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Hi, everyone. Welcome to this talk and thank you very much for coming. Um It's my pleasure to introduce Doctor Abhishek Gray who is a gastro uh reg that I've had the pleasure to work with. Um, so I'll hand over to him now. Hello, everyone. Um Good evening and thanks for joining uh this evening. I am. I understand you're all after work. So, uh you must be quite tired. So I'll try to uh keep it very short and succinct and um yeah, I'll make sure that things are basically sort of made suitable for your level. But prior to that, can I quickly just confirm that you are all able to hear me and able to see my presentation? You can just put a yes in the messages. Oh, perfect. So, uh today's presentation I have particularly um put it and tailored it for uh foundation doctors and, and above, below the level of the registrars who does the weekend covers and it could occasionally be called to the wards of in the Gastro wards and they face a lot of anxiety and apprehension about what they do. I, so the thing is why are the causes of concern. So I did sit with a couple of my um F one and F two s who I have worked with previously and a couple of things which I have actually understood is that I believe the, the acuity of these patients and the fact that they are so sick on the very first instance, sort of throws people off and make them a lot anxious. This is true that they can deteriorate very quickly if not intervene at the right time. But if intervened, they can all completely recover. And these interventions can be very simple. Most of them have got uh like guidelines on the internet or even your trusted internet where you, wherever you work and um but it just needs a knowledge of it and awareness about what's happening and where we go from here, things are very basic. There is no rocket science here when I was on F one at your level. I remember our um med medicine lead. Tell it to us that among all of the specialties, gastroenterology patients are the ones where in the signs and symptoms will just show it, show itself to you. There isn't any ECG S and I'm, I'm not disrespecting any other specialty but just comparing it with others, there is no ECG, there is no um there is no CT scan of the brains to sort of um interpret before you actually arrive for a diagnosis. There is no chest X ray to interpret before you arrive to a diagnosis. It's all in front of you. Examination wise, everything is in front of you. Abdominal examination is something that you could get the findings straight away. So it just needs awareness and a high suspicion index of what's going on. Um, unfortunately, in, in the DG HS of the district general hospitals where I presume most of you work, there is no out cover for uh gastroenterology except for breeders unless you have the fortune of working with a medical reg on call that day who is um from the gastroenterology. But uh from the out call is only for uh bleeders or the gi bleeders. And I know in London it is covered by the gi bleed drench, but outside London where I work. So I work personally in Surrey uh wherein it's covered by uh gi consultants actually. So they are only available for calls for patients who are acutely bleeding to decide whether they need to come in for endoscopy or not. Um Apart from that, uh they are usually not available for advice for any routine advice which you would otherwise get in hours. Um So it's basically a bleed only service out of hours. And my point here or my objective here is to uh make you aware of uh very common cases that may basically come up in the gastroenterology wards. And these basics would at least um allow you to manage the acute phase or to tide over the acute phase before help arrives. Um I have made the slides very interactive because I don't want to be the one talking and I believe you can derive maximum benefit out of it if you, if you actually interact and if you progressively uh you know, give the answers to what I'm asking uh or contribute in the management plans because, and, and II, honestly, II, promise I am not going to be judgmental on anyone. No questions or stupid questions, no answers or wrong answers. II completely understand if obviously, if there are certain answers which does not actually abide by uh what the right management should be. I will go through the principality of why you, what you are saying is not correct and why we need to do something different. OK. So speak out um indirect and I think uh that way we can make this session more fruitful. So our case number one, I'm just waiting it out. So you are on the weekend on call. And thankfully, your me committee has arranged for a nice pizza lunch which you all are now enjoying. The medical take is quite, quite uh the wards are stable and all of a sudden the ward cover f one gets fast fleet to see a patient who is in the ward admitted 3 to 4 days back with pneumonia and has suddenly become hypertensive. And I want you to basically look at the points which I mentioned OK, because that will have a lot of answers in it. You arrive, arrive to assist the patient, have a look at the drug chart as you would always do. So she has been started on treatment with Oxy and Cycin for her pneumonia, which I presume is the antibiotic of choice. And most of the drugs across the country, she is on paracetamol, she is on or off for her pain. She is also on Warfarin for a point to note that her dose has not been changed. She has the same dose as before you start to assess the patient and midway into it, you're suddenly alerted. Your, your the first cranial nerve is suddenly signaled by a very foul offensive odor. And in a couple of seconds, you notice her pretty sky green colored hospital gown, Truss suddenly become black. What do you do? Uh just volunteer, just tell how do you what, what do you do from here? The patient is in front of you. So I've given you the observations that's the observations of the monitor uh because the nurses have kindly adjusted to the monitor has currently done a 12 DCG prior prior to your arrival. You have done a systemic examination which is also normal. What are your thoughts? What's happening? Anyone? Yeah. Um You, you can just um sh unmute yourself and sh I think uh that would be more useful but someone's written hemorrhagic shock, someone's written a and major hemorrhage protocol. Yes. Good. So major hemorrhage protocol is something that you would straight away do. Good as a moment. Yes, Melina, yes, Melina from a, from an UP G um and what would you do? Yes, you would put out the major hemorrhage protocol. Um Why do you think you need to put out the major hemorrhage protocol? Why can't you, what would, what changes if you put out the measure? He protocol? Good. Stop Warfarin. Yeah, that is that. Yeah, that would that definitely we would do. We make sure that the patient does not receive a warfarin dose. But my question is what does major hemorrhage protocol change? If you put it out compared to if you try to manage it locally, then has anyone been a part of the blood transfusion is ready? Yes. So um with major hemorrhage protocol, we would note that a lot of people come in, you mobilize the entire trash team of the hospital because as someone quite rightly mentioned over here. Exactly good. So more senior health would arrive good. So what happens is the whole whole system is mobilized. As you can understand this situation is a period is it could be a potential period situation. And with per situation, you can suddenly the patient can suddenly become drowsy and lose the airway. And that way at that time, air prediction might be necessary. So you mobilize the medical reg you mobilize the crash call. I you mobilize the I two I two people, you mobilize the anesthetics and most importantly, immobilize the porters who will then come in and on your on your um request, they can get in blood through the flying squad. Now someone just say blood transfusion is ready. Can anyone tell me what blood group is? Those bloods that come through the flying squad? Oh good, good eg so or blood comes in. So how many as many number of units you want? And then when you, when all of this happens, how would you, so say for example, you want to now intervene, what would you do? You can shout out. So what would you do from here? So how many of you? Sorry, I just wanted to let you know um people can't unmute themselves so everything has to go through the chat. Oh, everything has to go through the chat. Ok. Ok. Sorry, sorry, sorry, I didn't know that. Ok. Oh, ok. Yeah, that's fine. So good. So rhesus fluids transfused. Yes, absolutely. So we give recess fluids, we transfuse them the the uh blood. How many of you would do a VBG? You agree? We shouldn't do a do AE BG. So we have done a V VG before and uh someone sent off bloods and the V VG shows an HB of 65. Uh Yes, to make sure airway is clear clear. No vomiting. Yeah. So the patient, this patient hasn't vomited thankfully uh airway is clear, but yeah, I'm coming on to a scenario where we might, we might have this issue. So we've got um hp of 65 ph of 7.37 lactator, 1.1. So what does lactator, 1.1 show lactator, 1.1 shows that the tissues, there is no tissue ischemia. As of now, the tissues are being perfused but the HB has fallen down so that, that's dangerous levels. Um PH is fine. So which means patients not acidotic. So not got normal PO two PCO two and bicarbon. So no problem with the lungs. So as you can understand. So uh doctor, when you mentioned about airways clear, no vomiting, as you can see with the BG values, uh PO two PCO two bicarbonate would be, would be a little off the charts, isn't it? If there is vomiting and then they aspirate the vomitus. So that, that sort of, you know, is, is a major reassuring factor that um the airway is more or less clear. So set of the bloods. What would you, what would you do? So, so ABC management, someone had said a two E assessment. Very uh very good. Uh Previously, Doctor Tira. So yes, a two E examination we would need to do um IV access. How many IV accesses do we need? I do need uh then uh as many as we can get. Um Yeah, I mean, we wouldn't want to uh two is ideal. Yes, two is ideal. Um we would want to put in so that our uh our um guidelines say two white board break Cannulas inside. But um in reality, we don't find much free can and I can assure you with someone with a BP uh in double digits, you would struggle to put a day can in. So, II prefer to put in green ones through the anal veins. And um if obviously green is a diff is difficult, uh pink is also fine. So our aim is basically one is for blood, one is for fluids or whatever medications we want to give, but one can, needs to be kept free for bloods, um, fluids. So between fluids and blood. So say for example, you have both at your arsenal. So you have got o negative blood with you and you have got fluid in your arsenal. Someone's hypotensive. What would you prefer to give? Is it blood or is it fluid? So blood replacement blood. So yeah, uh what will, what might happen if we get fluids? So say for example, um you have got a plasma light in front of you. Um, would we just push it through or we would still go with blood hemo dilation? So, yeah, that's correct. So, hemodilution. So we are already getting someone with an hp of 65. So the oxygen carrying capacity of the blood has significantly reduced. So if you are to, if you have to push fluids through it is definitely going to cause more hemodilution. Uh as Dr Dash has just mentioned and um this hemodilution will further impair uh perfusion of vital organs in our body. So yes, we would prefer to push in blood PPI how many of you would go for PPI how many of you would not give PPI you know, so I let me give you the answer. I think that that will make it easier. So um if you see normal practice is basically to give people just give PPI S because if, if there is an ulcer sitting down, you want to reduce the uh gastric and the secretions to further, further injure it and then further cause the bleed. Whereas um there's a uh there was a very old study which was done uh back in Hong Kong and that's known as the Hong Kong Protocol. The Hong Kong Protocol purely mentions that you give uh PPI S only if there, if you have done an endoscopy and there is a stigmata of recent bleed uh because sometimes PPI S can mask small ulcers. But um I mean there is no right or wrong answer to it. I have worked in multiple set ups and people have done differently. I think at, at the end of the day, it just boils down to what you are more comfortable doing. Uh If, if you, if you choose to give ppi you have your reasoning. If you choose not to, then I think you also have your reasoning because you can then refer to Hong Protocol um blood and clotting products we have already mentioned and um reversal of anticoagulation. So this patient was on Warfarin. So Warfarin, as we all know is a Vitamin K antagonist. So we basically need to give uh something which will regenerate the regenerate our uh clotting factors. And which is why we give Beriplex. And can someone tell me what Beriplex is? Because I've just used a brand name here. Um What is the, what is very actually has anyone seen? What is? OK. So, Beriplex is basically uh no, it's not Vitamin K Unfortunately, Vitamin K is available as phyto me and uh but Bex is basically two thrombin complex concentrate. So uh no, not pax pex is a is a, is a um is a solution of multivitamins. We give it for people suspected of uh thiamine deficiency, but it's not PEX. Unfortunately. Um So valle is basically prothrombin complex concentrated. It basically acts on the uh coagulation pathways to create to synthesize more Vitamin K and synthesize more um sorry, synthesize more clotting factors and that will uh in turn allow or um facilitate more clotting so that the bleeding is slowed down if not completely stopped. Um So it's very important if say, for example, the patients on uh do a uh like, you know Apixaban or Rivaroxaban, we all know that there are uh antidotes available. Now with the name of Adex and Alpha. Um that's a different discussion for some other time. But um there should be, there should be uh protocols existing in your trust um about use of these agents and they still still need to be um approved by uh the hematology reg of the consultant on call. But yes, um there are agents available now. Um this patient is hypertensive. So we clearly agree that this patient has gone into a shock and the management of shock is is aggressive fluid replacement. And when you're aggressively fluid replacing someone, it's very important to do a fluid balance uh monitoring and uh fluid balance monitoring is also we need to have a clear um measurement of what the output is. And catheter at that point of time is is very important because uh you don't want to cause androgenic heart failure in someone by giving them like a lot of blood products and a lot of fluids if necessary. So catheter is very important and that needs to go in the first instance, OGD. So once you have resuscitated the patient, once you have done your bits, um you have to do an O GD. So how will that happen? So you basically speak with the out of hours out of hours endoscopy consultant or the register, who, who uh whoever is on call in your trust and then brief him briefly or heard about the case. Go ahead and facilitate that usually out of hours it takes place in seaport, which is basically theaters. So a lot of people that again needs to immobilize, to facilitate the procedure. Now, how many of you have uh had this thought? And when, when someone actually explored this thought to me, I find it found it very amusing. But uh I think this is something that goes in the minds of a lot of people. Um, people have told me that patients been bleeding continuously. They've called up the gastro consultant uh on call and they say patients too unstable to scope at the moment. And uh please can you stabilize the patient and then let us know once things are getting better. And there has been the other end of the spectrum wherein they have called up the consultant and then briefed him or about the situation. And they say, well, the patient is not too stable. Why, why does he need an out for scope? We can do it maybe tomorrow morning when and also the the will be available. We don't need to do it on anesthesia. So this is this conflict between when patients too unstable to be scoped versus too stable to warrant an urgent scope. Um What do you think uh might happen? So say, for example, if this particular patient who's got a hemoglobin of possible around 65 or maybe around 70 because that's a BBg hemoglobin, what might happen if, if you scope this patient now without necessitating because ultimately, that's the definite of management, isn't it? So what might happen anyone? Oh, so um remember that when the hemoglobin is too low, the body is trying to compensate. So if you remember the patient was tachycardic at a heart rate of 120 BP, very low of 80 systolic. So remember the body is trying to compensate, the heart is trying to beat quite fast in order to uh maintain perfusion to our white organs, like brain, the kidneys and the and the heart itself. So while doing that, it's basically working in an overdrive. And if anyone works in an overdrive, they become stressed. And if you then put an endoscope down down the patient's food pipe, that creates a lot of additional stress, which might be too much for the heart to take in. Um There have been a lot of, there have been some instances where patients have had a cardiac arrest with a with a scope in and that that can happen because you can't stop it, but you have to minimize the impact of stress on the heart as much as possible. Uh And which is why it is very important that the patient is stabilized. At least with a target hemoglobin of 18 usual target hemoglobin. We uh we aim around 70 but except for gi bleeds, certain cardiac causes of ischemic heart disease and certain hematological conditions that we then uh uh go for, go for um a higher, higher um threshold of hemoglobin. So yes, uh they've been going to an arrest you to hypovolemic shock. Yes. II completely agree. That's exactly what I said. And uh type one, am I doctor you wrote? Type one? M I, so I think what would be basically type two M I rather than a type one M I. Um So yes, was it too stable to warrant an urgent scope? So the question might come. Well, we have stabilized the patient. Um Why can't you just come in and do it? Just remember because out of hours um if the, if the endoscopy is to happen, it basically needs the gastro consultant to come in the anesthetic team to mobilize endoscopy on call nurse to come in. The c support needs to be kept ready, which could otherwise have been used for more um more urgent procedures. So it's clearly about the balance as to should we do it now mobilizing the emergency team versus can we monitor and see if we can defer it to the morning next day? I appreciate that this is a decision which cannot be taken from your end. But this is a decision that will be taken by the endoscopist at the end of the day. But what I'm trying to, what I'm trying to um emphasize is that what rational we think of while we make certain decisions and though it might sound unpopular with uh with the on duty doctors at, at, at that point because it means that the definitive management is not being implemented, but sometimes we have to take a step back, assess the situation, take a stock of the situation and then then proceed in terms of uh what we do or uh for the best of the patient. So yeah, so the patient now it comes to vial bleeds. So how would we change our management? So say, for example, this one, we all know that it's possibly a non vital bleed, uh vital bleeds. When do we suspect it? So someone's bleeding out, someone's having a Mirena, someone's having hematolysis. Uh Number first question, when do we suspect it? And what group of patients should, can we suspect uh where it should be? So patients with alcoholic liver disease? So yes, I agree. So, II would just generically say liver disease because not, not always. Um all liver diseases are are due to alcohol. Yes, I agree that uh it it does, it does um occupy a major percentage of the etiology of liver diseases. But you can have uh certain people with uh portal vein thrombus which can cause portal hypertension causing collateral circulation, which you call as viruses and they can bleed. Uh patients can go into cirrhosis from nonalcoholic fatty liver disease. Yes, exactly. So, stigma of chronic liver disease, you might not be able to see it all the time. But yes, patients with portal hypertension um or mainly patients with a background of liver disease. You have to, you have to think about, think of the other lines. Um remember the signs of portal hypertension clinically. Um if you look at the bloods and and do a clinical examination or even look at the radiology reports, if someone's got background of liver disease, and um if you see that the platelets are low and they have got uh an ultrasound which was done previously, which mentions about splenomegaly. So low platelets and a splenomegaly on a background of liver disease is basically portal hypertension because portal hypertension would cause hypersplenism with the spleen uh working in overdrive spleen enlarges in size because obviously, it's, it's uh working too much. And while it does that it also starts uh eating up more of platelets. So you end up into a state of thrombocytopenia and the splenomegaly. So this these two, if you see in a in a liver patient, you can be absolutely assured that clinically, you could say that this patient has the total hypertension and obviously, things would come after that. So you can do an O GD for very screening, you can do a fibro stent to quantify the cirrhosis, but these will all come later. But clinically, these two findings and you know that we are we are dealing with a patient with portal tension. Now, uh what do you think uh with very, if I ask your opinion, how would it manifest, would it be hematosis or would it be Melina? I mean, either of them can happen but what's most common and, and very short leads? Right. So, Doctor Shiva Ramani, you feel it's Melina? Ok. So hematosis hematomas. So I would, I would say it's more hematomas unless, unless the patient, um, unless the patient is actually lying down in a position and, and is quite bed bound. Um, the reason behind. Yeah, II agree. It could be both coffee ground vomit. Yes, I mean it would be coffee ground vomit but saying that not always vital bleeds would be coughing on. You can see red blood coming out. The reason I'll explain to you because what happens is the viruses are mostly in our esophagus or in the gastric. Uh and, and the stomach rectal virus is completely different. They will manifest as Frank pr bleed. I'm not going into that aspect today. The other, other places were common places of viruses are our gastric fundus and our esophagus. And if ulcers bleed, they ooze if varix is bleed and have a good picture just coming up a bit gross picture. But it will give you an idea about how varices bleed. They are just like a fountain just like a fountain. So think about it. Uh There's a, there is a vessel which is bleeding and it's ruptured and it's just bleeding like a fountain into the stomach. The stomach will do a reverse cell to throw it out So it will be more hematomas rather than, rather than Melina. Yes, we will have some amount of Melena because of gravity. Some, some uh amount of blood will pass down, but most amount of blood will basically come out from the top end. Now. Coffee ground vomit. Yes, I agree. It could be coffee ground vomit. But most of the, if, if it's an active ongoing where you should breed the reason why it would not be coffee ground vomit. Because if you, if you reconnect the physiology, the blood basically needs to be digested by the gastric acids, which then creates a compound called as acid hematin. Now, this acid hematin is what gives the vomitus this coffee joint color. And when we say coffee, no color, you will face, you will see a lot of uh people explaining this to you. Any brown vomit or any dark vomit is is not coffee, no vomit, coffee, no vomit is is just like if, if people who drink coffee, if you look at the bottom of the cough, there are like coffee Granules. So they look just like that and it is just because of the compound forming. So now think about it, you, someone has actually been bleeding and then that blood has been digested by the gastric secretions, they will throw this out, but the patient is continuously bleeding. Now that blood will not get enough time to get digested by our gastric acids because the gastric acids will need to accumulate, will need to digest. So when they then vomit out, it will be fresh red blood coming out. And if it's fresh red blood coming out, most situations, it would be, it would be indicative of a varix. Now, why am I, why am I being very particular about, um, suspecting someone with a varix or not? Because if someone's got vial bleed that needs to be, that needs to be controlled straight away. And for that to be controlled, we need a particular drug called sterin. Now, I understand a lot of, a lot of you are aware about 30% you have seen 20 been given. Can someone tell if how does 20% act, what does it cause in one word? So, yes, exactly. Vasoconstriction, it causes vasoconstriction. So a systemic vasculated, it sort of constricts to then starve the viruses of any blood. Because at the end of the day, these varices are not supposed to be there. These viruses are collateral circulation because of portal hypertension and uh the changes in and around the liver. But these uh vasoconstriction will then the vessels constrict and then starve all the collateral vessels. So there is nothing to war it out, but there is nothing to bleed actually. So which is why 20% is very important and make sure that before you give 20% to anyone have a look at the ECG because as you can understand it starves the blood, it just constricts and the every, every possible place is stopped. So in people with ischemic heart disease that can actually precipitate another attack of ischemic heart disease. But the question comes, would you give Terlipressin in someone in the background of ischemic heart disease or would you not give? Because if you give, they might have an attack of M I, if you don't give, they bleed out. So I think at the point where saving a life is important, uh the person is going to die quicker from bleed rather than having an M I and then dying from there. And the best way to find out is basically looking at the ECG, have a look at the ECG have a look if there are previous Q waves or not because Q waves are indicative of previous ischemia. OK. So we can do that. Antibiotics. Yes, definitely give a third generation or fourth generation closin. Uh We use um we use Ceftrixone in our trust. It might be different in your place. So, um there are studies which has shown that giving antibiotics has actually improved uh outcomes of mortality in this uh in these cohort of patients. Um Since they LMO tube, um how many of you have seen one? It's not used much uh frequently these days because endoscopy is so readily available. Um You can, you can just go, go into youtube and see how they are deployed. It's basically uh there are three tubes with three endings like this. And one is an inhal ending. One is a gastric ending and they've got balloons in it. So I've recently done a case where we, uh, went down with a scope and we could only see blood inside the stomach, only see blood inside the stomach, nothing else. And the patient was actively bleeding. And then we realized that we won't be able, we are not finding a point to actually therapeutically intervene. So at which point, we had to put the six second in to, to, to get that pressure, pressure effect on the, on the stomach and, and, and avoid and, and sort of reduce any, any ongoing bleed from there. And that actually works. It's, it's a very unpleasant feeling because it's a big tube. It's a big thing that comes down, goes down, your uh goes down your food pipe, but it is life saving in some instances. Not, not always that it would be able to help, but sometimes it did help our patient because that patient is still alive. So, uh since taking mo tube is something worth having a look. Now, I'm going to show you if obviously that you are not able to remember the management because I II uh appreciate there's a lot of things to do. Just Google and find out this thing. So they had done an audit. A couple of uh I think it was done in 2022 when they came out with this um acute upper gi bleeding bundle. Now, this will have everything here. So just print it out. If you just Google and just say A B SG um um upper gi bleed bundle, it just comes up straight away, get it printed out, just it's just like a checklist, do everything what is mentioned over here and it's a very uh it's a very definitive um uh treatment guide for what you need to do with these patients. I particularly put this uh um thing here as you can see the top picture is what an esophagus looks like if um if they are um if, if it's normal and the one below is these um inflated bits. I don't know if you are able to see my mouse. I don't think you are able to, but um these ones are the viruses, the inflated ones are with the varices. And if you see the 12 o'clock uh engorged vein, there's a bit of a redness around the, around the top. Uh That's basically what we call as a red sign. This means impending rupture. And now for the picture that I was mentioning, so that's how a V bleeds like as you can understand, it can be calamitous and, and it, it, it's just burs out like a fountain. So if you're not able to control it, it literally patient will bleed to death straight away. Um For these patients, we basically need to do two types of scoring, which is basically the Glasgow black foot score, uh which is a preendoscopy score. It the theoretically anyone with scores of zero or even one can have an outpatient scope doesn't need to be done as an inpatient because they are relatively stable. Uh anyone above one are um they need to have an topa scope. But again, this scoring systems are a little uh they're a little misleading. So I would say at your level, just do the scoring when you refer and just uh speak with the uh speak with the consultant and then it's their decision whether they want to scope out hours or, or eight hours. Uh just like a pre endoscopy score. There is uh the Rockall score, which is a post endoscopy score. Basically, it mentions about the chances of uh mention about the prognosis. Like someone with a, a score of less than three has got good prognosis score of eight has got high risk of mortality. And um obviously, it it requires a calculation as you can see after endoscopy because uh from endoscopy, you are going to find out whether there's an evidence of bleeding or not and that's how it's scored. Um Now two pictures I II thought of showing you. So endoscope, this is, this is an endoscope, uh how it looks like. Uh This one basically goes up to the T two and not beyond that. So any any sources of bleeding up to T two can be visualized with a, with an endoscope. If the patient is bleeding somewhere else, unfortunately, won't be able to colonoscopy can only go up to the terminal ilium and not beyond that. So, a huge part of the small bowel can be uh it is literally unsual by endoscopes. We haven't yet um got the routine scopes to um to visualize this in a, in an acute setting. Yes, you can do um single balloon or double ball endoscopies. But again, that's, that's much more uh niche and complex and beyond the scope of today's discussion. Um So the endoscope goes in and this is a couple of therapeutic procedures that we do. So say, for example, this is an ulcer which is basically there on the G OJ. Um As you can see, there's an oozing blood from there and we just a apply the clip over here. So these are clips which you can deploy through the endoscope. You can also put injections. So this is basically this syringe is filled up with adrenaline and the end of this wire is basically a needle which comes out of scope and you can just inject around the bleeding site. Not this one though, because this is a very short bleed. But uh say for this one, if you just inject around the sites of the blood, so this adrenaline will cause some uh local vasoconstriction and pressure effect uh causing the blood to causing the bleeding to go down. I occasionally stop, but we usually don't stop with single therapy. We usually either go for double or sometimes triple therapy. So they can get either injection or clip or injection and something which is called as core or ABC that we call blood work, uh coagulation. So we go on to the ulcer site. So if, if we have to think about this particular ulcer, uh we would basically just take the pot over there, inject, find out the bleeding point where it's bleeding. So if you inject the adrenaline around, you will find the bleeding point because it will uh momentarily stop bleeding and then you just burn that area of the artery to burn the vessel and then you basically controlled bleeding. Does it work all the time? Uh No, not 100% but at least, um you have done something and endo ligation. So this is very important for vial bleeding. It's another look as to how they can bleed. And these vial, these are basically like rubber bands which basically go on to the top of it, suck the mucosa and then just put a band around there. Uh If you do an endoscope, this band, then the tissue underneath that, that sort of completely disappears, it wears off and the bleeding stops as you can see it goes on just looks like this. And uh six weeks down the line when we rescope them, it just becomes like this So you have basically destroyed the viruses and uh significantly reduced the chances of bleeding CT angio. So who do we do ct angios? So say, for example, uh we have found someone who has got a big ulcer, say, for example, and we trying to cauterize, but it's so big that we cannot, we cannot clip them or we cannot cauterize them. Because if you, if you cauterize beyond a certain point, you might, you can risk um perforating the bowel. So they, so when these patients have the initial endoscopy, they will either come to you and say this patient has got no evidence of um any, any source of bleeds in the upper gi tract up to D2 when, when the endoscope can go. And uh so if the patients should bleed further, they would need radiological intervention because it might be that the patient is bleeding from much below the small bowel or maybe D four or there on. Or the ulcer may be so big that endotherapy or endoscopic therapy is not possible because the clips are definitely not going to grab there. You're not going to be able to do a PC and there is no point putting a big area with uh adrenal injection. So what do you need to do? You need to starve the vessel that supplies the bleeding point? And that is where CT Angio comes into picture because what will happen is the radiologist will do a quick CT scan to then see where the bleeding point is. And then they will put in with uh put in some coils to put the angio and then we will completely embolize that vessel. So that vessel is gone, you are not bleeding anymore. So that's how these bleedings are controlled radiologically. Why do we not go in for CT angios and straight away if they are more definitive because you are destroying a vessel straight away. If we can give a chance for our endoscopic therapy to cause healing without destroying a certain vascular, we would want to do that. But wherein it's not possible, let's say, for example, the patient is going to be not very fit for a second scope. Then uh CT is what, what we prefer. Uh Just for a point, if someone's asking this question, there is no colonoscopic intervention of controlling bleed because we don't do that. No one for you. Someone's had a bleeding ulcer treated comes to the ward. Four days later, the nurse comes to you and say patient hasn't opened his bowels for the last uh four days. Uh hepatitis, minimal complaints of abdominal discomfort. As a gastroenterologist. I would you be very happy? Would you be sad? Would you be concerned? What would you do? What would you tell the nurse how many of you would be happy? How many of you would be sad? Even in deep thoughts, I can see nothing coming up. No wrong answers. No So, yeah, just shout out or probably just right down here. Ok. I think people are too deep with thoughts. So let me see. II as a gastroenterologist would be very happy or someone just said check bowel sounds any strictures. No. Uh, let's not go into, let's not dig into that territory. Um Yes, I would definitely check Bowel sounds to make sure that the patients are obstructed. Uh But yeah, there is no, the bowel sounds are completely fine and there are no strictures at all. So as a gastrologist, I'd be very happy because remember the best, the best available laxative to us is blood. Unfortunately, that's not marketed. So my point is if blood is inside your gi tract under no circumstances, it's going to stay there, the body is just going to throw it out whether by the down end or the top end. So if someone has not opened the bowels for the last four days, from a bleeding perspective, you can be absolutely assured that there is no bleeding ongoing, makes sense. So you can just tell the nurse. Ok, let's, let's um, I'm not worried about from the gi perspective, but let's give him some negatives and uh see how things go on. It might be that once you get the lax, there will be a bit of black stools coming out, but that's completely fine. As long as the HP doesn't drop, remember whatever blood has been there in the gi tract will need to come out. So you will have a bit of uh Monina in the first couple of days. But the the question to ask the patient is, are you looking at your stool color? Is it becoming light or not or are you, is it getting the normal yellow color back? So that is the question that we need to ask. So even if there are black stools, as long as the patient is stable, as long as the HP is not dropping, you can be completely reassured that there is nothing going on. So my second question, my second thing is interpreting lefties. Now, um this is something that are designed for face to face teaching where people are able to shout on. But I I believe there is a technical impairment here. So there are four sets of LFT S here which I have put down. So remember just for the interest of time, I'll go through it. So it is very important to understand. What aspect of LFT are we looking at? Is it the transaminases? What concerns us or is it something else? Remember, transaminases are released from hepatocytes or the liver cells when they break down because of a certain insult to them, they break down and they release the transaminases. So these transaminases are high transaminases are an indication of uh hepatocytes or liver damage that has happened. But does that mean that the damaged liver is not working? No, what our concern is whether the synthetic function of the liver is maintained or not. And the synthetic function of the liver is indicated by three parameters, albumin, bilirubin coordination. Apart from that, you are going to look at someone's developing ascitis or not. If they're decompensating or someone's becoming opic or not. Because remember, the urea cycle takes place inside the liver and if the liver is not working, ammonia would not be broken down into liver. This ammonia will go up to the brain causing them to have to. So these are the couple of things that we need to keep in mind. So if whenever you in N FT you are needing, you need to check these aspects. So with that background, let's delve into the first one. So what do you think of this one? Would you be very concerned about the patient? Is this patient uh about to die or about to become more unwell or there is something that you can just monitor? Ok. So let's come into that. So we're seeing a normal bilirubin here. We're seeing a normal inr here. So there is no coagulopathy. There is no hyperbilirubinemia albumin is normal. So what we can see the synthetic function is maintained. Yes, at moment, liver function is maintained. So, II would say synthetic function is maintained. That's the correct term. So whenever you present, so uh going forward, whenever you present to the consultants or 10 years, and if you have to mention about liver function. Always mention synthetic function is maintained because um liver function is more of an umbrella or a generic term. So as you can see, the synthetic function is maintained, what we are seeing over here is transaminases, rice. No, is it a posthepatic cause or a hepatic cause? Well, the L4 is more or less closer to our transaminases. So it's very likely uh hepatic cause. Now, why did this happen? A lot of reasons? Maybe some drugs, maybe alcohol, maybe starvation, maybe the ischemia, anything can happen. So something has actually hit the liver heart, which is why the hepatocytes have broken down. Now how to understand whether it's alcohol driven or non alcohol driven. Remember the, this is where your at and see someone mentions ability is normal. So no worry, II wouldn't, I wouldn't call it an obstructive picture because um I'm, I'm coming into an obstructive picture later, but I would not call it as an obstructive picture at this point in time just because the force is very similar to the alk transaminase and the aspartate transaminase. So remember the first sort of follows the transaminases. So unless the AOS is uh significantly and disproportionately raised compared to the transaminases, we would not uh consider obstruction clinically. Although every patient with liver functions needs to have a noninvasive liver screen and an ultrasound. At the first instance, without that, there is absolutely no point referring them to a gastroenterology registrar or consultant because we would just say do a liver screen, do an ultrasound and then come back to us and obviously the patients encephalopathic, in which case, you need to speak to a level three that is a critical care or maybe to the c support nurses. But uh as long as we don't have the answer to the liver screen or the ultrasound, there is not much we can do in terms of trying to target how and where we to be. Ok. So this one, so A and T is low in alcoholic. Yes, that's correct. So the ratio is very important. So I normally the ratio between transaminase to aspartate transaminase is two is to one in alcoholics. This ratio is completely reversed, it becomes 1 to 2. So the ast will be twice the number to ad in alcoholics. And obviously the comity would would go up but comity is, is a good indicator for alcohol, but it can also go up in certain other conditions. So this one is possibly it could be uh it it could be ischemia driven, it could be drug driven. Um it could be something else but it's definitely uh it could be an alcohol one, it could be, but alcohol is not the sole etiological factor here coming on to the second one. As you can see, we've got a billion of 300 with normal transaminases. Mm the T of 514 either is the over here. So in this situation is what we call as a classical picture of alcoholic hepatitis, right? Because the bili is through the roof, the GGT is again raised as doctor Moman mentioned. And uh INR is also deranged. So something has hit the liver really hard. The synthetic function is deranged. As you can see if there is hyperbilirubinemia, there is coagulopathy. So the synthetic function is gone. The ast is more or less double ish if not completely double. And uh the GGT is also quite raised at first is again, more or less. All right. So this is what is a classical picture of alcoholic hepatitis. Obviously, the history would give you the answer. This one is what we call is an obstructive picture. As you can see the billy raised more than normal, but it's not alarming levels. There are disproportionately raised out force inr is normal and the rest of the transaminases abnormal. So this is what I would strongly suspect uh observe the picture. And the fourth one, it's a little tricky. It could be anything because the bills raised. S are raised. Four is also gone up. So it could either be something like a but syndrome wherein there is a portal obstruction by a thrombus. It could be a stone sitting down there. It could be anything or it could be say, for example, a stone was there and it has now passed out and the liver functions are now normalizing So this is something that would need uh very careful history, taking investigations and um and imaging, cross sectional imaging. This is a real life experience and, and, and I had this experience literally a month back in my previous hospital and this has taught me a lot of things. And the reason I have put it down is because this is something that you are very likely to come across. So this is an 18 year old otherwise fit and find girl presents to us following three days, history of nausea and vomiting, generalized loss of appetite. She returned from a holiday to Italy last week and the bloods basically showed this amount. So these levels so initially seen by us, I was um I saw her liver screens were sent off. Ultrasound scan was done, which was all normal. So there was no obstructive cause, no posthepatic cause. OK, just to mention that there is no history of alcohol abuse, um just social drinking, but obviously she hadn't drunk for the last one or two months. Um So this was a test. So inflammatory markers were fine, more or less. OK? Um A LD is significantly raised and this has not happened. No, the time when I got involved with this patient was when I was handed over by the night team over the weekend and I was the more medical age on Sunday morning when this patient I was handed over that this patient has been becoming very agitated, abusive to her parents. I mean, she is someone who was literally like was very sad when her parents were leaving her in the hospital. But now she was abusive, she was beating them, she was punching them, pulling out her intravenous lines. She also had two episodes of hypoglycemia overnight and and the morning when we saw her date two blood tests, this was what it was. So how many of you can tell me which are the indicators which are indicating towards what's happening. What are the red flags here? So when I was handed over, I was handed over saying, well, the patients bit um agitated, I think she's a galic but her liver functions are improving. The ad is coming down to four digits from five digits. Uh Billy is not very raised at 96. Exactly odd behavior, very odd behavior, but that is where my first points come in. So your high index of suspicion will help you over here. And yes, the patient was encephalopathic, but why would she be encephalopathic? Because encephalopathy is a sign of liver failure. So if you look at the bloods, you would see that there are a lot of indicators which indicates that the liver is failing. So look at the bilirubin on the first glance, it might seem ok, it's, it's raised but it's not significantly raised. But look at the day zero, bilirubin 42 day two, bilirubin, it's 96. It's literally doubled. Look at the inr it's gone up from 1.1 to 5.4. So we have got hyperbilirubinemia, we have got coagulopathy. She's encephalopathic. And remember one of the, one of the symptoms of liver, liver failure is hypoglycemia because the gluconeogenetic pathway is then impaired. So this patient has got hypo four signs of liver failure. So she was an impending liver failure who basically went into the stage of an acute liver failure. Yes. Raised I and transaminases. Well, transaminases is coming down. So again, ii personally, I am not particularly very interested about transaminases. And as long as they are coming down, they're as good as useless to me in this scenario. So raised inr coagulopathy, hypoglycemia, hyper BM and encephalopathy are the ones which will click in my mind that OK, this patient needs to be intervened. This patient needs to have discussion with the tertiary unit with the liver I two and possibly for a liver transplant. So we discussed this patient with Kings and Kings immediately delighted her there for a potential liver transplant assessment. This patient would not survive without a liver transplant. So the take home points do not forget the signs of liver failure, bili hypoglycemia and nephropathy escalate immediately. As definite treatment might not be in your center, it might be in a different center. So people in London, Kings and Royal free of the centers, people up North Leeds is your center. Um I think to the East. Um Edinburg does um transplants so and so forth. So yeah, keep your eyes open. Anything unusual to your eyes could actually be unusual, which might be missed out by your colleagues. So just escalate and escalate, escalate, escalate and, and things. So no questions or stupid questions and you are not wasting her at this time and you might actually end up saving her life and your s the patient's family, your colleagues would be actually thankful for your, for your um awareness. So, thank you. And I look forward to further questions if you have, unless I've already already overloaded you with a lot of information if er, no one has any questions, um just wanna say thank you very much. Um Abhishek, it was a great talk. Thank you, everyone else also for attending. Um I've put a link for the feedback form. So if you could fill that in um after which you can claim your um atten certificate. Thank you very much and thank you Abhishek once again. Thank you, Marish. Uh pleasure to see you again, right? I'll end the, I'll, I'll end the live now. Um If anyone needs er, anything else you can email mind the bleep, er, if you need any help about the feedback form certificate. Abhishek. Thank you very much once again and thank you everyone else for attending.