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Hi, everyone. Uh, can you guys see the screen? All right. Ok. Um, we can see it. Um, people will be interacting with us uh, on the chat. Um, you can, um, start the presentation in like a minute or two in a minute. Ok, that's great. Thank you. Um, you guys can get started with the presentation. Ok. Um Hi, everyone. Um, I'm Doctor Nasim. Um, we're gonna be presenting on gastro emergencies today. Um, I'll be doing the first half and, uh, we have my colleague, Doctor, uh Selvan, he'll be doing the, the rest of it. Um, the second half, um, while we're doing the presentation though, um, I won't be able to see the chat but if you guys have any questions or any comments or anything, you can put them in the chat and uh Doctor Theresa will pick up on it. All right. So, um, if everyone can see, we'll just get started. Um, so we'll just start off with the case first. Um, so a 52 year old lady presents to the A&E with severe abdominal pain, getting progressively worse for the last three days associated with nausea and vomiting and she has been having intermittent abdominal pain for the last two years, mostly after eating food. She didn't think much of it and put it down on indigestion on further questioning. She says the pain radiates to her back. Uh, no fevers, no hematosis bowels opened, um, this morning, no changes, no low urinary tract symptoms, no unintentional weight loss. Um, for her past medical history, she's got some hypercholesterolemia hypertension. She takes some atorvastatin and Ramipril for her social history. She works as an office clerk, lives with her husband. She's mobile independent. She does not smoke and drinks alcohol socially. So with that history, um does anyone have any ideas um, what we might be talking about or um, what do you guys think in general if you can just write on the right on the chat or guys feel free to unmute yourself and speak if you would like or message in the chart either is fine. I believe the participants don't have that function to unmute and talk. Um, they can, um, type on the chart. Ok. Yeah. Ok. Ok. Um, so, um, that's fine. Um, we'll just go on to the examinations then uh from the end of the bed, she's sitting on the bed leaning forward. She appears to be in pain. Her chest is clear, equal air entry into both lungs. Her heart sounds are normal. Abdomen is soft, it's tender um, in the epigastric region. Mostly she's got a bit of guarding her news is three, which is for the res break of 24 and her heart rate of 109 other OBS are stable. She's had a 12 lead ECG as well which shows sinus tachycardia. Um, and for her investigations, um, her ene are fine. Uh, her at is a little bit uh, elevated. Bilirubin is fine. CRP is slightly elevated as well at 55. Um, hemoglobin and white cells are normal. So, amylase is also elevated. Um Any ideas? Anyone, what do you guys think if you can just pop it in the chart? Uh If you can make this interactive, I think it'll be really good for you guys as well. Anything. No. OK, then. So um you guys might have guessed it already. Anyway, we're gonna be talking about acute pancreatitis. Um It's acute pancreatitis is characterized by inflammation of the exocrine pancreas and is associated with acinar cell injury and both a local and systemic inflammatory response. It can be either self-limiting with mild pancreatic edema or have severe systemic inflammation with pancreatic necrosis, organ failure and death. Um So some of the causes. Um I think mostly in med school we, we learn um I get smashed which is um which is a good, which is a good way to learn. Um causes of pancreatitis. I think mostly when I was in med school, I remembered scorpion bites the most. Um So I is for idiopathic pancreatitis, which is around 10% but in the UK, the most common cause of acute pancreatitis is gallstones. Um alcohol being the second commonest cause in the UK at 25%. Um E RCP is also um one of the causes. So five in 100 patients having E RCP developed pancreatitis with one in 500 having severe pancreatitis which can be fatal. Um Other causes as you can see on the screen such as blunt trauma, uh steroid. Um So surgical procedures near the pancreas metabolic conditions. Um if infections such as mumps, coxsackie four B four virus, mycoplasma pneumonia infection. So, certain drugs, um it could also be acute on chronic pancreatitis, um certain autoimmune conditions. Um and also uh very important to remember. Pancreatic adenocarcinoma, cholangiocarcinoma, and periampullary tumors can also cause pancreatitis. So, for diagnosis, normally you'd need atypical history um and also elevated serum amylase or lipase three times of the upper normal limit. Um which would be 300 imaging CT MRI or ultrasound uh with changes consistent with acute pancreatitis. So, normally a history would involve something like severe epigastric pain, which our lady in the case had, which irradiates to the back exacerbated by movement, um alleviated by leaning forward, nausea, vomiting, um and other things like risk factors for gallstones. Alcohol history is also very important. Um As for physical examination, normally you'll have a tender abdomen which may be just tender, there might be voluntary guarding uh tachycardia tachypnea. Um There may also be reduced, bowel sounds if it's associated with ileus, um, fever can happen if there's necrosis of the pancreas associated with infection. Uh, reduced breath sounds in cases of pleural effusion. Um, I just wanted to show you those pictures. So the first one is the colon sign. It's, um, uh, hemorrhagic pancreatitis. Um, and also the second one is, um, gray turn side, uh, sign it's on the side, the fat flank area, you get some bleeding there. Um ok. For investigations, normally you do um a full set of labs. Um You might find deranged user knees um for having uh AKI I due to secondary third space fluid loss and IV fluid depletion. Uh you can have deranged LFT S in case uh the uh cause was a biliary stone. Uh You can have deranged serum Myla and lipase levels. C RP is an indicator of severity and progression of inflammation. Um Ultrasound abdomen is the preferred initial imaging method as it has a sensitivity of 75%. If systemically unwell, you can consider a Multiphase contrast enhanced CT Abdel vs which uh you do to rule out peripancreatic collections. Any necrosis, abscesses or vascular complications such as portal vein, thrombosis, PSE uh pseudoaneurysms and hemorrhages. M RCP can also be done to um detect or exclude biliary and pancreatic stones or if you want to plan any drainage of um collections. Um As for treatment, main goal of the treatment would be to alleviate symptoms and prevent complications by reducing pancreatic secretory stimuli. So, normally you'd treat with IV um and replace any electrolytes. You can keep the patients near by mouth when there's nausea and vomiting. Um Otherwise you treat the symptoms, uh pain relief and antiemetics. If there's signs of organ failure or if there's uh the Glasgow Emery score is more than three or the patchy score is more than eight, you can assess for HD U admission. Um If and if there's any imaging proved pancreatic collection, you can also consider ir drain. Um If there's necrosis of the pancreas with infection of the collection, you can consider antibiotics. Normally. Um For pancreatitis, you wouldn't use antibiotics because it'd be um a sterile sort of pancreatitis. However, when there's necrosis and uh when there's a collection, they are susceptible to infections. Any questions, anyone um or any comments, if there's anything you can pop in the chat, that's the first case. OK. If there's none, we can move on um to the case too. If anyone has any questions, we can still take them or if anyone has any questions, we can take them at the end as well. Ok. So I think we'll just go ahead and start with our case too. So this the second one is um a 28 year old gentleman presents to the A&E with bloody diarrhea. He complains of having 8 to 9 episodes of type 6 to 7 stools for the last three days, um, associated with abdominal pain, bloating and fatigue, pain, relieved on opening bowels, denies eating out recently. No sick contacts, no fevers, no low urinary tract symptoms. No unintentional weight loss denies any cough, cold symptoms. For his past medical history. He's got ulcerative colitis, um, drug history. He's on Octa 2.4 g, uh, twice a day. AOL, 0.75 g. Suppository once a day for his social history. He works as a personal trainer. He lives alone. Mobile Independent denies any recent travel does not smoke or drink alcohol. Um I'm guessing most people know what we're going, where we're going with this or is there any ideas? Any questions what you guys think is going on? Ok. On examination, he's got conjunctival, pallor, abdomen is distended, um tender in the lower le le lower left quadrant, no guarding chest clear, equal air entry, both lungs, heart sounds are normal. Uh New score is one for his heart rate. 109 a 12 lead E CG shows sinus tachycardia investigations. His potassium is a bit low at 2.4. His hemoglobin is 90 otherwise. Um mostly OK. CRP is slightly raised. So, so one person Saba uh said that could it be toxic mega colon toxin? That's a very good. Um That's very good. Um It could be um but uh it could be one of the what the pa patient is presenting with. Um, we just might need to find out what has caused the toxic megacolon because normally it happens in certain uh conditions as well. But that's a really good shout. Any, any other comments, if you guys were suspecting toxic megacodon, what uh what kinds of things would be pointing towards that in the examination? Do you think? Sorry. Uh Was that a question towards me or uh no, no to, to anyone uh anyone? OK. So there's a, there's a couple of things mentioned in the examination above that it could point towards that. So, abdominal distention, um you would expect slightly more guarding with toxic mega but ultimately, um what would diagnose it is called imaging? Um So imaging would also be part of the management. Anyway. Um it's just that when you're suspecting toxic megacolon, um you need, you need to do things a bit quicker. Um maybe change things a bit in the e to e assessment. Um And then once you get the abdominal x-ray, then that I can confirm. Mm Yeah. It's basically like um what K we said um if you're suspecting obviously an acute abdomen um or something like toxic colon, you'd need to do an A two E and you need to escalate it uh accordingly. Um OK. So um what we're talking about is an ulcerative colitis flare in this gentleman cause he's got a past medical history of ulcerative colitis. Um UC is a chronic inflammatory disease which is characterized by mucosal inflammation starting distally in the rectum with continuous extension, proximally for variable distance, often with an abrupt demarcation between inflamed and noninflamed mucosal. According to the B SG, typically patients with experience periods of relapse and remission and up to 90% will have one or more relapse after the first attack. So it's very important to um sort of keep an eye out for flares in patients with UC. So risk factors. Um The risk of ulcerative colitis is greatest in the first degree relatives. Um Interestingly, appendicectomy before adulthood is thought to be protective against the development of UC. Um The exact physiolog are not really uh not known. Uh NSAID uh use may exacerbate UC and increase the risk of disease flare ups as well. So for a history of um UC presentation, you'd need um some bloody diarrhea, fecal urgency or incontinence, nocturnal defecation, tenderness, abdominal pain, it would be mostly in the low left, lower quadrant, um, pain relieved on opening bowels, fatigue fever. Uh family history might be there as well. Um Examination if there's significant loss of blood, you'd find some pallor abdomen might be distended, there might be tenderness. Um You might also find some extraintestinal manifestations such as arthritis, erythema, nodosum after mouth, ulcers at theri or uveitis. Um, examination can be normal when it's mild to moderate disease. So, um however, uh bloody diarrhea and um frequency is uh in a patient with ulcerative colitis is pretty indicative of uh a flare up. So, for investigations. You do FDC uh to uh uh see how much anemia there is due to the blood loss. C RP is a good indicator of inflammation in UC. Uh fecal calprotectin suggests active inflammation in IBD U. Use any you can do to assess for dehydration and electrolyte derangement because there's a lot of diarrhea and you might be losing potassium and other electrolytes. Um LFT S low albumin can indicate protein losing enteropathy, nutritional status. Um You can also do other tests to rule out other causes of diarrhea such as thyroid functions where in hypothyroidism, you can also have diarrhea. You can do celiac studies um to as a differential diagnosis for diarrhea, stool culture, um to rule out an infective diarrhea, uh very important to rule out C diff and other causes as well. Um Iron studies B12 folate to assess nutritional deficiencies due to loss or malabsorption. Um For you see, it's very important that you do flexible sigmoidoscopy, which is the first picture. You only do it. Uh you only scope until the sigmoid colon, but most of the time this is um sufficient in the early stages um to assess as uh it's a distal disease. Um colonoscopy with biopsy mostly, uh you'd need it for uh diagnosing because you need to see the entire colon, which is where you see mostly effects and um you'll be able to take biopsies to actually see whether it is or Crohn's um abdominal X rays like Ky mentioned to identify any evolving toxic megacolon or bowel obstruction, which is very important. Um as patients with IBD can um have toxic megacolon. Um just wanted to mention a couple of things. Um So another thing you can test for is um Albumin as well. I think it's already mentioned there, but Albumin, especially when it's low in IBD can be a sign of a poor outcome after treatment. So it's along with C RP is probably one of the more important ones to have a look out for. And the other thing is when present with symptoms like this. Um, it's very important to look at what's already happened in the clinics in the past. So patients that you see often have regular in clinic, um, like annually or even, um more frequently than that. But it's very important to see what treatments they've been on previously, um, whether they've had surgery in the past. Um But it's when you know all of that information first, then you can see, ok, they've tried this, this and this and it hasn't worked. Um And you can see what the other options are then. So it's very important to get a full picture of what happened in the past first. Yeah, of course. Any questions, anyone. Ok. So this is just a little bit of histology. Um, as you can see on the left side, that's the normal colon. Um and the UCS on the right side you can see the crypt distortion and the abscesses. Um it's just a little bit of um just to get an idea. Um So sometimes uh when patients present with diarrhea and blood in the stools, you might not be able to differentiate between UC and Crohn's. Sometimes even in histology, it's sometimes difficult. However, there are things that are different or more common in UC and more common in Crohn's. So, uh for UC abdominal pain, you may or may not have it. But in Crohn's disease, it's more common uh depth of inflammation and you see is mucosal. Um whereas in Crohn's disease, it's transmural affects the whole length of the uh bowel wall and uh diarrhea is more severe in UC, whereas it's less severe in Crohn's disease um as for distribution, uh UC has a diffuse contiguous spread involving the rectum as, as the proximal gi tract. Um And it's the opposite for Crohn's disease, almost segmental noncontiguous spread where you have the skip lesions. Um less common rectal involvement and mostly involves the entire gi tract. Otherwise, um fistulas are rare and you see, whereas it's more common in Crohn's disease. So, um this is the modified true Love and wits criteria for classifying the severity of UC. So, as you can see, it's based on how many bloody stools you have per day, your pulse temperature, hemoglobin and C RP. We don't normally use E sr too much, but we could um that's also one of the criteria. Um So as you can see, it goes from mild to moderate to severe. Um I'll just give you guys a chance to look through. So obviously, as you can see temperature as well, um the more the higher your temperature, the more severe it is along with the number of stools per day. Um And as your inflammatory response increases, um your pulse and everything goes higher and the more blood you lose, um your hemoglobin goes lower and the C RP, the more higher it is. Uh it's a marker of inflammation. Ok. So, complications like we've discussed toxic megacolon. Um You can see in this x-ray that this chronic dilatation, especially in the transverse colon, you'd measure it. Um it should be normally more than 60 millimeters to be diagnosed. Um uh and there's a loss of post administration as well as if you can see it's uh there's no sort of posture in the transverse colon bed. Um Sometimes there might be evolving toxic megacolon. So you might need to do serial abdominal x rays or you might even need to do CT abdo pelvis to get a better look at the bowels. Can I make bowel obstruction, bowel, perforation, intestinal strictures, fistulas. Um One other very important thing to um note with you see is there's a chance of colorectal cancer around 3 to 5%. Um There's a higher risk if it's early onset of disease and longer duration and if they also have uh primary sclerosing cholangitis. Um Obviously, there's also the psychosocial impact, anxiety and depression, especially the worse you have it, the more number of flareups you have. And um if, especially if you've had got surgery and you've got a stoma, um all of these things can affect um socially as well. Ok. Um So the B SG guidelines for treatment of it's quite, it's quite in depth. Basically, you treat with five A SA um and then you treat with orally and also with enema and then you escalate the dose depending on how much where you start. And then you monitor for, monitor your renal functions as it's nephrotoxic, you do it initially um after three months of starting and then after initiation, like you do it annually um for patients with mild to moderate or moderate to severe UC uh or flare ups, you can give oral prednisoLONE, 40 mg and wean it down in 6 to 8 weeks if they're tolerating and if they're improving on it, um for up patients on maintenance therapy of high dose mesalazine, but they've had more than two courses of oral steroids in the last year or if they've got refractory, see, then you'd need to think about escalating to biologics or thiopurine at the TNF um loads of biologic options available. I think we start normally uh Infliximab or otherwise Adalimumab or there's loads of other ones as well. Um For osteo colitis. Um if the, um sort of uh mesalazine and the prednisoLONE and the Infliximab. Uh They don't work initially. You can give a rescue therapy of IV Infliximab certain regime or if that doesn't work within seven days. Um, they might need a surgical review for subtotal cholest uh with ileostomy as you can see in the picture. So you remove the colon and then you form an ileostomy and then they'll have a stoma there. Any questions, anyone? Oh, that's great. Um That would be the first half of the uh presentation. Um I think I'll stop sharing there if there's any more questions as well. Just, um, pop it on the chart. We'll be able to see. Can you guys see the presentation? Yes. Yes, you can see the presentation. Um So I'm gonna be talking about the next uh few cases here. Um So we've got a 52 year old man who has brought him to Ed after a fainting episode at work. Um, he was unsteady at his, on a feet, um, and fell to the ground, sorry, uh, fell to the ground without losing consciousness. He also had abdominal pain for a few hours and vomited dark material. Um, he doesn't really have any past medical history of not, but he does have uh chronic back pain. Um, and in terms of drug history, uh he's been taking Ibuprofen daily over the counter for his back pain, any initial thoughts so far, um, we'll just talk a bit more about this. Um, so one of the, uh, students have said upper gi bleed. Yeah. So that's certainly something you're thinking about, especially with, uh, abdominal pain, um, with Ibuprofen. Um, and he seems to be, um, sort of hely unstable as well in terms of his symptoms. Hopefully we'll get on to the examination. We've got other, um, input as well. Esophageal viruses, good shots. Yeah, that's a, that's a very good shot. Um So viruses is uh can, can be a cause of uh symptoms like this, but it's often it's the cause of um it's the ology of the condition itself. So if you, if you suspect a bleed, for example, then viruses would be the cause of that bleed. Um So yeah, that's a very good, very good shot as well. Um In terms of his observations, his BP is 85/50. Um heart rate is 125 respiratory rate is 28. Um and a certain temperature are normal on examination from the end of the bed, he looks pale. Um he's got tenderness in the epigastric region. Um he hasn't got any guarding or rebound tenderness. Um but on digital rectal exam, you do find some Melina. Um so having heard all of that and seen the examination results, what would you do at this point? A two E assessment? Yeah, so as any emergency A two E is, is what you should start with. Um So start with airways, make sure they're patent. Um, make sure his breathing is ok. Um Look at the circulation part is where you find that he's hypotensive. Um, he's tachycardic. Um, so you and he looks pale as well from the end of the bed. Um, so he looks hely unstable. He, he's obviously gone into shock. Um So at this point, you would put two wide wall cannulas in both, um, both arms and then give him some uh fluid resuscitation. Um Another important thing is also to get um a group and save done as well. Um Because if the blood's come back, the hemoglobin's low, um then you can transfuse some blood or if you feel that he's actively bleeding, then you can give some group oo um immediately by activating the major hem hemorrhage protocol. Um And then you would finish your examination by looking at um in e you would see the abdominal tenderness and with any gastro examination, always do a digital rectal exam. Um And that's where you find Melina. We've got other um comments, a two E assessment escalate as appropriate to gen surge, likely diagnosis, bleeding from ulcer. Good shot. Yes. Yes. So, um that's a good point as well. So if you're suspecting a bleed from the ulcer, um what do you think caused the ulcer in the first place for in this case? Maybe we can just go back to the history. Yeah. Is there any risk factors that this uh gentleman has that you guys think. Yeah, nsaids, Ibuprofen, um, Nsaids um is a big risk factor in this case. Um So how, um, Nsaids cause ulcers is basically they inhibit um, prostaglandins, um prostaglandins uh protect the mucosa. So when you, uh, when it's blocked, that's when it's causing mucosal damage. Um, and then when these peptic ulcers start bleeding, that's when the, um, you get the coffee ground, vomiting hematemesis. Um And you get Melina as well. Um So yeah, anything like nsaids is a big risk factor. So, um you guys guessed correctly. That's a upper gi bleeds we're gonna talk about. So before you move on really quickly, um K I just wanted to say um the member that said uh at assessment escalate appropriate to gen surge, likely diagnosis, bleeding from an ulcer. I just want to uh so, um how different departments work? Um I in certain hospitals, they have different um escalation pathways when it comes to upper gi bleeds in the UK. The first person that we escalate to as the f one would be the person who's gastro on call. So gen surge is not gonna really touch any patients who would present with uh a case like this. Um Your best bet would be definitely to, to call whoever is on call for gastroenterology. Either that's the um the registrar or the consultant, they would be the best help. And if this person is hemodynamically unstable as Well, uh, JJ Serge will be happy to come but they, their hands are pretty tight in what they can do when it comes to scoping them and trying to get it resolved. Um, just on that same note, um, even, even when you escalate to gastro, um, it will be after you resuscitate and after they are somewhat stable you, they won't be, um, scooping someone who's absolutely, um, hemodynamically, unstable like that unless there's no other choice. Um So as Ky was saying, you need to resuscitate accordingly as per um the with the fluids and any bloods, any anything necessary like that. All right. Um So we're gonna talk about some of the common causes of upper gi bleeds. Um So, gastric ulcers, um esophagitis, uh H pylori uh which tends to cause gastritis, duodenitis and uh gastric erosions as well. Um Nsaids like in this case, uh esophageal varices like someone mentioned earlier. Um mallory wise to. So these uh tears occur in the digestive tract, especially when there's been a lot of vomiting in the first place. Um Often it's a slightly more fresh blood uh as opposed to um more coffee ground in color. Um But in that case, you would have to investigate what caused the vomiting in the first place. Um and pausal hypertensive gastropathy as well. So, um this condition is caused when there's portal hypertension. Um Also hypertension is normally caused by liver disease, things like cirrhosis. Um What that causes is some venous congestion around uh the stomach. Um And it basically causes damage around the mucosa as well. Um So these are the common conditions that cause upper gi bleeds in terms of signs and symptoms um in your history. Um if there's any abdominal pain, uh do a Socrates assessment. Um but obviously, you won't be getting too much if the patient's very unwell. Um So the history normally happens after you resuscitate the patient. Um Ask about how many episodes of vomiting they've had, if this is the first time, if they've had any dark stools, any reflux in the past, um or any liver disease, um drug history as we've talked about uh things like steroids and nsaids, which can cause ulcers and um alcohol history as well in terms of science. Um In this case, uh there was hypotension and tachycardia. Um things like clubbing goya Parma, erythema, they're signs of uh chronic liver disease. Um So that, that's the, that's the things you would find on the gastro examination, uh uh jaundice, uh epigastric tenderness, um Hepatomegaly. Um And as we mentioned before pr exam, uh you would find Melina. Um So for upper gi believe there is there are methods to risk assess. Um And these are the two scores that we can use. There's a blusher score and a rock score. Um The Blaser score is normally used pre endoscopy. Um So this, this course we usually use um when you're risk assessing someone, whether they can be discharged and managed as an outpatient or whether they definitely needs to be kept in. Um, just take time. Have a look at the table though. Um, so normally if the, if the score is less than one, then you can say, ok, they, they're safe enough to be discharged and they can have an outpatient O GD and managed as an outpatient. Um, any scores higher than that, then you would consider keeping them in. Um Rockall score is um a, a good predictor of mortality. Um So if you have a look at the table there, you can see um the things you call for things like shock, um other comorbidities, um anything you found on endoscopy, so any signs of bleeding uh and the actual diagnosis as well. Um So if you um having a score of maybe seven or above, um you're having more than a 27% chance of mortality. Um So it's, it's a very good method to, to see uh what the outcomes are in terms of management. Um Like we've talked about already, the a to reassessment is very important initially to resuscitate. Uh blood transfusion is important. Um Normally, if the hemoglobin level is less than 70 you would uh transfuse um other reasons you would transfuse as well is if there's been a large uh drop in the hemoglobin as well. Um You would consider Vitamin K if there is a raised. Uh I nr um normally, if it's greater than 1.5 you would consider giving Vitamin K Um IV PPI is um not always given. So sometimes it's not recommended pre endoscopy to give IVP P. But if you have done the endoscopy and you've found um a possible site of bleeding or if there's clotting shows that uh that shows that there's been previous bleeding, then it's a very good method of stabilizing the clots as well. So things like IV preop is very good to use antibiotics, um, is very good uh to use as well. Normally for prophylaxis, um, it's not routinely given. Um but uh measure the infection markers on the bloods. Um And then you can risk assess and see whether they need the antibiotics. Um Normally the endoscopy needs to be done within 24 hours. Obviously, it can be done a lot sooner. Um After you've called the gastroenterologist on call, whether they've got active bleeding, but if you think they've got active bleeding, they may need it a lot sooner. Um And within the endoscopy itself, they may use things like adrenaline injections, um, and endo clips as well, uh which stops the bleeding from the vessels. Um, when things, when the bleed has stopped, sometimes they can rebleed as well. Um And in those cases, a repeat O GD may be needed. Um And when it's treated on the repeat O GD and it still hasn't stopped. Um, it's at that point where you would um, refer to interventional radiology or er, or surgery where you can consider embolization or other other treatments. Um, variceal bleeds we've touched on a bit. Um, previously. Um, so there are, there are several treatments, things like terlipressin band ligation, er, and transjugular intrahepatic porto systemic shunts as well. Um, so when the viruses are normally around the esoph esophagus, then band ligation is preferred. Um Terlipressin often is started as soon as a variceal bleed is suspected, but the thing that will stop the bleed ultimately will be the band ligation. Um And when those two things haven't really worked, then you can consider the um transjugular treatment. Have you guys got any questions with anything I've covered so far? All right. So we'll uh move on to question. Um So a 62 year old man presented with um a one day history of dark stools and hematemesis on examination, his heart rate was 100 and five. BP was 90/55 and his abdomen was distended with shifting dullness and it was non tender on bloods. You can see that the hemoglobin has dropped to 68. The white cell count is 5.6 and the platelet count is 97. Um He's already been resuscitated. He's been taken to theater for uh O GD under general anesthetic. Um And you can see in the endoscopy that he's got large viruses um around the lower esophagus, er with carry red spot, but there's no active bleeding and some blood is seen around the stomach. Um, amongst those options. What do you, what do you guys think is the best management at this point? Just pop it in the chart, guys, don't worry about being wrong or anything like that. It's, this is all for good discussion and uh we'll all be learning. Gruffy po has said it's a ok. Any other shots? Five seconds. Um Saba is saying, I'm confused as usually there is initial management and most appropriate. So which one were you looking for? Um So most appropriate management I would say. So what the question should say is what's the most appropriate management at this stage? Uh E is subset E OK. More taking Graphy Paul said E if A is not enough. Yeah. So the correct answer is E um the, I think there's, there's been a mixture of A&E in terms of the answers given. Um And this is a very difficult question. So don't worry if you've got it wrong. Um So the two things I did mention earlier, tin and bind ligation, they both do work. So tin is given for hemostasis of the bleeding. Um But if you read the question here, it says um he's got large varices around the esophagus. Uh He's got cherry red spot but no active bleeding. Um So appropriate management at this stage, he's already been taken to endoscopy. He's got no active bleeding. So, hemostasis has happened already. Um But he's got a cherry red spot, which basically means um he's got a chance of rebleeding. Um So when he's already in endoscopy, then band ligation is the best option here. But obviously, when he gets back to the ward, then Charley press would, would, would start up there. But the first thing he would do at this stage when he's at endoscopy is band ligation. Um So you had those who answered e well done. Um But this is a very difficult question. Any other questions? If not, we can move on to the next case. So uh we've got another case. So a 40 year 48 year old woman with a history of migraine headaches presents to the ed with altered mental status over the last several hours. She was found by her husband acutely disorientated and increasingly somnolent. Her husband reports that she has consistently consistently been taking pain medications and started taking additional 500 mg, paracetamol pills several days ago for lower back pain. Further history reveals a medication list with multiple paracetamol containing preparations on examination. You find that there's a, a scleral icterus, there's mild right, upper quadrant tenderness and there's asterixis as well on bloods. The prominent er results are the A LT has increased to 6498. The bilirubins jumped up to 95.8 and the I nr 6.8. Um So out of all the things you've heard there. What do you guys think might be going on? Um Ky, there was uh one question from one of the students r um she's asked, when would we use beta blockers in the previous case? I think. Oh, that's a, that's a good question. So beta blockers are normally used for um primary and secondary uh prevention. So they don't really give much use in an acute stage. But when you found that when the O GD has been done and hemostasis has been achieved, um and the patient is more stable. Um usually beta blockers is given a secondary prevention to prevent further bleeding from the viruses that they may already have. Um So normally a patient with varices will need to be monitored and further OG DS will need to be planned. So, in, in that stage, they will need uh to be on beta blockers really. Um So, but in the acute management, it doesn't really give, give much, but that's a great question, right? So back to case four, any thoughts on this one so far. So uh the things we're um thinking about here is basically um um from the history, sorry, sorry. Um There's been some comments. Um Guffy has said liver toxicity, Saba has said paracetamol overdose. Um Those are very good shelves. Uh And they're both technically correct, but what has those things caused? Ultimately, what's the condition here we're talking about or Yeah. What's specifically to do with the liver? What are we talking about here? Uh We've got some suggestions, liver failure. Yeah, that's absolutely correct. So, um, the uh the patient here has gone into acute liver failure. Um So we'll talk a bit about what things uh cause liver failure, how, you know, they've got a acute liver failure and then we'll come back to the case and see um how you can tell Basically. So, normally liver failure presents with a triad of jaundice coagulopathy where the inr is created at 1.5. Um and hepatic encephalopathy as well. Normally, when you see all the, all three of those things suspects acute liver failure. Um So something that's uh often mischarged as liver, acute liver failure is where there's no preexisting liver disease. Obviously, it can w when the, when the patients have previous liver disease that can cause people to go into liver failure. But when it's acute, normally there's no previous course and it's a new presentation. Um So bear that in mind as well. Um And the two phrases we I've mentioned are fulminant, hepatic failure and acute hepatic necrosis. Those two phrases are also used in, in exchange for acute liver failure, but more commonly nowadays, acute liver failure is used. Um So if you go back to Asia, um the ac is massively increased. Um So there there has been hepatic toxicity and uh he hepatic injury. Um the bilirubin jumped. So you know, there's jaundice and you can see that on examination as well. That's coagulopathy because the I NR has increased to 6.8 which is above the threshold of 1.5. And if you go back to history, um it says that the, the patient was found with altered mental status, um acutely disorientated and increasingly somnolent. So those kind of things point you more towards hepatopathy. Um So that's, that's what you're looking for in terms of history and examination. Um in the history. Obviously, when you can see that the patient is jaundiced and they'll tell you that they look yellow as well. Um find out when that came on. So was that a few days ago, a few weeks ago or has it been there for even longer than that to find out when that came on? Um That point is very important because acute liver failure can also be categorized as um hyperacute, acute and subacute. Um the hyperacute phase is I think within a few days of jaundice, um acute phase is slightly f er longer than that. So maybe weeks. Um and then the subacute phase is slightly weeks to months. Um So find out when the jaundice came on really um again, with pain. Socrates is very important, alcohol use chronic pain as in this case, um was not really chronic, but because of the headache, she's been overdosing on the paracetamol um which has ultimately caused this uh liver injury. Um Any previous drug history, travel history is important. Um This is where you're thinking of things like um viral hepatitis. Um Have they had any tattoos abroad? Um, have they taken any supplements recently? These kinds of things also point you towards liver injury as well. So try and get a full picture and in terms of the signs on examination, you're looking for abdominal tenderness in the right upper quadrant, jaundice, nausea and vomiting, hepatomegaly, um abnormal pupil reflexes, muscle rigidity, uh decerebrate posturing. So these kinds of things point towards encephalopathy, um slightly more difficult to pick up. But when you're suspecting liver failure, always remember to do a neurological exam as well. Um Without that, you can't really say how bad the encephalopathy is or whether they have it in the first place in terms of investigations. Um So as I mentioned before, I nr is very important to have a look at. Um if you're suspecting autoimmune hepatitis, then measure the antibody um antibody levels. A viral hep screener toxicology screen for drug use. And uh in this case, paracetamol level will be very important as well. Um Sometimes it can be very obvious what the cause is. So in this case, um your first differential would be paracetamol toxicity. But when you've started treatment and you've not necessarily seen any improvements, then by all means, think about all the other things that can cause uh acute liver failure as well. So always keep an open mind. Um in terms of imaging ultrasound abdomen, uh it is very important to do very early on. So you can spot things like cirrhosis, any biliary obstruction, any liver changes. Um And if you're uh suspecting biliary obstruction, then M RCP would be a uh an excellent add on test. Um So if you find any stones um that, that may have caused the patient to go into acute liver failure, it's very important. Um a slightly more uh well, slightly more uncommon test as an ultra Doppler of the herpetic vein. So this is when you think of things like uh Bod Chiari syndrome. Um So on this test, you're looking for things like um uh the flow of the uh blood in the hepatic vein, um the amount of signal there is there. So those kinds of things pointing towards whether there has been any uh thrombosis in the in the portal system. Um And you've been looking at B ra month at point. Liver biopsy is also done, but normally this is not done in the initial stages and biopsies take time to manage time to organize and get the results back as well. So the management of acute liver failure is not going to be hinging on liver biopsies. It can be done as a uh it's a very good procedure to confirm your initial diagnosis. But normally it's done when you don't really know what's going on and that's your last port of call or you know what the diagnosis is and you want to confirm it, but normally liver biopsies take time to organize. So, hepatic encephalopathy, um, is quite, uh, slightly more challenging to, uh, grade. So, as you can see in the picture on the top right corner, um, that's asterixis or also called the hepatic flap. So, what you would do is ask the patient to put their hands up, er, put their hands back and stay in that position for say, like 30 seconds. And what you would see is the, the hands would start flapping and that does, that doesn't necessarily happen continuously. It can be completely normal and then suddenly you will see a flap and it will go back to normal and it will go back to a flap. So always s examine over an extended period of time and um look out for those random flaps before they come back to normal again. Well, normal as in, in the examination and there are different levels of grading. So there's 1 to 4, so one being the mildest and four being the most severe. Um, so there's impaired awareness, sleep changes, maybe the attention span changed. That's on the milder end. If they become more lethargic and they become more confused, then their grade of think opathy would be a lot higher. Um, a good way to monitor. Um, well, uh measuring ammonia levels is not a good way to monitor is what I meant to say um a, a build up of ammonia is the, is basically the toxin that causes the encephalopathy. Um Usually a level greater than two shows that it's poor prognosis. Um And you can measure it uh at any point in the admission, but it doesn't necessarily provide any outlook on their monitoring as well. So if the ma levels drop, it doesn't mean that the encephalopathy is resolving. Um So it's a good idea to get and measure when they first present with the encephalopathy, measure the levels of hernia and then see what their outcomes are likely to be. Um If the patient's got known cirrhosis um caused by infection, electrolyte, imbalance, diarrhea, vomiting, constipation, uh upper gi bleeds, these are the kinds of things that you're uh looking out for as well. Um Just one more thing um when we were talking about um liver injuries and also I think from the case itself, there was a paracetamol um overdose, I mean, maybe not overdose, maybe there was a toxicity. Um It's always important to remember that um to weigh your patients or to just have a rough idea of how much they might weigh based on just uh just having a look at them whether they might be over 50 K GS or not. Um Because normally we just tend to um prescribe the 1000 mg of paracetamol four times a day and if it's regular, um this might be too much uh uh for a patient who weighs less than 50 K GS. So it's just a small thing to keep in mind. All right. So, um in terms of management of acute liver failure, um when it's obviously it's very difficult to grade encephalopathy. So as an F one, by all means escalate to your seniors at this. Not, not at this point. When you first suspect acute liver failure, always escalate and um always ask for a bit of help grading things like this. It's not easy. Um Normally grade two and above is managed in ITU. Um And as an F one, it definitely it won't be you that's discussing with ITU for transfer, it would be registrar and above. But at your stage, it's important to be able to recognize what, what they're presenting with and being able to tell the registrar exactly what's going on, especially if they're not around. Um in it. They can always uh they can also prevent sepsis, uh manage other complications like cerebral edema and as well. And normally they're incubated if it's grade three or four um liver transplant assessment, uh it's very good to do that very early on. Um often liver transplants won't be done in the the hospital or trust urine um or in your local region. So have an idea of where the nearest liver unit is, where they'll be doing these assessments and transplanting as well. So when patients present with acute liver failure and um you know that it's heading towards a liver transplant. Um always refer early and don't worry if you don't know how to do that. Um The consultants and registrars will guide you on how to refer and who to refer to as well. Uh regular blood glucose monitoring is very important as well. Um So in acute liver failure, hypoglycemia is quite common. Um the liver is a very important organ for um glucose regulation. Um It's the primary site of gluco neogenesis. And so when that uh process has stopped regular hypos is uh is a possibility. So, always replace with IV glucose whenever you suspect it or see it on blood glucose monitoring, uh electrolytes can be deranged as well. So always monitor things like sodium potassium magnesium and these electrolytes will need to be monitored often twice a day, um or sometimes less than that, but usually it's twice a day when they're in acute liver failure, um cultures to monitor infections. Um and just a couple of things uh focusing on the cause of the liver failure. So, if you're suspecting viral hepatitis, so the screen has come back positive, then you would start thinking about um antivirals, uh paracetamol um toxicity. So, acetylcysteine infusions, um checking of the paracetamol levels, um whether it's coming down um with paracetamol toxicity, you can often um find a table. Um It might be on the, on your trust guidelines or in the B NF. Um So have a look at the table, see if the paracetamol level's too high, then um you can often follow the guidance that's on the and as we mentioned before B Chiari syndrome as well. Um So when uh this is a, a condition where there's thrombosis or uh some kind of clot in the portal system, um and that's treated with anticoagulation, which is long term. Um angioplasties can be done as well. Any questions before we move on to another, another question, I think as well. Just to mention um when we're talking about liver transplant and all of these things, it's very important to have um an alcohol history for the patient because if they are consuming alcohol actively or currently um and if they don't, don't have a plan to stop, they probably won't be a candidate for liver transplant. It's a very good point. Oh, so um I got another question. So a 20 year old woman has presented to Ed with four weeks of abdominal pain and swelling. She had no significant past medical history and does not drink alcohol. Her only medication was the oral contraceptive pill on examination. She had tender hepatomegaly with shifting dullness consistent with ascites. What is the most likely diagnosis? So, pop your answers in the chart. Uh We've got some comments. Um autoimmune hepatitis will affect the transplant. Does um do you know Cobby um whether autoimmune hepatitis affects transplant? So, um autoimmune hepatitis can be controlled um in the acute stage with IV steroids. Um I'm unsure as to whether the long term outcome, whether they can go ahead for, to a transplant is possible. So, I don't know if you know, if anything. So with autoimmune hepatitis, typically, um, the cases that I have seen the woman ha are, well, they're not exactly women, they're actually quite teenage years. Majority of the patients I've seen they're female and they present very young. So you will on the gastro or you'll see a 17 year old sometimes 19 twenties. Um And because of they're, they're so young and the only other comorbidity that they have is autoimmune hepatitis. They still put them on the transplant list. Um A and K, you, you are correct. Um We try to dampen the immune response so that when the liver transplants goes through it, you know, it doesn't reject and also um the same uh condition doesn't um you know, do the same thing um which damages the liver, but it's, it is quite a complex. Uh It's, it's quite a complex thing with the transplant. Um like the criteria, but they, they typically will look over the case and, and still decide whether or not the patient needs uh wi will still have the transplant but no, it does not exclude them. Um We've got two members um replying uh but Chiari um yeah. Option B. Yep. So uh that is uh the correct answer. Um So in this case, the um patients presented with abdominal pain and swelling. Um they're on the pill. Um and they've got tender hepatomegaly and shifting illness as well. So I know that acute liver failure doesn't necessarily need to present uh or it, it doesn't necessarily need the patient to have previous liver disease, but they can present acutely with hepatomegaly and ascites in this case because ascites can build up very quickly uh in a short space of time. So the thing that's pointing you towards Budd Chiari syndrome is the oral contraceptive pill, which puts the the patient at a hypercoagulable state. Other things that do that as well is things like pregnancy, um pregnancy, um any he disorders as well, they put a hypercoagulable state. Um So yeah, in this case, you're thinking about uh about chiari um acute pancreatitis. Um doesn't usually present like this. Uh the abnormal pain would be epigastric doesn't really present with hepatomegaly. Um So it doesn't point towards that. Um cholecystitis, uh liver cirrhosis, not really. Um thinking about that as well. Malignancy is possible. Um But in this case, the oral contraceptive pill is the, is the main point to take away here. So, malignancy can cause um this presentation, but it would be the pill that's causing the blood cure syndrome. Does that make any sense? Um I think we're at the end of the presentation. So, if you guys have any questions from either the previous um cases or from even now you can just pop it in the chat. Also, guys, please uh make sure to give us some feedback by completing the um feedback form which I've just posted in the chart. Um It will be really helpful for us to um improve our teaching for our next future sessions. Thank you Hosner for posting it. Um And yes, please guys. Um please do provide feedback. It's really helpful. Um Any uh any constructive criticism as well as all, all well placed.