Okay, that was a lot to cover, so I'll do my best to see if I can do the same. Okay, so just a schematic again to orient ourselves back to the past esophagus, stomach, and we're now getting into the small intestine. So what I'm going to try to cover right now would be disorders involving the small intestine to include celiac disease, obscure GI bleeding, small bowel obstruction, and mesenteric ischemia. So celiac disease is an autoimmune disease of the small intestine, specifically involving the duodenum. We have exposure of gluten, which is then leading to an immune system to respond inappropriately and causing inflammation and thus damage to the small intestine. Not all is known as to, you know, what causes it in certain populations, but there is a genetic predisposition. We see some HLA, DQ2, DQ8 type of genetic mutations that we know are being passed down in 1 in 10, you know, if there's a family history, 1 in 10 chance you can have it passed down. What is gluten? So, you know, we are living in a very healthy society nowadays compared to before. So this is something most people already understand, but just to break it down, gluten is protein that is found in wheat, barley, and rye, not just wheat alone. So it gives the dough its doughy texture, but it's found not just in food, but in cosmetics, hair products, skin products. So some people are just purely avoiding gluten in their diet. They could still be inadvertently getting gluten, other pathways. So we have to educate the patient if they truly have celiac disease to, you know, understand all the environmental factors that could be exposing them. So the other, excuse me, I'm going to go back. The other thing that I wanted to kind of mention here is there's true celiac disease and there's something that's also gotten more popular, which is gluten sensitivity. And I think that's our biggest challenge as gastroenterologists, a lot of people will come in with outside just, you know, testing or just symptom, constellation of symptoms that people would think, oh, you must have celiac disease, but without proper testing, accurate testing, they could be miscategorized. And then they're going down this lifelong, you know, gluten free diet, which is not just, you know, kind of a burden to them, but also it's costly because gluten free products are not cheap and you have to keep looking for them. And that lifestyle is a permanent lifestyle. So we have to be, you know, at some point, make sure they had a proper testing and we'll go into that and to, you know, be accurately classified. So if we don't know that they have celiac disease, how do these patients present? Some of them are completely asymptomatic and they happen to have a genetic family history. That's how we, you know, test them and find them ahead of time. But if we don't, you know, test in a timely manner, things kind of progress to more severe coming on the right side of the slide. So some people would just have fatigue and anemia as a beginning complaint. So we talked about the duodenum being like an iron area where iron absorption is done. So we'll have iron deficiency is common finding. Sometimes we'll have like B12 and folic acid deficiencies as well. And then their main constellation would be fatigue. Other times as things progress, we'll have abdominal pain, cramping and diarrhea being one of the more common complaints. And then we get more severe with malabsorption, weight loss leading to that. And then in children, we can see growth failures and then obviously bone density impact because of vitamin nutrient malabsorption, so that can lead to osteoporosis as well. So diagnosis, again, we typically can use serological less invasive techniques. But the key is to be on a gluten-rich diet, not gluten-free. So a lot of times I'll get patients who are already on a gluten-free diet to symptomatically control their symptoms, but they don't know they have celiac disease. So we actually do recommend, for accuracy purposes, they go into a gluten-rich challenge. So they'll eat a certain amount of gluten daily for a couple of weeks, and then we'll test them with blood work. And the type of blood test that we do recommend is tissue transglutaminase antibody or TTG for short, and specifically the IgA type. And this is first line. It has a high specificity and sensitivity. So that's why we recommend that over some of the other options that are older, like deaminated, glidin, peptide, and endomyceal antibodies. Sometimes you'll see doctor's offices ordering a panel of tests that'll include all of them as well. You have to be somewhat mindful because this is an IgA test. You have to know that sometimes people can have other immune deficiencies like IgA deficiencies, and then this test could be somewhat not as accurate. Endoscopic biopsies are the gold standard of the small bowel to diagnose celiac disease. So sometimes you can have no symptoms, and we're looking because somebody has iron deficiency, and we find this, and we're not sure if they have celiac or something else going on. So then we will take them to endoscopy. Or you can just go straight to endoscopy and skip the blood test. So again, endoscopy is banking on the fact that you have gluten exposure. So if you're already on a gluten-free diet, that can sometimes underrepresent the damage. So we could call it a normal biopsy and miss celiac disease in some patients. So again, if they're on a gluten-free diet, we encourage gluten challenge. Now if somebody already has celiac disease, we're not going to re-challenge them if they've been accurately diagnosed. So then we do surveillance biopsies just to know how they're doing also. So you just have to have it the right context. So if you're going in for initial diagnosis, we recommend on gluten. But if you have already been diagnosed and you're on a gluten-free diet, then we want to see how it's regenerating and looking off of gluten. So context matters. So what does it look like when we do endoscopy? For the duodenum, we can see a couple of different changes. We'll see reduced folds, blunting of the villi can do that. They look more flattened. There's a scalloping, kind of like this scallop appearance that we can see on the surface right here of the wall. Because of the nodular appearance, things like that, it just gives rise to these types of findings. So typically when we see these, these are kind of alerting us that, hey, something might be going on. But this is not necessarily only celiac disease can do that. Any kind of inflammatory process, Crohn's disease, other things can also mimic these things. But these are kind of related to celiac disease as well. So what is our treatment? We don't have a medicine, but we typically go on a gluten-free diet, strict avoidance. So it's not that, oh, I'm going to eat a gluten, you know, bread here and there that can still lead to active symptoms. If you really want good control and lack of downstream complications, like the flow chart showed earlier with like vitamin deficiencies, osteoporosis, other complications that you don't want for these patients, then you need to be on a strict gluten-free diet. Other times we do introduce steroids and things in refractory patients, but this is usually the foundation of treatment. Moving on to the next topic, which is obscure gastrointestinal bleeding. So this is not your obvious bleeding where you have melanoma, like Dr. Guha mentioned, or hematochezia, which may come later, which is bright red blood. This is a patient who's typically has had endoscopy and a colonoscopy. We haven't found the source, which is about 10% of these gastrointestinal bleeding. So then we further subcategorize that into occult, obscure occult GI bleed, and obscure overt GI bleed. So in occult patients, you know, we don't see blood loss from day to day, but they may be continuing to drop their blood counts, showing signs of anemia. And then in overt bleeding, you're seeing either melanoma or hematochezia, but you just haven't been able to locate where it could be coming from. So in these types of scenarios, obscure bleeding, you typically have 75% of those cases coming from the small intestine, and the 25% can still be upper GI or colonic sources. So there are multiple causes that affect the small intestines to bleed. So sometimes it can be inflammatory, such as in the first top left. We have Crohn's disease, inflammatory bowel disease, which can affect the entirety of our GI tract, known very commonly to affect the small bowel, deep penetrating ulcers that could be oozing and bleeding over time. There can be ulcer disease as well, associated not just with Crohn's. But if somebody is taking a lot of ibuprofen, Motrin, the NSAIDs, like Dr. Guha mentioned, it can not just affect the beginning portion of the small bowel, like the duodenum, but sometimes further down as well, like in the jejunum and the ileum. So those can bleed. And then, of course, these arterial vessels that stick out from the surface called dulafoil. I mean, you can't miss these. These are, when you find them, they're quite satisfying. It's like a jet stream of a pump. And these are sometimes difficult because they're so small, and they can dive down under the surface of the lining. So we have a high chance of missing them on our initial look. That's why we have to keep looking. And then, of course, angioictasias can affect any part of the GI tract, not just in the stomach. That was mentioned previously, like gave or other portions of small intestine are common to see. And these are just like spider-like veins, an artery in a vein kind of malforming into this really small millimeters at times of lesions that can be difficult to locate. Then we have anatomical defects called Meckel's diverticulum that we can see in the distal small intestine, and that can also lead to bleeding sources, vessels. And lastly, growths anywhere in the GI tract, like tumors that can also be hypervascular and ooze and bleed. So how do we evaluate obscure GI bleeding? So typically, we start, if somebody is presenting with overt bleeding with melanoma, you would think it'd be an upper GI source. You'd try an upper endoscopy. If you think it's a really brisk bleed, you might be missing something lower with hematochezia. We still sometimes do both directions of endoscopy and colonoscopy, or in a sequence. We start with an upper. We don't find a source. We go for the lower, because most of the time, we'll find the source in those two locations. But if we don't, then we think there may be something in the small intestine. So we deploy these pill cameras called capsule endoscopy, where it's kind of like a huge, described as a multivitamin, rounded, soft capsule, which has a video device inside that's taking images as it traverses through the small intestine. And this is something that we can dispose. It's disposable. And the patient does not have to fetch back, typically. And it's recording the entire mucosal surface of the small intestine. And we can see if there's any kind of lesions there, and then make strategies as to what to do next. So this is a capsule endoscopy. This is a video of what, as a pill camera, is going through the peristaltic motion of the small intestine and traversing. And then we're seeing some abnormalities come into view. So again, like I mentioned, it's a disposable miniature camera, helpful to see the lining of the small intestine. The pill is swallowed. So sometimes patients have tracheostomies, other reasons that they cannot swallow, where you have to sometimes place it into the small intestine via endoscopy. And you have a wireless recorder device that is the pill camera is transmitting data directly to that. And that's what we download the images and watch a video. Sometimes it can be an 8 to 12 hour video. So we typically put it on a faster rate of watching. And then we can slow down, stop, where we think there may be abnormalities. There's already AI involved. In this, where they use known markings, like red spots. And they'll hone in the provider to look at that area more carefully. It does not always correlate to an abnormality. But you may want to look at that segment a little bit more carefully, rather than zipping by it. So what can we see? We can see active bleeding on pill camera, where we see fresh blood. We sometimes don't always see the cause of what's bleeding. But we know that now we have localized it to a portion of the bowel. So we know the source is coming from the small intestine. We can see growth, like this tumor growing into the small intestine. We can see these blood vessels nicely, called angioectasia. So we know not only the location, but also the cause. And of course, we can see these small ulcers, which can also be the location and the cause. So not everything is perfect with the pill camera. Of course, it still requires a preparation for the patient. They have to take a laxative, like a colonoscopy. Typically, it's a little less than the colonoscopy at volume. But nonetheless, the effect of that is still what they have to go through. It does examine the small intestine. That's where it's focused. So right now, we don't have it to look at the stomach, or the colon, specifically, or even the esophagus, because it's just zipping right past that area. We're not distending that portion of the anatomy as well. So it's primarily to look at the small intestine. The other problem is, it's just like a video. We cannot clean something to look if it's a dirty clean out. I don't have a window shield wiper to clean up my lens or suction like I would an endoscopy. So if it's not a good clean out, I can have poor views or not see what I'm looking for. And it could be not of value. And also, if we find something like an ulcer or something abnormal, we can't take biopsies. It hones in to us of the location or what's happening. But now we have to go back and follow it up with another procedure. So that's time and effort for the patient and us. So of course, it's, like I said, an 8 to 10 to 12-hour video. So it takes time reading it. And some of us who read it a lot, we've gotten more efficient. We are visual, like how to look at four screens at one. We've gotten used to those kind of techniques. And we can read it a little bit faster. But say, if a first-year fellow is starting to read it, it could take them time. Yes, go ahead. I'm just curious, what percent, and if you could put a percent, I know you're just taking a guess. What percentage of times do you look at one of these readings and then have to go back and confirm yourself versus look at it and say, it's probably good? So the question is, what percentage of time am I missing something, and I have to go back and do it again, or I have to re-review it? I guess I'm just curious, do you usually give an endopil or one of these capsules with the assumption that you're always going to go back and just confirm yourself? Or do you give it and say, maybe I don't, like depending on what it shows, maybe I don't have to go back and look at this person again? Right. So we all read our own. So typically, all of us are reading it. So AI is not going to read this for you. They're not going to generate a report. So we're not there yet, at least. So we, as human beings, are reading it. So somebody is manually reading the images. Now, we can still miss things because, again, it's dependent on multiple things. Cleanout is one of the biggest barriers to having a good study. Some of our patients are very ill. They're sedentary. They're sitting in a hospital bed. Our diet restrictions are not perfect. They get a food tray that's meant not to be given to them, but they eat it. So a lot of things can factor. And of course, the motility is the other factor. Sometimes the pill camera doesn't even make it to the colon to exit the entirety of the small intestine because the patients are on opioids or they have motility disorders that maybe we didn't realize. It's sitting in the stomach for five hours, and now we only have three hours of transit time, but we didn't make it to the entirety. So maybe there was a lesion where we didn't see it. So then we're repeating the study. If the prep was not good, then we're repeating the study. Say we've done the rigmarole of endoscopy, colonoscopy, pill camera, still haven't been able to localize the bleeding. There are other modalities which I'll talk about. And everything is just negative, but we know it's coming from the bowel. So then we would sometimes repeat it to gain yield because maybe in that moment something is actively bleeding, and then we'll capture it. We use it sometimes in Crohn's disease as diagnostic for small intestine where our cameras are not reaching deep further down on endoscopy and colonoscopy. And sometimes we have NSAIDs that are mimicking Crohn's or some other pathology. So we'll want to look with a pill camera because some of these patients look negative on CT scans. MRIs don't pick up pathology. So we do commonly go back and repeat these studies if I'm answering your question. I don't know if I have a percentage of time I do that. I think it depends on what the indication for the study would be. So bleeding is probably the most common use of it to repeat. And then surveillance for celiac or Crohn's, things like that, has been known to be used as well. Does that answer your question? It does. Thank you very much. Yes. So I know you started saying that you can use it for diagnosis, but I guess I was wondering, is this a form of diagnosis currently? Or would you have to go back and take a biopsy still? Or would you be able to go right into a procedure or something? Right. So yes and no. You can use it as just like a diagnostic tool rather than a formal diagnosis. Like you can use it in one of your armamentarium of tools. However, like say in Crohn's patients, like Dr. Abraham takes care of, sometimes there's really classic visual changes, like deep ulcers, multiple skipped ulcers. And then you put it in the context of a history. Like there's no NSAID history. There's a family history. They have inflammatory markers that are rising. And so I think if you put it together with multiple other modalities, then you can have a higher yield from it. And then you can sometimes rely on that itself, whether rather than going back and doing an enteroscopy and taking a biopsy to prove Crohn's. But for bleeding, it's not helpful. You diagnose the bleeding, but you have to go and control the bleeding. So you can't do anything. It's not as therapeutic as more of a diagnostic imaging tool. So yeah, it depends on what you're using it for. So of course, the last thing I want to say is risk of retention with this pill camera. So if somebody who's had a known stricture like Crohn's or a malignancy, you don't want to go send this down there necessarily because it can get stuck. And then we're stuck with some sort of retrieval mode, whether it's endoscopic, depending on where in the GI tract it's stuck, or surgical, which could be a big deal for some of these weak patients who they're not good surgical candidates. Now, I'll have a couple of surgeons that I work with who actually want us to deploy, especially with bowel obstructions that are difficult, like partial bowel obstructions that are difficult. And they'll say, if it gets stuck, I know exactly where I'm going to operate. So I think that's a side comment. But that's usually not what we should be doing. If you know this patient cannot have surgery, do not put them in that boat. Yes. There is a, do you know the retention percentage with pill cameras? I don't know if I know that on top of my head. I can get back to you, though. That's OK. I'm just curious if it's something that- It's, I mean, if you find that, so remember, any tool that we use, we should be finding the right patient for it. So if you use it in the right patient population, you should not, it should be low. But- Yeah, so the studies can be skewed based on how aggressive were they in preventing, you know, like appropriately figuring out which patient you should do it on versus not doing the patency capsule first before considering the actual regular capsule. So, I mean, I've had my share of capsule retention. I think I had three patients ever in my career where a capsule was retained. But in all those cases, these were active Crohn's patients, and we couldn't figure it out based on imaging or colonoscopy because it was deep in the small intestine. So in a sense, I mean, of course, the patients are aware of the risk. We have to put them, you know, tell them risk benefits. But in all three cases, it was actually beneficial for the patient because we found the area, and then the surgeon was actually able to go and locate that disease, resect that, and then reanestimose them. So in some cases, it could be a benefit because we find where the lesion is. In some cases, it could be like even a small bowel cancer, and it was causing obstruction, and maybe it wasn't picked up on MRE or CT entomography, and it can be beneficial. So patients, we have to explain the risk of doing the capsule, but you can actually prevent it by doing a patency first in those high-risk patients that you're, let's say it's a 90-year-old, you don't want to put them through surgery, you know. But what if I had a diagnosis? You want to do a patency first before doing the regular capsule. So a patency capsule, oh, go ahead, Dr. Prabhakar. No, no, sorry. So the national rate is 1.5% to 2%, and the, so we use the patency capsule in, as Dr. Abram was mentioning, in certain conditions. But the number that you need to know is 1.5% to 2%. Thank you. So lastly, I want to say one more thing. A patency capsule is basically like a barium shape and size of an actual capsule, but then it'll disintegrate and dissolve if it gets stuck somewhere. So we use that commonly in patients we classify as maybe a risk for retention. And so we do that first, and we get x-rays a couple days later to see has it passed. If it passes, then, you know, we're not completely out of the woodwork, but we may be able to get past. So then we then talk to the patient risk-benefit. I think one more question, and I'd like to move forward with the slides. Go ahead. Yeah. We might be getting ahead. But when you do find a bleed or, you know, whatever it is you find, can you usually go in endoscopically or, like, you know, what's after that? Right. So sometimes, you know, these do take some time because you have to let one day of just the study with the pill camera, and then the next day you're looking and reviewing the images. Based on your day, like you went over our days, it could be at the tail end of that day that we sat down and watched the images for that. And so then we finally diagnose the patient, OK, they need an enteroscopy or another endoscopy because it's reachable in the proximal small bowel. So the next day we typically try to take them back for, you know, endoscopy. Now some of these are done outpatient, so then those, you know, you have to get them in a timely manner rescheduled for endoscopy based on their labs and how sick they are. OK. Moving forward, we're finishing up the obscure GI bleed, so we talked about endoscopy, colonoscopy as tools, capsule endoscopy. And then there's deep enteroscopy, so this is device-assisted enteroscopy, so going deeper in the small intestine. So one of the devices that exists is balloon-assisted, and then we also have tube-assisted, more like a spiral. So there's double balloon, just as the name is, there's two balloons at the tip of the catheter and the camera, and then there's also a single balloon, which is just one balloon. Not all facilities have double balloon, but most facilities have single balloon. So balloon-assisted enteroscopy, it's basically the endoscope is advanced through the small intestine by inflating and deflating the balloon, and the goal we're trying to do with both of these type of device-assisted enteroscopy is to pleat the small bowel. So you're just trying to, you know, if you have a drawstring, like in a pants, you're tightening that string, so you're pleating those folds to make things, you know, shorter. And that, because a small intestine, like we talked about, is very long, so no camera exists the entire length of the small intestine. So we have to pleat to cover surface area and move forward. And that's what these different balloons or spiral tubes provide. So it's a push and pull technique. We can evaluate the entire small intestine that may not be reachable with endoscopy, traditional endoscopy, the EGD and colonoscopy, and we can even get to the terminal ilium. There's anterograde enteroscopy, which is going through the mouth into the esophagus stomach and then moving forward in the small intestine. And then there's retrograde, which is through the rectum, doing a whole colonoscopy, getting into the ileocecal valve and then marching backwards from the ilium up towards the jejunum. Which approach we want to do depends, say, like on the location of your bleeding. So if it's, you know, on a pill camera, we decide it's located in the fourth portion of the duodenum, then doing a retrograde doesn't make sense. So we would do anterograde approach because it's more proximal, excuse me, from the mouth. And we would try to get to the lesion. But if it's sitting in the ilium, an anterograde approach has a high risk of failure because of length that we have to cover. So we definitely want to try retrograde. It sounds very easy, but it's not as technically easy as some of our therapeutic endoscopists will tell you because we're fraught with, you know, anatomy changes, somebody who's had multiple surgeries and they have adhesion, scar tissue, risk of perforation, bleeding risk, just hematomas, all these things that can, you know, make you want to think twice about do you want to proceed with these type of modalities, but they exist. So this is a cartoon image showing you how we inflate the first balloon and we inflate the second. And then we are pleating, so it made it shorter, as you can see. So now we have a more straight camera, so then we can keep advancing instead of looping in the bowel. And that's how we typically move forward. So I'll just show it. Again. Sorry. Okay. Let's try that again. I think the cartoon should move now. Moving our distal end and then we're ballooning, and then you can see as we push and then we pull, and so it's now pleated together, and now we can advance further than a regular endoscope, which we couldn't get that far. Now rotational endoscopy is similar. We have endoscopy. That's, again, trying to look at the small intestine, but instead of balloon, we're using a spiral-shaped overtube, so it's more of a rotary clockwise and counterclockwise maneuvers to pleat, and it allows the spiral to pleat the small intestine and our colon in a rapid controlled manner. So this is what it looks like, again, to the small intestine, the spiral, and then up here you can see some of the pleating happening to shorten and then thus move forward. A lot of times we use fluoroscopy to see what's happening, how deep we're going, because it can be such a long distance, sometimes we get lost in the length. Again, once we find what we're going in for, we can, like if there was an angioictasia, we can cauterize and take care of that bleeding lesion, or if there was a blood vessel, an artery sticking out, we can put a clip, different modalities that were already discussed, and then if there's something like a tumor that you want to resect, you can do that or take a biopsy of, so we know what we're dealing with and we can have pathology to treat. So these are all different means to an end. Again, we talked about the endoscopies capsule and then deep enteroscopy, and then lastly there's radiological methods of GI bleed. This is called a tagged red blood cell scan, so basically they tag your radiology, tags your red blood cells as it circulates, you're going to see in the early phases of the imaging, you know, where the common aorta, iliac, and femoral branches are, and of course you're excreting it in the bladder, so you'll see the contrast there, but later in the delayed images you'll see kind of what we call this, excuse me, like a blush. So things are kind of oozing out into the luminal intestinal tract, and then we'll see that, and then the radiologist has the hard job of locating where is it. Also the flow rate of the bleed matters, so this is usually 0.1 mL per hour, so that's important, so if you have a brisk bleed versus a slow ooze, knowing which patient to offer which scan and to have high yield. So we commonly can miss the location, because if you are, if you scan somebody at the time of bleeding, you may be able to capture it, but then by the time the reality is they get a hospital stretcher, get into the radiology suite, something actually gets tagged and then scanned, it may be in an inactive bleeding state, so then it looks negative. That doesn't mean that the patient's not bleeding, it's just at the time of scan we may have missed it. Now the good thing about a tagged RBC scan is it stays active for a couple of days, so if you've tagged somebody and then you missed something or you didn't capture it, but then they show evidence of bleeding again within 24 or 48 hours, you can re-scan them and try to capture it again for yield, so it could be a little faster yield. Then of course we have angiographies with radiology, so it's like a, where they inject dye into your arterial system and then get the beautiful, you know, vascular map into the bowel and then they see if there's, again, extravasation of contrast or blush in any particular area and to kind of hone in. The nice thing about an angiography is sometimes it can lead to therapeutic interventions by interventional radiology where they can embolize depending on, you know, what it is and where the location might be. So that's showing a blush right here and then they're putting a coil embolization to cut off the supply to that bleeding source, so now the bleeding is controlled that way. It's not perfect. If we intervene, we can obviously lead to ischemic injury and other complications, but this is a modality sometimes. Yes? So you mentioned before with treating a re-bleed, going back in, I'm just curious about the methodology of when you're treating something prophylactically or just kind of going in and not seeing bleeding right away versus, sorry, treating a re-bleed. Would there be any change in the algorithm or how do you kind of think through that? Yeah, absolutely. There are multiple algorithms for gastrointestinal bleeding and that's what we try to teach our fellows. So say you have somebody, this is their first time having a gastrointestinal bleed and we haven't found, so we're going and looking for, like, so we may burn through multiple modalities to localize and treat, but sometimes there are disease disorders that we know. So if a known gastric cancer patient is coming in on chemo and they're bleeding, you know the likelihood would be in their stomach from the cancer potentially, so you may just target an upper endoscopy instead of a colonoscopy. Also, if they're recurrent bleeding, you know, you may have already done this work up and say a month ago and they're back in the hospital a month later. And if you know the source like angioictasias are known to come back and form again, more common in the small intestine, then you may want to target that site from the beginning and go into an enteroscopy from the get-go instead of going through like the same algorithm of endoscopy, colonoscopy. So yes, that is correct. So if we know a source or we have a high suspicion for a source, we may choose a certain path rather than just blindly endoscopy, colonoscopy, and so forth. Okay. So treatments, just to wrap up, the GI bleed depends on etiology, severity of bleed. We can obviously use supportive care like iron supplementation, blood transfusions. We have our endoscopic hemostasis tools that we discussed and prior to CLIP, chemo spray, other things. Then we have our radiological colleagues who help us with angiography, with embolization. And last but not least, there's surgical options. This is usually our last resort depending on what it is. A couple more topics to cover, and I'm going over time, so I'm going to withhold questions until I can finish and then certainly ask your questions. So there's mechanical or functional bowel obstruction in the small intestine. That's what a small bowel obstruction is. So it prevents normal transit of digestion moving forward, and these can be medical emergencies. So symptoms that patients present with are abdominal pain, distension, nausea, vomiting, constipation, given that things are not moving forward and they're backing up. So for the small intestine, we can have multiple causes, including large bowel as well, adhesions being really common. If you have multiple surgical interventions in the abdomen, just by having surgery can create adhesions or scarring, and they can prevent peristalsis or proper motility. And over time, that can lead to complete obstruction in patients, and it can even flip the bowel or torse the bowel because of the fixed nature of the adhesion. Other causes are hernias that can be present in the abdominal cavity. So we have a weakness in a bowel muscle wall, and so then our internal organs protrude out into the hernia sac. And depending on, we call this a neck of the hernia. Sometimes if it's small, it can get trapped in there and can lead to bowel obstruction. And then the worse, the longer it stays in there, it can lead to strangulation and ischemic injury, and those become emergencies. Other times, the bowel loop is going in and out, in and out. So sometimes people can have intermittent obstruction, and they resolve with time. It just depends. And of course, there can be growths in the bowel, which include tumors, benign or malignant, and then they can also be space occupying, so they can present, the bigger they are, with more obstructive symptoms. And this is more of a surgical specimen that was resected in the size of the tumor. Other causes are something called intussusception, common in children, but also in adults. We can have basically telescoping of the intestinal wall into the other intestinal neighboring lumen. So again, it's acting like an obstructive source, and this can be transient coming in and out. So sometimes these can be very difficult to pin down. Patients come in with recurrent complaints of obstruction. We scan them. We don't find it because it's already un-telescoped out. So it can be sometimes difficult, and you have to know kind of the situation where you might be suspecting something like this. And then lastly, strictures, which are inflammatory or malignant, depending on the cause. So narrowing in the lumen, and it can be seen on radiological, this apple core-like stricture. This is probably seen in Crohn's more commonly. And then last but not least, due to motility disorders, we can also see besores, which are just this stagnant food and medication debris, and that just solidifies and just stays there. These are rare, but common to see in obstructive patients and also in dysmotility, like gastroparesis and things like that. OK. Diagnosis, we can use x-ray of the abdomen, which we can see dilated loops of small bowel. And radiologically, they commonly cause the appearance of air fluid level, where the air will rise and the fluid will be below. So you can see this kind of deep, straight line. The fluid is below densely, and then the air rises. So it leads to this air fluid level appearance and can be a sign of a bowel obstruction. CT scans are generally more helpful because they can also give us the location of the bowel obstruction rather than x-ray. But they do also show dilated loops of small bowel. We can see transition point, where proximal, above the obstruction, it's dilated and more pressurized. And then below, it's decompressed, more collapsed. So that can be the transition point. And then it can also help us know the cause, like is there a tumor, or is there a volvulus, or interception, things like that, rather than just that there is a possible obstruction. Treatment, typically, we do conservative treatment with nasogastric tube for decompression, prevent the patient from vomiting so much and having aspiration risk, and also decompress the dilated loops of bowel and all the fluid sitting there. So it's a tube that goes through the nose, typically, into the back of the esophagus, back of the throat into the esophagus and the stomach, typically, and then suctions intermittently any of the bile and gastric juices. And then we want to correct electrolytes, because somebody's been vomiting, and they're dehydrated, and resuscitate them in fluids. And usually with that, a lot of our patients can unobstruct or move forward, and they don't always need surgery. But some patients don't move forward. They just stay in an obstructive state. And the longer they are obstructed, they can obviously have further risk of perforation or ischemic injury. So thus, we do surgery in those. And these are just different types of anastomosis that they're showing. In the interest of time, I'm going to move forward. Last topic is mesenteric ischemia. There's inflammation and injury to the small intestine due to inadequate blood supply. So we have our major artery here, the aorta that has three different sections, the celiac artery. Then we have the superior mesenteric artery, the SMA. And then we have the inferior mesenteric artery right here, the IMA, that feeds into the small and large bowel. And then we have offshoots, like smaller branches coming from all of these. So mesenteric ischemia, again, is inflammation and injury, both of the small intestine due to inadequate blood supply. We further divide that into acute and chronic mesenteric ischemia. So with acute, you're going to have, say, like an acute obstruction, like a blood clot that comes through that vessel. And it leads to acute, severe abdominal pain, can lead to blood pressure changes. And you can have abdominal tenderness that is out of proportion to the physical exam. I mean, you're barely pressing in there, just jumping off the bed. Chronic mesenteric ischemia is more like plaque disease, atherosclerotic disease, like heart disease. And you have postprandial, like after eating, abdominal pain, weight loss, because you have fear of eating. The patient will just eat small portions, like, I don't want to deal with the abdominal pain that's going to come. I know it's coming. And again, you can have abdominal tenderness that is out of proportion to the exam. So acute mesenteric ischemia, this is just a schematic showing the blood clot right here. And that leads to the clot that's obstructing the flow in that territory of the blood supply, and then leading to this blue ischemic kind of pattern to the bowels. And it can be devastating for some of our patients. There are also clotting disorders, lots of things, autoimmune processes that can lead to this. And this is what the surgical specimen looks like. This is the part of the bowel that didn't get blood flow, so it's nice and dusky looking. And this is our healthy looking tissue. So chronic mesenteric ischemia, occlusion or narrowing of at least two or three of the mesenteric arteries, seen in patients with atherosclerosis, like CAD, and other things they may be having. Abdominal pain due to poor blood supply to small intestine, again, that's what's having almost like ischemic kind of like heart attack, like injury to your bowels. So this is, I think, supposed to show right here, plaque, and that's leading to poor supply in that territory of the bowel. Diagnosis, again, we can use angiogram like the radiologists have, CT angiograms, which are less invasive than angiograms, and the MRI angiograms can be helpful in certain vascular disorders or anatomies. And then we also have Doppler ultrasound available. And I think this is just showing in a CT image like a clot sitting right there. Angiography is also helpful because it can be therapeutic. You can put a stent as this diagram, a radiologist putting a stent right there, a vascular surgery. And of course, surgery for management of acute definitely, and then for chronic sometimes, if they meet enough criteria, enough plaque to make that a clinically significant obstruction, then they need to be bypassed or resected. That's it.

small intestine disorders

celiac disease

obscure GI bleeding

small bowel obstruction

mesenteric ischemia

gluten

capsule endoscopy

nasogastric tube decompression