So, I have the pleasure of talking about stricturing and penetrating Crohn's disease and this is important to me because I actually have stricturing Crohn's, so this is a topic that's near and dear to my heart. So if you haven't, that was my lead into these, if you haven't read these papers, I highly recommend you do and bookmark them because they're nice references and they're a really good atlas and glossary to refer to if you forget what are the parameters that make something fall into a certain category. So these are the two references, if you ever need to make decisions, that I would turn to first and I mostly had nothing to do with that. They're really well written and again, I almost had nothing to do with that. So here we are, why do we identify phenotypic features of Crohn's based on these recommendations? And one of our co-speakers today did a study to look at how good we are at doing that and we, using the standard references, we're almost perfect in our observer agreement on identifying strictures and penetrating disease and that's important because we all want to be doing the same job at all of the different places where we're going to be doing that job. So if you, again, take a gander at that paper, I'm going to define and show you some images and talk about the pathophysiology of these diseases and this is really a summary of this phenotypic presentation. So up to 30% of patients with Crohn's will present with stricturing disease at diagnosis and the lifetime risk for patients with Crohn's of developing a stricture is approximately 50% and this is similar in both pediatric and adult populations. Most stricturing disease happens at the TI or the ileocecal valve, not all, and you'll see that over and over again in the images, but early, but that's an important place to start looking. It's not the only place you should look and we're really important to identify the multiplicity of strictures that we'll see in patients, but that may be your starting point. Just remember that early strictures have both an inflammatory and a scar formation component to them so they can coexist and they most often do coexist. Most of the medical therapies that patients with Crohn's disease are given are targeted to reduce the inflammatory component or inflammation. They don't target or reverse fibrosis and that's important because if you can get to it early, you may be able to intervene on their scar formation, but if there's already well-formed stricture and upstream dilatation, you may not, we may not be able to make that go away with just medication and in fact, most strictures will need surgical resection. So this is a full sentence with a lot of very sophisticated words that I don't understand, but basically stricture pathology is very complicated. There are a lot of components, there are inflammatory cells on path, there are cytokines involved in this process, mesenchymal cells do things, there's an intestinal biome that gets involved and what happens is there is a transmural extracellular matrix accumulation, read, a stricture is formed. So you can imagine why this is so complicated because if you're trying to target medical therapy to this, you have to sort of get into all of these different types of contributors. So what they see on path will be a combination of bowel fibrosis and increased smooth muscle. It's most often associated when pathologic resected, most patients have active inflammation on path as well. There's a genetic component to fibrosinosing disease, I don't think we understand it particularly well, and then there's this really fancy world called epigenetic factors and I'm not even sure what the definition is, but that's just, there's more out there that we don't know. I do know how to define a stricture though. So a stricture is an area of bowel that has luminal narrowing and it's focal and the bowel preceding it is dilated and to meet this definition, you need pre-stenotic dilatation of three centimeters or greater. If you don't have that, if there's not enough pre-stenotic dilatation to be present or if there's none present, then you're going down the probable stricture definition and that will include a couple of things. Either you also identify a coexisting fistula or the proximal stricture decompresses the bowel from, another stricture is decompressing the bowel from the distal stricture or if you're, have the ability to look at it on multiple sequences like with MR, the luminal narrowing persists on multiple sequences. I forgot. There are other definitions. There are other groups who have defined stricturing disease components. One of them I've listed here. You can see that to some extent, there's some variability including this one from the constrict group where they talk about increased wall thickness and luminal narrowing of greater than 50% but then you have to take into account things like anastomotic strictures which happen at the area of prior resection where wall thickness is not necessarily present. So a good rule of thumb is to think about it with a focal stenosis and then upstream dilatation. Something to remember, most patients' clinical symptoms don't correlate with the presence of strictures. So if the patient is going to present with physical symptoms, it's going to be symptoms of obstruction and it's important to image them to look for the imaging findings of stenotic disease and multiple stenosis which can coexist at the same time. So again, CT image, here are the findings you want to look for. Again, what I've identified here with the arrow is luminal narrowing, wall thickening and upstream dilatation and you can see in this one, I don't even need to put a caliper on it, that's clearly greater than three centimeters. Apparently, you got to be there. Okay. Strictures can happen in multiple places. This is what makes us the expert. So the clinician may think there's a stricture and want the patient imaged but it's our job to look for more and you can see on this coronal image that there are multiple strictures. We're not done when we identify more. We have to run the entire bowel to make sure there aren't additional strictures. Here's another patient with multifocal stricturing disease. This patient had both colonic and small bowel strictures. So some of what we do is try to help distinguish between the phrebotic component and the inflammatory component of a stricture but that remains controversial and there's no standard method of imaging and they often overlap. So don't feel bad if you're not all that helpful to your clinical colleagues in this area. Some of the things we look for is increased signal intensity on T2 rated images but for a sort of layperson like myself, I like to describe everything I see and then work with our clinicians to figure out what they think they can manage. So the next thing that follows after a stricture is penetrating disease and penetrating disease generally arises with stricturing disease present and an episode or a situation of active inflammation. The stricture and the fistula or the evidence of penetrating disease is going to be above the strictured segment, so upstream of the stricture. It's typically, again, associated with active inflammation and patients with ileal disease are at higher risk of developing fistulizing disease than other patients. Included in penetrating disease are sinus tracts, fistula, inflammatory masses and abscesses. Just remember that perianal disease is a separate process and we're not going to talk about it in this talk. Penetrating disease pathology includes a couple of entities together. There are mechanical factors if you think about the increased interluminal pressure from downstream strictures and there's also an inflammatory process that includes those cytokines and lymphatics that contribute to penetrating disease. So this is a sinus tract on this axial image and it's a blind ending tract that goes beyond the bowel wall but doesn't reach another piece of bowel or skin or another organ. So they're blind ending and they're going to be, they're going to follow inflammation on MR and CT. A fistula, in contrast, is a communication from the bowel to another epithelialized surface. So the nomenclature follows what it's going to and, again, this will follow inflammation on both MR and CT. In this case, this is an enterocolic fistula and you can see that it's connecting colon to small bowel. This is a patient with an entrovesical fistula connecting small bowel to bladder. Inflammatory masses used to be called phlegmons. We now call them inflammatory masses. They're an inflammatory process without significant fluid. These we don't drain because nothing would come out. And they look mass-like and are going to be bright on T2 and sort of follow soft tissue on CT. An abscess typically forms from a sinus tract and it will become a walled-off collection and you'll see enhancing walls and it will follow fluid attenuation on CT and fluid on MR or complicated fluid on MR. This is another abscess at the dome of the bladder and right by the terminal ilium and you can see that they can contain air, they can contain fluid, and fluid and air as well. Another patient with complex fistula and once it starts to become very complex, they start to look somewhat stellate. You can see here this is beginning to look stellate and on this one, another case where it's all pulled together and very stellate or clover-like in appearance, bringing multiple bowel loops together. So what do we know about emerging biomarkers? To be honest, the results have been mixed in the literature and I don't think we're quite ready for hard and fast designation yet in our reports. Why is it important for us to think about stricturing disease? Because we're the person who's going to identify all of the strictures and all of the complications from this disease process and we're a very important part in the multidisciplinary approach to this patient population. So a couple things I want to bring up as far as therapy. As I noted early in the talk, medical management typically involves bowel rest and the treatment of complications, but the medications we give patients at this point don't actually fix a stricture. Most of these patients will go on to surgery. Your surgeons are going to be plus minus on balloon dilatation. The abscesses are often treated percutaneously first and the patient is treated with medications to try to improve their nutrition before they go to the OR. And if you think about it, fistula closure is going to be impaired by constant bowel irritation and poor nutrition. So this is the patient population that we try to buff up before they go to the operating room. Once these patients are resected, the goal is to keep the patient in remission and that they do with medical management. So in order for medication to be successful as far as what we're going to see and how the patient's going to respond, it needs to improve both the clinical symptoms and the imaging findings. Improving the clinical symptoms alone is not going to be sufficient, and imaging should be included in the endpoints of medication trials. This is what we have to look forward to in the future. The literature is updating daily. We all look forward to medication modification that can be successful in humans. We're really at the murine model right now, but there's more to come. I'm easy to reach if you need me, and I appreciate your attention. Well, it's great to be back. So you're going to see here we're going to talk about CT and MRI assessment of disease activity in the setting of Crohn's disease and a little bit about treatment response and reporting. And we're going to talk about subjective assessment of response, objective assessment of response, and then wrap up by discussing reporting of treatment response. So if my first slide looks familiar, it's because Tracy just gave the exact same first slide in her talk. Hers was in words and mine are in images, but these are those two papers that really are a foundation for reviewing these examinations and making interpretations and reporting them. One is the radiology paper in 2018 that was co-published in gastroenterology, and that's the, you know, how to perform and how to report these examinations, and then we came along in 2020 with an imaging glossary, which I think is very valuable. This comes from a 2018 article, and I think it's critical to understand how to report these examinations. We have to recognize the manifestations and how you go from no inflammation to active inflammation to luminal narrowing to stricturing and to penetrating disease, as Tracy went through. And there is sort of a chronologic order here that occurs in most patients, and we need to know that when we see luminal narrowing with active inflammation, when we see stricturing, we then need to look, for example, for penetrating complications. So kind of knowing what to look for will take you, you know, at least a long way down the road. So why is it important to accurately report disease activity and treatment response? Well, also, as Tracy mentioned, enterography, so this is MRE and CTE, are increasingly becoming a treatment target. We're looking for transmural healing. And it turns out if you can heal the bowel wall by imaging, by CT or MR enterography, your odds of needing steroids, your odds of being hospitalized, your odds of needing surgery for a bowel resection all go down considerably. Another reason why it's a very important image is that in any given year, 37.4% of patients will transition from, for example, being in complete remission to now being out of remission or vice versa. They're moving back and forth between states. And it's important to know where a patient is so we can treat them as an individual patient. Also, as mentioned, symptoms in labs do not correlate well with disease activity. We've seen this in our own research. This has been published in many, many papers. There are correlations. They're mild to moderate, but they're not strong. And for any given individual patient, they may not be that helpful. Also, symptoms in labs fail to predict disease-related complications, as we saw, and that's our strictures and fistulas. So moving on to subjective assessment of disease activity. So what do we look for? Well, this is what we've looked for for, you know, literally decades now as we've been performing these examinations. But we need to be intentional about it. We need to look for bowel wall thickening. And we need to have a definition for that. If we go back to that SAR AGA paper, or Dr. Ramola's work, you know, it's typically more than about three millimeters. We want to look for intramural edema, which we're not going to see on CT imaging. We're going to see that on MR, as increased T2-weighted signal or restricted diffusion. We're looking for post-contrast hyperenhancement. We're looking for inflammatory changes in the adjacent soft tissues or the mesentery. And then more and more, I'm finding as image quality has improved over the years, and you can see up here on this top left image, we can actually start to see areas of ulceration and pseudopolyp formation. And when we see that by imaging, generally it suggests that the degree of active inflammation is quite severe. And also, as Tracy mentioned, once we find that first segment, we need to run the bowel. We need to, you know, is there a second, is there a third, is there a fourth segment? At some point, I'm not going to describe if there's 10 segments. You know, I'm going to say multiple segments and then describe perhaps the one or two most severe or the segments that have associated complicated disease, but we want to give an overall extent. And then subjectively, once we've looked for all of these findings, we're going to synthesize them into impressions. So what are the pros of subjective disease assessment? Well, it's generally simple, relatively speaking. It's relatively fast. We've all done it for a while. We're pretty good at it. And it's still the current standard of care. This is where we live for the most part. That said, when I reported an examination versus Dr. Al-Hawari, Dr. Dane, you know, our inter-reader agreement may not be great. We're not doing things in a standardized way. It's subjective. It's not objective. And then if we're moving into research, whether we're looking at clinical reports and trying to extract features for research or whether we're actually looking at the exam sort of a priori for research, subjective probably isn't the way to go. We need more objective assessments of disease activity. Now, subjectively, this is a patient, this is, we can learn a lot of her single-shot imaging. I feel like I make 95% of my findings off the single-shot imaging. There's bowel wall thickening. There's intramural edema. There's pseudopulps here. There's ulcerations. This is a patient with very, very inflamed bowel. Six months later, the same segment of bowel, you know, most patients don't respond like this. This patient did. You can see the terminally exact same anatomic location. Those findings have all resolved. So this is a great treatment response. Here's another patient, marked bowel wall thickening, marked post-contrast enhancement. You can see the vasorector are engorged. A year later, the patient actually feels very good. They're on their biologic. They're feeling fine. Their labs look better. And this is what the bowel still looks like, very, very, very actively inflamed. There's progression of disease. There's pseudopulps and ulcers here, and this patient feels fine. This is, you know, this is why we need to image. Additional findings, and I'll move through this very quickly. This goes back to Tracy's talk. We want to also mention if there's luminal narrowing, if there's upstream dilation or not, and then talk about how it's changed compared to the prior. Is it, you know, is it the same, better, or worse, or perhaps has it resolved? Because this luminal narrowing and stricturing disease is associated with bad outcomes, including the increased need for surgery, and as Tracy mentioned, the degree of upstream dilation does seem to have a degree, does seem to influence outcomes, including surgery. Penetrating disease, again, we're going to describe that as better, same, or worse. At our institution, 67% of patients who come in with penetrating disease that's new will go to surgery within one year. That's the state of affairs where we're at right now, and you can see in this paper the hazard ratio is quite high for penetrating disease as far as need for going to the OR. So that's what we do now. What about objective assessment of disease activity? Well, I break this down into a few ways to look at it, and this is not all-inclusive. There are lots of sort of preclinical biomarkers that us and others are looking at that are out there that may or may not come to fruition, but right now what's out there, there are these complex indices, and I include the MARIA score in that. The Claremont score, which we'll see is variation on a theme. It's very similar to the MARIA score, and then there are others. There is what I'll call a simple index, which is the simplified MARIA score, and then if you have a dual-energy CT scanner, and we've seen this out of the NYU group here, it's been able to show that we can actually look at the iodine concentration in the bowel wall and get at disease activity. Briefly, the MARIA score, I mentioned this, I consider this to be complex. It's not that complex, but it does involve some math. You're going to need single-shot imaging, typically, and then pre- and post-contrast imaging, and from that, you can derive the bowel wall thickness, the degree of enhancement, whether or not there's intramural edema. You can see there's extensive intramural edema in this patient, and whether there are ulcers. Look at all these ulcers. The lumen here is very serrated, very lumpy, bumpy. Contrast is going into the wall. So this is a patient that's going to have a very high MARIA score, and from Jordi's work, we can see that when we correlate it with endoscopic indices of severity, that the correlation is actually quite good. Claremont's score, I mentioned, was variation on a theme. Let's take out the post-contrast imaging and let's add in diffusion-weighted imaging. And it turns out it correlates very, very highly with the MREA score, especially for small bowel disease. And this is a patient who's going to have, again, a very high Claremont score. So they're going to have bowel wall thickening, check intramural edema presenting as restricted diffusion and or increased T2-weighted signal. They're going to have ulcers, which this patient has if we go up and down their bowel. And then you're going to throw in the ADC value. One of the issues I have with the Claremont score is that ADC values, despite our efforts, there's a lot of variability depending on B values you choose, how you fit your curve or line, you know, mono-exponential versus bi-exponential, different scanners between vendors within the same vendor. There's a lot of sources of variability there. So I'm not a big fan of using ADC clinically at this point. So moving on to the simplified MREA, I put this in my bucket of simple indices. This is relatively new. This is also out of Jordi's group. It avoids the need for IV contrast enhancement. You can get at individual bowel segments as far as disease activity, and you can sum them to get a global intestinal inflammatory score. And it only really requires, in my mind at least, one or two high-quality, non-contrast image acquisitions. So we can do this in just, you know, literally less than five minutes. And for the findings we're going to look for, if we do single-shot imaging with and without FATSEP, we're probably good to go to get at the simplified MREA score. So there was a derivation cohort. There was a validation cohort. And basically, if you have bowel wall thickening, you get a point. Intramural edema, you get a point. Perianteric inflammatory changes, desenteric inflammation, you get a point. And if you see ulcers, you get two points, because ulcers are indicative of severe active inflammation. And they found if your score was greater than or equal to one or greater than or equal to two, you can see these areas under the curve of .91 and .94, which are actually very, very good for getting an active inflammation and severe inflammation by endoscopy, respectively. And then when they correlate with endoscopy, it also looked very good. And it correlated, as you would expect, with the original MREA score. So here, you really, again, only need one or two high-quality sequences. There's bowel wall thickening. There's intramural edema. There are ulcers here. And if we went up and down, there's perianteric inflammation. You get five points. This is our patient, same patient we saw earlier. All of those findings have resolved, which is amazing. They've gone from five to zero. Here's another patient. Again, as we go up and down, five points. There's actually a nice little ulcer right here, a little divot in the bowel wall. And then six months later, all of the findings are gone with the exception of a little bit of bowel wall thickening, you can see. So they've gone from five point to one point. This is something that we can very easily do in our brains. You could work into standardized reports and templates. And you have a number, you know, we're more than a number. But at the same time, our clinicians do like objective sort of indices that can be followed over time. I mentioned dual-energy CT in the work out of NYU. And Dr. Dane, sitting here in the front row, they very nicely showed using dual-energy technique, you could quantify the amount of iodine or contrast material in the bowel wall and get at active inflammation versus no active inflammation in the area under the curve or accuracy at least was greater than 90%. So we're going to wrap up by talking about reporting of treatment response. So this is taken from the SAR AGA paper. Basically, we're going to want to have a certain number of impressions for enterographies. And the first impression should probably relate to active inflammation, whether it's present or absent. And then there should be some statement about the severity of it and the extent. And then don't forget, if there are prior exams, is it better, same, or worse? We're going to want a statement about luminal narrowing and stricturing disease, whether it's present or not. If there's an overt stricture or not. And then if there are priors, how it's changed over time. And then we're going to want a penetrating disease statement, present or absent. What type is it? And has it changed over time if there are priors? So this is taken actually out of my PowerScribe. And there's no pH on here. I think I did a good job hiding it. But I want you to focus on the impressions. Notice there's an, everybody, when we report these exams, and we have 20 radiologists, pediatric radiologists who read these enterographies, they're going to start with an inflammation state, present or absent, and go from there. Then they're going to go with a luminal narrowing stricture statement, present or absent, and then a penetrating disease statement. And we have that in our GI docs. Love it. Because they can go, you know, they don't get lost in our, you know, we like to think we're sort of like poets when we dictate. But when we use the standardized reports, they know exactly where to go and find what they want to find. We know this, just a couple more slides here. Free text reports lack organization. They're a source of ordering doctor frustration because of, you know, mistakes, mispertinent findings, those sorts of things. When we standardize, we improve our communication. We ensure that important findings are captured. We ultimately add value. We improve our inter-radiologist agreement very likely. And we probably improve outcomes through standardization of care. Although I have a question mark there, because it'd be nice to actually show that. There are other benefits of standardized reporting, including looking at outcomes, looking at doing QI activities, and then facilitating research as well, both within an institution and actually between institutions too. So this is the last paper I'll leave you with. This is out of Duke. And they looked at a bunch of enterographies and had them reported unstructured and then structured and looked for 15 key findings. And basically, no surprise, when you structure reporting, you reported basically all of the findings versus when you took an unstructured approach, you had about half of them. And then I think as important, the referring clinicians had a preference for the structured report. They could find what they needed to find, and we added value. So to wrap up, MRI and CT are very important radiologic biomarkers of Crohn's disease activity these days. And they have been shown to correlate with meaningful outcomes, which is very important. We can use them to accurately assess treatment response. So make sure we report whether it's responding or not. And today, our assessments are still mostly subjective. However, I think going forward, our reports are going to be increasingly objective. And that's not a bad thing, and we need to embrace the future. Thank you. There we go. All right, my name is Barry Dane. I'm a body radiologist at NYU. And this talk is CT and MR Enterography in Crohn's Disease, Patient Preparation and Techniques. Here's our outline of what we'll discuss. We'll start by talking about patient preparation, and we'll start by talking about what patients can do before they arrive, and details of oral contrast administration. We'll then talk about imaging technique for CT Enterography and MR Enterography separately. But we'll start with before arrival. And in this section, we'll answer questions of if patients should be fasting or have a colon preparation. So on your left is a coronal trufisp, and the right is an axial single-shot fast spin echo from an MR Enterography. And you can see that the stomach is distended with retained debris. I don't think I can get the mouse over there. So is this a gastric outlet obstruction? No, this is a patient who's not fasting. It's recommended that patients fast for four to six hours before their exam, because that will reduce filling defects within bowel, and will improve oral contrast consumption compliance. Now, what about colon preparation? So recall that enterography is a tailored evaluation of the small bowel. And the Society of Abdominal Radiology Crohn's Disease Disease Focus Panel did a survey of 16 institutions and found that none of these institutions were using a colon preparation, which makes sense, because it's an exam for small bowel. So colon preparation is not necessary for enterography exams. So now let's talk about oral contrast administration. We'll do this for CT Enterography and MR Enterography separately. But first, we'll start by talking about common principles to both. So the first is that oral contrast consumption is usually done under 60 minutes for optimal terminal alial distension. Our center uses 45 minutes. And keep in mind, you may need to go shorter for patients with surgically altered anatomy, such as 30 to 45 minutes. The target adult volume is usually 1000 to 1450 milliliters, with most centers using more than 900 milliliters. But keep in mind, giving too much, more than 1800 milliliters, can induce diarrhea and cramps and reduce compliance. So here is a coronal image from a CT Enterography with intravenous and neutral oral contrast. And you can see that there's poor small bowel distension. And that's because the patient did not complete the 900 cc's of 0.1% barium solution. Next is that you need to have visualization of the interface between the bowel wall and lumen. So here's a coronal image from a CT with intravenous and positive oral contrast, so not enterography. And you can see that while there is adequate small bowel distension, you can't make out the wall, because it's obscured by the positive oral contrast. Whereas in this CT Enterography with intravenous and neutral oral contrast, which would be less than 30 Hounsfield units on CT, you can see that not only is there excellent bowel distension, but you can very clearly make out the wall, which is really important, particularly in Crohn's, to look for areas of active inflammation. On MRI, the contrast should be T2 bright and T1 dark to maximize visualization of this interface. And finally, the last common principle is that there needs to be uniform bowel distension, and for that to occur, patients have to take consistent, steady sips. They shouldn't gulp the contrast, and that really is best if patients are supervised. So here's a coronal image from a CT performed with intravenous and neutral oral contrast, and you can see that there is distended small bowel, but there's a transition point with a caliber change in the distal ileum. So is this a small bowel obstruction? That's actually how this was interpreted, but this is a patient who was unsupervised while they were drinking. And here's the follow-up CT in the same patient a few hours later without oral contrast, and you can see that there's normal caliber small bowel in this patient with no bowel obstruction. So that's it for common principles. Now we'll talk about CT enterography oral contrast. The CT enterography oral contrast agents, again, have measure less than 30 Hounsfield units, and these are some of the agents that can be used. You can use water, milk, lactulose, polyethylene glycol, methylcellulose, sorbitol, mannitol, a commercial sugar alcohol beverage known as Brisa, and a commercial 0.1% barium suspension known as Volumen. There was a recent study looking at these four commonly used agents, and they found that polyethylene glycol and 0.1% barium solution distended small bowel better than water and methylcellulose. So here's a coronal image from a CT performed with intravenous contrast in a patient who drank water instead of the 0.1% barium suspension, and you can see that while there's excellent gastric distention, there's no small bowel distention. So what can you take away from this? Well, if you give patients water PO immediately before an enterography exam, it can be used to help distend the stomach and duodenum, and at our center we give patients 300 cc's of water right before their enterography for this purpose. But keep in mind that if only water is used as an oral contrast agent, you should consider scanning patients earlier, such as 30 minutes after drinking, because it's readily absorbed. That same survey by the Society of Abdominal Radiology Crohn's Disease Disease Focus Panel surveyed the 16 institutions and found that 44% of them were using the commercial flavored sugar beverage or Brisa, 38% were using the 0.1% barium solution or Volumen, 13% were using Manitol, and 6% were using polyethylene glycol. And 75% of the surveyed institutions had a nurse or technologist monitoring oral contrast ingestion. So now we'll talk about MR enterography oral contrast. Oral contrast helps distend small bowel, which can minimize false positive neural enhancement and wall thickening. So here's an axial image from a T1 fat suppressed sequence with intravenous contrast, and you can see this segment of distal ileum is narrowed with apparent wall thickening and enhancement. So is that actively inflamed? Well, in the same exam, here's the axial single shot fast spin echo, and you can see that that same segment is normal, and it was also normal on endoscopy and biopsy. Again, it should be T2 bright and T1 dark to maximize image contrast with the bowel wall. And another perk of oral contrast is that it can displace intraluminal bowel gas, which on MR can cause susceptibility artifacts. The same survey found that 50% of institutions were using the commercial flavored sugar beverage or Brisa, 31% were using .1% barium solution or Volumen, 13% used Manitol, and 6% used polyethylene glycol. And 69% of the surveyed institutions had a nurse or technologist monitoring oral contrast ingestion. So that's it for the patient preparation portion of the talk. Now we'll talk about imaging technique, and we'll start with CT enterography. So here's a coronal image from a CT in a patient who drank neutral oral contrast but then declined intravenous contrast. So while you can see that there's excellent small bowel distention, you can't see the bowel wall. So intravenous contrast is required for enterography. You need it in order to see areas of neural enhancement and particularly active disease in Crohn's. CT enterography exams are usually performed between 50 and 70 seconds post-injection, which is in the enteric to portal venous phases. Most centers use greater than 3 cc's per second power injection. And for single phase CT enterography, which is most commonly performed for Crohn's disease, it should use 300 milligram per milliliter iodine concentration. Patients are usually scanned supine and make sure to include the perineum because there is a high incidence of perianal disease in Crohn's patients, and you should get axial, coronal, and sagittal reformats. Here are additional technical parameters from our protocol for your review. So now finally we'll conclude by talking about MRE imaging technique. It should use a phased array surface coil if possible based on patient body habitus, and you should cover as much bowel as possible, including the anal region. And that's because the lifetime risk of perianal involvement is 30 to 50% in Crohn's patients. But interestingly, only 13% of institutions routinely obtain these dedicated small field of view perianal images. We recently added them to our routine MR enterography protocol for this reason. Now should patients be scanned supine or prone? Well, there really is no consensus, but supine is better tolerated and used by most institutions. So now we can talk about the sequences. There should be a pre-contrast rapid sequence because bowel motion is not corrected with breath hold or triggering techniques. So you need a motion insensitive T2-weighted image, which is most commonly single shot fast spin echo at 81% of institutions as shown here. There also should be a fluid sensitive sequence because this helps identify fluid collections, mural edema as shown by the blue arrow, fistulas such as this simple fluid filled enteroenteric fistula shown by the white arrow, and sinus tracts. And this can be with a single shot fast spin echo or a T2-weighted fat suppressed image. Diffusion-weighted imaging is also helpful with multiple B values. We acquire a B0 and a B800 at our center. The low B value is effectively a T2 fat suppressed image, which can help identify edema and fluid, whereas the high B value can help identify active bowel inflammation, abscess, and lymph nodes. Intravenous contrast is also very helpful. It should be with a standard extracellular gadolinium-based contrast agent. We weight-based our contrast administration at our center. And it's great to get multiple post-contrast phases. So you know that MR patients, that there's no ionizing radiation, so you get that benefit of getting multiple phases. You could consider getting a late arterial or enteric phase, a portal venous phase, and a delayed phase, at least two minutes to look for fibrosis, which tends to show more progressive enhancement, maybe more homogeneous appearance of the wall, whereas active inflammation will tend to show earlier enhancement. Now one thing that MR is subject to that CT isn't is bowel motion, just because of the sheer length of the exam. And something you can do to overcome that is give a pharmacologic bowel pyrolytic, which 81% of the surveyed centers do. In the US, we most commonly use glucagon, which is short-acting. So it should be given immediately before the motion-sensitive sequences, which are pretty much the IV contrast-enhanced sequences. So for that reason, it may require exam interruption. And 85% of the centers that use a pyrolytic do interrupt their exams. It can be given IM or IV. IM lasts longer and has fewer side effects, but is less reliable. So for that reason, we do give IV. And finally, dosing. Seventy-five percent of institutions use a fixed dose. So on your left is a coronal image from a single-shot FASP and echo, and you can see that it's largely unaffected by bowel motion. We give IV glucagon right before the post-contrast sequences, and you can see on the right, this coronal T1 fat-suppressed image with intravenous contrast is markedly degraded by bowel motion in this patient who declined intravenous glucagon. And finally, there are optional sequences, which you could include, which would include a dynamic real-time SINAE single-shot balance-steady state-free procession. This really can aid the detection of affected segments, and it helps with the functional significance of narrowing or strictures, but only routinely used in 25% of institutions, and it's not in our routine protocol either. Here are the additional technical parameters for our protocol on a 1.5-Tesla scanner, and that's it. So we spoke about patient preparation and imaging technique for enterography in Crohn's disease. Thank you for your time and attention. Hello, everyone. I'm Sudha Anupindi from the Children's Hospital of Philadelphia. I want to thank the organizers for inviting me to speak this year at our SINAE on bowel drosophila Crohn's disease and how to get started. I have no disclosures, but I do want to mention that I will mention ultrasound contrast agents, which are currently off-label use for imaging IBD. So what do we know about the background of bowel ultrasound in general? Several societies, including the Society for Ultrasound in Medicine and Biology and additional European societies, ECCO and ESCAR, as well as the European Society for Pediatric Gastroenterology, Nutrition, and Hepatology, have set some current guidelines where they recommend utilizing ultrasound as the initial diagnosis for IBD, especially in Crohn's patients, to manage patients with IBD in Crohn's particularly. And in addition, our publication in 2020 highlighted a survey data showing underutilization of bowel ultrasound in North America. But what we concluded from our survey data was there was very high interest among GI practitioners to pursue this modality. So during this session, I would like to show a methodical step-by-step of how to proceed with starting your bowel ultrasound program. First, we're going to talk about justification. You should have a vision to why you want to do bowel ultrasound. Then what is the preparation needed for doing this, followed by how to perform the examinations. Next, we want to collaborate and introduce the exams, show off our great images, and finally educate. So let's first talk about justification. Justification for the bowel ultrasound. Well, there are a lot of advantages of using bowel ultrasound. One, there's no radiation. It's a portable exam, easily performed. It's very easy to perform. And in addition, it is very patient-friendly. It can be an excellent alternative when a patient cannot have a CT or MRE. And when a patient needs sedation or general anesthesia for a CT or MRE and they're very high risk, ultrasound is an excellent alternative exam. Finally, you have the equipment in your department already. You have to use it to your maximum potential. In addition, you can justify using bowel ultrasound because there's a lot of value to your department. It will help you bring collaboration with your GI clinicians. You can perform very targeted examinations, and this can also be a driver for imaging younger Crohn's disease patients. Next, let's move on to preparation. Preparation for performing the bowel ultrasounds includes two separate categories. One, you need to acquire your personnel. And this means identifying a lead ultrasound tech with possibly additional alternative two and three techs to start as an ultrasound team. You want to identify a GI clinician who's going to be your advocate to help identify patients that you can scan. Next, you also need a colleague. Doing this alone is not sustainable in any practice. Having a few colleagues or even a fellow or a resident who are eager to be involved in this project would be extremely beneficial in the long run for sustainability. Next, you need schedulers and ancillary persons. They would be the people who call, schedule, and schedule your patients. You need the people who call, schedule a case, and they need instructions for their patients. You also need the right people to help provide and develop orders in the EMR for referring dogs. Finally, this is a billable and reimbursable study, and that will require some expertise as well. Next, once you've got the justification for doing this in a vision and you have prepared and gotten your imaging team, let's go ahead and see how to perform the exams. Well, you have to have a plan of how to perform the exam and implement a protocol. And you also need to secure a volunteer patient. This could be a trainee, a radiologist, or securing a ultrasound technologist, which we have used in our practice as a volunteer patient. You want to build a roadmap and educate the ultrasound techs through dedicated in-service. Finally, it is really useful and beneficial if you localize or focus your studies in specific clinical questions, such as localized ileocecal disease or localized disease in follow-up from a baseline MRE and CTE. And then once you have all of this in place, you just want to do it. You want to use high-frequency imaging, both the linear probe and a curved, less, a lower frequency probe would be very helpful. And that curved, lower frequency probe is useful to look at the deeper areas in the pelvis. You want to use harmonics to help reduce artifacts and increase conspicuity of the bowel wall. And panoramic imaging is also very beneficial to be able to show these beautiful images to your GI clinicians in a conference-like setting. Remember that the bowel ultrasound technique is not really super new. It really was initiated from the ultrasound appendicitis technique that was developed in the early 2000s. It's based on a graded compression, both anterior compression with the probe, with a posterior manual compression with your hand from behind. This will help isolate a loop of interest. It will help displace air in the bowel so you can see the bowel wall, and that shorter distance for improved visualization of the bowel wall pathology. So where do we start? We start in the right lower quadrant using the linear probe. We look at the TI, the ileocecal valve and cecum, and then proceed along the length of the colon all the way down. Then you want, in a zigzag fashion, use your probe, linear probe, to look at the small bowel in the jejunum and in the mid ileum. Finally, you want to use the curb, lower frequency megahertz probe, to use to look at the pelvis, sweep the quadrants for fluid or abscesses, and use the bladder as a well-descended acoustic window to look at the rectosigmoid. In addition to looking at bowel wall, measuring it, using color doppler to look at hyperemia, you also want to look outside of the bowel wall and evaluate the mesentery. Once the examinations are performed, it's time to collaborate and introduce. You want to show off these beautiful images. So once you've incorporated bowel ultrasound into your practice, you want to introduce the bowel ultrasound to the IBD clinicians, perhaps in an IBD conference. And you also want to introduce it to the radiologists. Your best advocates and the people who are going to promote this imaging modality are the people who work with you on a daily basis. Then you want to teach them the value of the bowel ultrasound and this will help foster feasibility of collaborative research studies. When you share these studies at an IBD conference or to your radiology colleagues, you want to show them that bowel ultrasound has capability and clinical value. Show them these beautiful panoramic images of a normal TI next to a disease loop of TI, or show them how you can use ultrasound to correlate with MRE findings or CTE findings. As in this case, I'm showing you a diseased, thickened, enhancing, inflamed loop at the TI of the ileocecal bowel. And here is that same area on ultrasound, which is hyperemic and thickened. So once you have done the justification preparation, you perform the exams, you've shown them to the right stakeholders, you want to educate. And education can mean several things. We have several articles already published on how to do it. We have pictorial reviews that help guide an interpretation of the studies. And finally, there's plenty of evidence-based articles to stress the value of ultrasound and the accuracy of assessing disease activity, which will be extremely helpful when talking to your GI clinicians to get their full support. There are also several educational resources online, both from the European Ultrasound and Medicine and Biology Society and the International Contrast Ultrasound Society. So you can do advanced bowel ultrasound imaging with IV contrast if you so desire. And if you already have IV contrast, you already have IV contrast on board at your institution. Ultrasound contrast agents are safe. They're not nephrotoxic. They're becoming more widely available. And this will help you with your standard grayscale and color doppler imaging to provide additional quantitative measures. In addition, if you are looking to start an ultrasound contrast program in addition to a bowel ultrasound program, this is a great article from our institution at CHOP that helps define how best to approach that. So in summary, have a vision and a desire to start a bowel ultrasound program, create an imaging team, then perform the exams, incorporating it into your practice. Share those cases with both the GI practitioners and your radiology colleagues. And finally, collaborate and continue to educate. Thank you for your attention. Thank you, Tracy. And sorry for going a little bit over the time. Thank you for staying around to listen to the last talk. And thanks for Tracy and Jonathan to invite me to talk on MRI of perineal fistula. So what's better at the end of the presentation is to talk about the button. So the outline I'm going to go with the presentation is to talk about the perineal fistula, starting with anatomy, focus a little bit on the etiology, although we're talking mostly today on Crohn's disease, and then go to Crohn's disease perineal fistula classification. Talk a little bit about treatment and why we need this important classification and how to affect treatment. And in the end, touch a little bit on treatment response and how we report that. So what's the anatomy of the perineal region? So basically the important structures that we need to know about in the anal region is the internal sphincter, which is the continuation of the circular muscles in the lower rectum. We have the anal gland crypts, and we see why these are very important that they're usually at the level of the dentate line. We have the external sphincter, which is a smooth muscle and skeletal muscle, sorry. And it outlines the outer edge of the anal canal and it's mostly responsible for the continence mechanism. And we have this very important space, which is called the intersphincteric space in between the internal and external sphincter. On the axial images, this is the internal sphincter. This is the external sphincter, which usually is a U-shaped structure and that important space in the space. Other important structures in the perineal region that we need to be aware of is the ischorectal space, which is lateral to the external sphincter and the supra-elevator space, which indicates basically the deep pelvis above the level of the internal sphincter. The way we usually reference the perineal region is a lot of radiologists like the clock face, but basically when you talk to the clinicians and the surgeons, they hate that because when we see the patient, they are in the supine position on the scanner, but when they examine the patient, they are either in a decubitus or prone position. So their nine o'clock is different than what you're seeing as a nine o'clock. So if you use anterior and posterior, right and left, they know exactly, irrespective of the patient position, where the anterior right side of the patient is. So I encourage you to use that. What are the causes of perineal fistula? And one of the trick questions I always use with the trainees, I always ask them, what's the most common cause of perineal fistula? And they always say Crohn's disease. And the reason is because that's mostly what they see, but actually 90% of the cases are due to this cryptoglandular hypothesis related to those gland crypts that I showed you earlier, and we'll show that in a second. The second most common is Crohn's disease, but again, as many speakers have alluded to, this is very common. It develops up to a third of the patient, and it's usually related to rectal and anal disease. So what is that cryptoglandular hypothesis? Basically, you remember those glands, it gets blocked and infected. Now what happens is there's one way for the infection to move, and it moves towards that very important space we call the intersphincteric space. And this is what forms a deep anal infection or sepsis. And then that abscess has to break somewhere. So it has several routes to do that. Either it goes through that intersphincteric space up to the outer skin, or it goes across the external sphincter into the inter-eschiorectal space, and then goes to the skin. Or it goes actually up into the deep pelvis and then crosses back through that levator plate back into the skin. So these are multiple pathways for the infection to spread. What's the difference in Crohn's disease? The initiating event in Crohn's disease is actually rectal and anal disease. So what happened, basically, we have these strictures and deep mucosal ulcers that can form along the internal anal sphincter. And over time, they extend, especially due to the force of defecation. And the peculiar thing about these Crohn's disease-related fistulas, they basically cross the internal sphincter into that important intersphincteric space. And then from there, go into all these spaces. And more often, actually, we see them moving into all these directions, as opposed to the routine griptoglandular fistula, which usually is a single tract going into one space. It's usually intersphincteric. This is an extrasphincteric fistula. So how do you classify perianal fistulas? So the classification is mostly based on the location and the cause. So the simple fistulas are usually those idiopathic or griptoglandular. They're usually a single tract. They are intersphincteric space. They do not cross that external sphincter, which is very important for continence. And or the low transphincteric fistulas that don't involve much of the external sphincter. The complex one are usually these cross-disease-related one. They usually are branching or have multiple tracts going on either to the skin or to the deep pelfus. They're usually high transphincteric fistulas, so they have a significant impact on continence mechanism if there's injury to the muscle, and even can be extra or suprasphincteric. What's the classification? So there have been classically two classifications, Parkes, which is a surgical-based, and Morris, which was MRI-based, developed based on the Parkes situation. And the way we classify these is, one, based on the tract course, and two, if there's an abscess. So the simplest grade one, the one we start off, is the intersphincteric fistula. Two would be the same plus an abscess. Three would be the transphincteric, and four, you guess, with an abscess. And the fifth one is the most complex, which is basically the supra-elevator that starts in the deep pelvis and goes out, or the trans-elevator that goes up and then goes back to the skin across the external sphincter and elevator plate. So now we covered the anatomy. Our next is the treatment goals. What is the treatment goal for a perineal fistula? One is we need to drain that local infection. We need to make sure that it is drained because this is the only way it will heal. Two, we want to eradicate that fistula's tract because if that tract stays there, it's gonna continue to be communicating with the bowel lumen and has an infection. We want it to heal completely without recurrence, especially in the patients who have Crohn's disease. And most importantly, to maintain continence. We don't want to convert the patient to his continence by treatment, so we want to solve the issue of an infection or an abscess or pain and get the patient to be in continence. So this is a very important goal, especially for the surgeons. Typically, if there's a perianal abscess, like you see in this case, the approach is very simple. You start with surgery with incision and drainage, and then you can leave that wound open and basically it will clear. If we have a fistula tract with an internal and external opening, what basically, all of these patients will go to the exam under anesthesia. The surgeon will basically do the exam, use a fistula probe to identify the external and internal opening, and then what they do, they basically place these non-cutting c-tons. There are cutting c-tons that have been used, but now they're less used, and now they're using these non-cutting c-tons to avoid muscle injury, and basically place that loop that will help the infection clear, just to keep the tract patient for the infection to clear up. There are other methods that are more specialized, and you find them in some centers. I wouldn't find them more in the general community, but more in the academic centers, including the indirect advancement flap, which basically moving part of the mucosa to cover the internal opening so it will heal, or a ligation of an intersphincteric fistula tract, or a lift procedure where they try to excise the intersphincteric fistula. There are also now newer agents where they inject mesenchymal, or adipose-derived stem cell injections, trying to induce healing of the tract itself, and there are other plugs, fibrin glues, laser ablation, but as I said, these are more specialized centers that deal with these on a constant basis. So what's the role of imaging? Role of imaging, mainly at acute presentation of anorectal abscesses is not much, because usually at physical exam, you can feel the abscess, all you need to do is just incise and drain that. However, if you present with a patient with Crohn's disease, you know that they have a high likelihood they're gonna have a complex fistula, so you are more inclined to image these patients, because very often, what you see on the surface does not represent the entire disease. Third, you wanna rule out an abscess in a patient with Crohn's disease before starting immunotherapeutic therapy, because you don't want that abscess to blow up. Another way we do it, and actually, this is why we see more often of these patients, because we do follow-ups, and follow-up to assess treatment and to see new symptoms, evaluate for recurrence. So did we miss a branching fistula tract with surgery? Trying to identify pus that's trapped in that interstitial space and hasn't yet opened up to the skin. There is insufficient response to medical therapy, so we're trying to give entity enough, we're giving antibiotics, but still the patient's complaining of symptoms or drainage. And in the end, it's there to assess that treatment response, especially in clinical trials. So what measure do you use, CT versus MRE? If the question is abscess, both modalities actually can answer that question for us, because we can visualize, as in this case, you see an abscess on both modalities. But if the question is, I wanna see the fistula tract itself, MRE definitely wins over CT, because of the higher signal-to-noise ratio and the distinction of the muscle groups, layers, interstitial space, and everything else. So we need an MRE in that. And I had a slide here, but I removed it, to respond to the earlier comment. I'm actually one of the opponents of doing a field of view, small field of view for pelvic MRI. I prefer to have a full, dedicated MR pelvic examination for a fistula. So you can do the MR examination. For the full bowel evaluation, and there is a specific about the bowel, I prefer doing a dedicated full examination of the MRI pelvis. But I know many institutions do a form of a hybrid protocol. What do you need in your protocol? You need, basically, essentially, these high-resolution T2-weighted images that are great to outline the muscle groups, the fat planes, the spaces, and you need a T2-fat-sat image to highlight edema. You want a post-contrast image to highlight the inflammation and the increased contrast uptake. It's preferable to do multi-planar acquisition, especially in the sagittal, coronal, or you can do oblique along the internal sphincter in the axial or coronal plane to better delineate the entire muscle, see the opening, and so on and so forth. Optional, some institutions use a post-phase T1-weighted imaging, diffusion-weighted imaging to highlight more edema. So these are more optional. So what are the checklists that we have to go through? Is one, is there a fistula? If there is a fistula, is it a single tract that has a secondary tract? Where are exactly the internal and external openings so the children know they have a roadmap where to start and where to poke to find us those openings? What's the relationship of the fistula to the sphincter complex? And I've said this is very relevant. What's the activity and the inflammation in that fistula? Is there edema manifesting as a high T2 signal? And is there inflammation by the increased contrast? And the last, most important question to answer is, is there associated abscess? Few quick examples to show. This is just a sinus tract. It goes from the anal region into the skin, overlying tissue, but does not reach the skin. This is a type one, a low intersphincteric fistula, a linear tract coming outside from the internal sphincter through the intersphincteric canal over to the allelic skin. This is a type two, same tract with an abscess or a horseshoe abscess in the intersphincteric space. A type three, you can see now the fistula tract crosses the external sphincter. A four, same, crosses the external sphincter and has an associated abscess with it, highlighted in blue. And the five are these horrible complex fistulas where you see there's a long fistula tract extending from the deep pelvis, from the rectum, going across the levator plate and going all the way to the skin. And you can see there are multiple abscesses along the way in this patient. This is a branching fistula. We can see more than one opening to the external skin. This is a complex anovaginal fistula, which are usually anterior, between the anterior wall of the anal sphincter and the posterior wall of the vagina. And these are complex and difficult to heal. This is an example of a seton. Usually it is a low signal. It's a signal void and indicates the presence of the seton in the tract. Sometimes it's relevant to make sure that they put the seton in the appropriate tract and we've seen cases where they missed that. This is an example of the treatment response. On the left side of the image, you can see on the T2 image, there is a bright signal indicating the fluid and the edema along the tract. On the right side, you can see how after the fistula healed, it's now a dark linear tract. So this is now a scarred fistula. It's no longer active. It does not have inflammation. Same thing on the bottom. You can see on the left side, there's a lot of inflammation and activity early. Later on, basically it disappeared. This is like the minimum enhancement in the linear tract. On the right side, on the right perianal region, you can see that other fistula still has some enhancement. So there is some activity there. The one on the left has completely healed or scarred. There are multiple, if you participate in clinical trials, you can offer that to your clinical colleagues. There's a Van Asch index. There's a new one and Jordi here is also a participant in that group for the Magnifi CD index, which basically takes a combination of all what we talked about. The tract, how complex it is. Is it involving the external sphincter? Is there a fistula, sorry, how long is the fistula? Is there an inflammatory mass or an abscess? And the more you have that complexity, you get a higher score. And you can use that in the follow-up. So if an original fistula has a score of 10 and the follow-up is a three, that you know that there is a response to the treatment. Last, this is another paper I would also encourage by Cynthia Senterland from our group also, the FP has published the topics in magnetic resonance imaging. It's a great review about the fistula, perennial fistula, and also offers this standardized reporting. It looks big and I always, cautious people, whenever you see these templates, everybody say, oh, it's too big. Yeah, because it contains all the elements. No fistula has all of these. It's impossible. So even the most, worst complex fistula you're gonna fill, it's gonna be half of this field. And that's, I'm talking the worst. So basically, just making cover. And if you do it in a structured manner, you make sure that you're talking about the openings, you're saying where is every track, how far it goes, is there an absence? You make sure it is inclusive of all the relevant information. So in conclusion, basically MRI can help in the pretreatment and preoperative evaluation of perennial fistulas, in particular, with suspected complex fistulas in the setting of Crohn's disease. Classify fistulas properly according to their location, relationship of the track to the sphincter complex. And if there is an unassociated, undrained infection or abscess, this is extremely relevant. And we can use also MRI for follow-up to assess why there is a recurrence of the symptoms of the drainage. And two, is the treatment response, especially in trials. And thank you for your time.

Crohn's disease

stricturing

penetrating

imaging techniques

inflammation

fibrosis

fistulae

MRI

surgical interventions

treatment strategies