Good afternoon, my name is Dr. Olga Brook and I work at Beth Israel Dickens Medical Center in Boston and at Harvard Medical School. I'm going to talk today about lower GI bleed. So we'll talk about definitions, algorithm for treatment of patients with lower GI bleed and what is the role of imaging. So first of all, this is a clinical guideline published in 2012. So you can see here there are a lot of text, however, the CTA appears on only one spot here. So where is that CTA and what is the role of CTA? First of all, it's only reserved for high-risk patients. What are those high-risk patients? Are patients who are hemodynamically unstable, whether it's tachycardic, low blood pressure, altered mental status, or syncope, with lower hematocrit, and patients older than the age of 60. So only high-risk patients. Next though, we don't administer CTA to all patients who is high-risk. But first, all those patients needs to be resuscitated with fluids, upper endoscopy should be performed to rule out upper GI bleed, and only then if the patients remain hemodynamic unstable and intolerant for colonoscopy prep, then those patients will undergo CTA. Otherwise, colonoscopy is the way to go. So what are the causes for lower GI bleed? There are a lot of causes, but most common is really diverticular disease, and then we have a few zebras. So this is the typical patient that presents with lower GI bleed to the emergency department. This is a 90-year-old woman, extensive primary rectum. She is hypotensive, she is tachycardic, and her hematocrit is low. So what is the imaging, what is the next step? What is the appropriate next step? We can perform angiography, because potentially if we see the bleed, we can treat immediately. However, this is invasive procedure, so we don't really want to expose patients to invasive procedure unless absolutely necessary. Colonoscopy, as we'll see, as you can see, as you saw in the guideline, is a good way to go. And then we have TAGRA-BC scan and CTA. So should we do colonoscopy? Well, it is a preferred method because it's not just diagnostic, but also therapeutic. However, it does require prep time, and this patient does not have that prep time. She needs to be treated immediately. And also, in this patient, if they even try to do colonoscopy, they won't be able to see much because there is so much bleeding. So then what is the appropriate modality, CTA or TAGRA-BC scan? So CTA is very quick, but TAGRA-BC scan is much more sensitive for the slower bleeds. TAGRA-BC scan also does not require intravenous contrast. However, it will be difficult to differentiate on TAGRA-BC scan between the venous and arterial bleeds. On the other hand, it's very good for intermediate bleeds because you can bring the patient up to 24 hours later. And the intermediate bleeds is the most commonly what we see is the reticular bleeds. CTA is useful if the patient is bleeding right now, but if the patient bled until 20 minutes ago and now stopped, it's very difficult to diagnose that bleeding. CTA will provide much better anatomical definitions, which could be quite useful. So what about that sensitivity? So TAGRA-BC scan has been shown in prior papers to be much more sensitive than CTA for a bleed. Sensitive meaning we can detect much lower rate of bleeding. However, angiography has a very similar detection rate of bleeding as CTA. So if we do detect bleeding with TAGRA-BC scan, let's say 0.2 milliliters per minute, it does not mean necessarily that we will be able to see it on angiography. And if we treat with angiography, we have to see the source of bleeding with angiography. So it's really not that helpful to have a TAGRA-BC scan. So what is the protocol that we use for a rule-out GI bleed? We call it mesenteric bleed CTA protocol, and it consists of three phases, non-contrast lateral arterial and portovenous phases. In our institution, we use a different amount of contrast depending on the patient BMI, because we need to see it a little bit better in the larger patients. But we also use lower KBP, doxygenated iodine, in smaller patients. Because we can forgive more noise in smaller patients. What is the extravasation? Extravasation is basically contrast outside of the vessel. In this case, it's intraluminal contrast. And we need to make sure that it's not present on the non-contrast phase, because it could be food, tablets, oral contrast, or inspected stool. Next term that we need to know is arterial versus venous bleeds. Arterial bleeds, in general, are brisk, they appear on the arterial phase, they progress in portovenous phase. Importantly, though, they can be embolized with angiography. Venous bleeds are usually slow, and they appear on the portovenous phase, and in general cannot really be embolized unless this is a very sealed bleed. Sentinel clot is another term that you need to know. Basically, as we said, the reticular bleeds are frequently intermittent, and the patient may have bled 20 minutes ago, but not anymore, and what we will see is the high-density material in the bowel, and that's actually just clot there, and that's called sentinel clot. Let's go through a few cases. This is your typical patient, so this is arterial phase, multiple images in arterial phase showing the ecto-extremization in the descending colon, coronal images to confirm that, you can see all this contrast there. It was not present on the non-contrast phase, just bloomy, and was worse on the portovenous phase, so this is your typical patient with diverticular bleed, you can see the patient has multiple diverticular, and that's what caused the bleeding. The patient underwent angiography, and this is IMA run, that you can see this pseudoaneurysm in descending colon. When we put a microcatheter close to the site of pseudoaneurysm, we could see again the pseudoaneurysm on the delayed phase. You can actually see that there is ecto-extremization into the sigmoid colon. This was successfully embolized, you can see those cute small coils in this vasorector going towards that side of the bleeding, and on this angiogram post-embolization basically shows that there is no other vessels going to that area, and that's important, very infrequently we see this colorectalization. Most vasorector, if you really embolize just vasorector, this is end vessel. In this case, this is 80-year-old woman, possible ectomy with massive GI bleed. So what do we have here? What I'm showing you is two different phases, late arterial and portal venous phase. So in the portal venous phase, it's much easier to see this active extrovasation in the right colon, right? But you can also see that it's actually present on the arterial phase, and that's important, because then this patient can be treated with angiography. You can also see that this whole right colon is full of high-density material, and this is the centenal clot as well. This patient underwent angiography, and this is the area that was suspicious, and you can see, surprise, there is no active extrovasation. Why? Well, most GI bleeds, they actually stop by themselves, even the arterial ones. In this case, 75-year-old woman, acute or chronic GI bleed, and again, what I'm showing you here is late arterial and portal venous phases. So do we see active extrovasation on the late arterial phase? I don't see anything, but on the portal venous phase, you can see that there is actually contrast in the small bowel. So what is this? Is this venous bleed? Is this slow bleed, right? Those are really two options. I would say, because I see so much of arterial vessels here, it's not that this patient's heart does not pump, right? So there is definitely enough contrast that was brought on the arterial phase. There's enough opacification of arterial system here to rule out arterial sores. So this is really the venous bleed, and because of this diagnosis, you can't really treat it based on angiography, and the only treatment is basically surgical. Thankfully, it stopped bleeding on its own. This is the next case. This is a 45-year-old woman with cirrhosis and portal hepatitis and ongoing lower GI bleed. What we see here is, again, late arterial phase and portal venous phase. On the late arterial phase, I don't see any sores or bleeding, however, suddenly, on the portal venous phase, what we can see is all this small bowel full with high-density material. Where did this come from? Is this oral contrast? Well, first of all, the patient was not given oral contrast, but more than that, on the non-contrast study, you can see there is nothing dense there. So this is something that appeared within those 50 seconds, right? So this is just a very, very brisk bleed, right? So to feel that much of bowel, this is very brisk. So what's happening here, this is a very rare entity. As you can see here, patient is carrying cirrhosis cleaver, all those collaterals, and this area is actually collateral between the SMV and the gonadal vein that ruptured into the small bowel, okay? And that's what we see here. This patient was embolized through TIPS approach, so TIPS placed, and then this catheter is now in the SMV, and you can see here a connection between SMV and the gonadal vein. When the balloon was inflated, the contrast injected, you can see suddenly we have contrast in that small bowel. This was successfully embolized with TIPS approach, and patient stabilized. In summary, colonoscopy with QPREP is the first choice, a diagnostic and therapeutic modality for majority of lower GIB patients. CTA is a great tool for unstable high-risk patients. Dr. Abassis can tell, should be reserved for patients with abnormal renal function. Thank you, and if you have any questions, please reach out by email. My name is Daniele Marin. I'm one of the abdominal imaging faculty at Duke University. These are my financial disclosures. So the goal of this presentation is to share with you my approach to incidental focal liver lesions in a non-cirrhotic liver. These focal liver lesions are a common clinical problem. We see them on a daily clinical basis, and they are oftentimes encountered incidentally during imaging examination performed for unrelated reasons. It is important to realize that the vast majority of these lesions are benign, even if the patient has a known history of a primary malignancy. The goal of imaging is really whenever possible to establish a firm diagnosis and to prevent additional follow-up. In the event a confident diagnosis cannot be reached, imaging should provide appropriate management recommendations and occasionally, in a small subset of patients, guidance for a potential liver biopsy. There are different imaging modalities that have been used for the characterization of focal liver lesions, including ultrasound, CT, and MRI, and there are new technologies that can be used to expand our ability to characterize these lesions, including contrast against ultrasound, dual NRGCT, and the use of epithelial contrast agents. Before we go into a description of different lesion categories, I just want to say that the fundamental principle for the characterization of focal liver lesions is to have the appropriate imaging technique and the appropriate imaging protocol, as indicated, for example, in this MRI protocol, which includes multiple acquisition before contrast administration, multiple phases after contrast administration, including the delayed ability to face images. I cannot stress enough the importance of the appropriate imaging technique and, in particular, the appropriate injection rate for the acquisition of the late hepatic arterial phase. This is an example of two different patients undergoing hepatic arterial phase imaging with different injection rates. You can see the one on the right. The injection was very small because the patient actually underwent hand bolus injection due to vascular access, and you can see the profound impact of the smaller injection rate on the quality of the arterial phase images. One of the strategies we have with MRI to enable appropriate detection of the optimal timing of the arterial phase is the acquisition of a multi-phasic arterial phase during a single breath hold. So, after the acquisition of the appropriate imaging technique, the first question I ask myself when I see an incidental focal liver lesion is whether or not the lesion is solid or cystic. Cystic liver lesions, also known as benign hepatic cysts or epithelial cysts, are very common. They've been described in about 3% of the general population, and the diagnosis of this lesion is fairly straightforward. Generally, these lesions present with anechoic and increased neurotransmission on ultrasound. On CT, they have attenuation consistent with water density and lack of enhancement on the post-contrast images. And on MRI, they present typically with a—typically, they always present with a very bright signal intensity on the T-weighted images, as shown in this example. Occasionally, the diagnosis of a simple cyst can be somewhat challenging. This is an example of a patient that had a lesion that was iso-dense to the background liver parenchyma during the non—on the non-contrast images. On the post-contrast images, the lesion demonstrated no evidence of internal enhancement. There was—the lesion measured fluid attenuation and was consistent with a simple hepatic cyst, and the reason why the appearance of this lesion was so equivocal on the non-contrast images is the—due to the underlying hepatic steatosis that decreased the attenuation of the background liver parenchyma. Another situation where cyst can be challenging to diagnose is when these lesions are very small in size, as indicated in this example. In this situation, the attenuation measurements of the—on CT can be challenging due to the potential confounding of partial volume. Another situation where they can confuse the—in the diagnosis of a simple cyst is when we are dealing with a larger lesion, particularly when the lesion has a complex appearance with the—for example, with the presence of internal septations, as indicated in this case. Occasionally, the differential diagnosis with a more—some more rare entities, such as a biliary cystadenoma, can be challenging, but in general, if the set are small in size, the enhancement is imperceptible, and the lesion has, you know, like a very smooth, like contours, the diagnosis should be fairly straightforward. Another situation where the diagnosis of a simple cyst can be somewhat—can be challenging is in patients with treated metastatic disease. The classic example is gastrointestinal stromal tumor. You can see this patient presented in 2010 with a large gastric mass, which was proven to be a surgery in gastrointestinal stromal tumors. After a few years, the lesion presented with a new liver lesion, which was consistent with metastatic disease. The lesion was treated using antigenic therapy and underwent a complete cystic degeneration, as indicated on the image in the right lower corner. It would be very challenging to differentiate this lesion from a simple cyst on these images only without knowledge of the prior clinical history. After I determined that the lesion is not cystic, the second question I ask myself is whether or not the lesion is following the blood pool. Blood pool enhancement is defined as enhancement within the lesion or at the periphery of the lesion, which mirrors the blood pool, which is the aorta or the portal venous phase—or the portal vein in the portal venous phase. As indicated in this example, we have a large hepatic mass with multiple areas of peripheral enhancement and central—more central enhancement. These areas of enhancement are isodense on CT compared to the blood pool. There is also progressive and centripetal enhancement of the lesion on the portal venous phase images, which is consistent with a benign hepatic hemangioma—in this case, a giant hemangioma because the lesion was larger than 10 centimeters in size. Occasionally, I have—I want to say that blood pool enhancement to me is a more important imaging characteristic compared to peripheral or discontinuous enhancement or progressive enhancement for the diagnosis of hemangioma. This is an example of a smaller lesion in the periphery of the liver, which showed homogeneous enhancement on the arterial phase and sustained enhancement on the portal venous phase. The lesion, if you pay close attention, the lesion is actually mirroring the enhancement or the attenuation of the blood pool, and this was consistent—shown to be a capillary hemangioma on subsequent MRI. This lesion can be very challenging to diagnose, particularly, as in this example, in the context of cirrhosis. If I determine that the lesion is not cystic and does not follow the blood pool, the next question I ask myself is whether or not the lesion is hypervascular. There is a fairly broad differential for hypervascular liver lesions, including benign entities, more commonly focal nodular hyperplasia and adenoma, or malignant entities, such as metastatic disease or HCC. Focal nodular hyperplasia is a common benign hepatic neoplasm, which originates from a congenital anomaly of the arterial blood supply to the liver. The diagnosis of focal nodular hyperplasia is fairly straightforward on CT and relies on homogeneous and even enhancement of the lesion on the arterial phase, with the exception of the central scar. The lesion fades to isodensity on the portal venous and the late phase and demonstrates delayed enhancement of the central fibrous scar on the delayed images. Focal nodular hyperplasia has been described in association with hepatic hemangioma in a fair number of cases. It is not uncommon for focal nodular hyperplasia to demonstrate somewhat atypical imaging findings, such as the absence of a central scar, a T2 high signal intensity on MRI, or the presence of somewhat a washout on the delayed images. Hepatic adenoma is the second common hypervascular liver lesion in a non-cirrhotic liver. There is a wide variety of different subtypes of hepatic adenoma, which have been described. Each of these subtypes has a very characteristic or different imaging appearance and very different prognostic implication. It is important to be aware of the inflammatory and beta-catenin subtypes of hepatic adenomas because they have increased propensity of bleeding or potentially malignant degeneration. I'm not going to describe the characteristic imaging findings of each individual subtype, but I want to point out some of the imaging characteristics that I look for in the diagnosis of hepatic adenoma. The first thing I look for is intra-lesional fat content, as demonstrated in this example by the drop of signal intensity of the lesion on the opposed phase images. The second imaging characteristic is the presence of areas of hemorrhage, as indicated at the bottom on the bottom image, by the areas of increased signal intensity on the T1-weighted fat cell image. On the T2-weighted images, hepatic adenomas can be a very characteristic increased signal intensity, particularly the inflammatory subtype. And as indicated in this example, the increased T2 signal intensity can be seen at the periphery of the lesion, also known as the atal sign. On the post-contrast images, the hepatic adenomas can have different degree of arterial enhancement. In this case, in this example, it was fairly bright. And on the portal venous phase and equilibrium phase, there could be some degree of washout. But again, this is fairly variable in clinical practice. One way we can actually facilitate the differential diagnosis between hepatic adenoma and FNH is the use of hepatobiliary contrast agents. These contrast agents are taken up by the normal hepatocytes commonly seen in the FNH, but they are generally not taken up in hepatic adenomas because of the downregulation of these transporters in the adenomas. This is an example of a classic focal nodular hyperplasia lesion demonstrating homogeneous vivid and homogeneous enhancement on the arterial phase and delayed uptake of the contrast agent during the hepatobiliary phase. As opposed to this other example of a patient with multiple liver lesions, this one in the peripheral portion of the right periclobe demonstrates vivid and homogeneous enhancement on the arterial phase, which can simulate a focal nodular hyperplasia. On the delayed hepatobiliary phase images, however, you can see that the lesion demonstrates lack of uptake of the contrast agent, and this was consistent with the hepatic adenoma as subsequently proven by a biopsy. It is important to be aware of the fact that a small subset of hepatic adenomas can actually take up the contrast agent on the delayed hepatobiliary phase images. These are generally the beta-catenin subtype of hepatic adenomas, and it's been shown that beta-catenin activation can actually lead to overexpression of some of the OATP transporters that are responsible for the uptake of the hepatobiliary contrast agent. It's been discussed that potentially we can use the information of the uptake of the contrast agent to stratify and to characterize the risk of malignant degeneration of a hepatic adenoma. Hypervascular liver lesions, as we mentioned before, can also be malignant, and this includes generally metastatic disease, HCC in a non-cirrhotic liver, and fibromyalar HCC. Generally speaking, there are clues in the images or in the clinical history that can point in the right direction in the right diagnosis, and metastatic disease is generally associated with a known history of primary malignancy, and HCC in a non-cirrhotic liver and fibromyalar HCC tend to present as larger masses with heterogeneous enhancement. Occasionally, the differential diagnosis between FNH and ephemeral mellar HCC can be challenging. However, there are some important imaging findings that you can use, including presence of calcifications within the central scar, the T2 signal intensity of the scar itself, or presence of anopathy that allows a differential diagnosis between these two lesions. If the lesions are not hypervascular, the only possibility is that you are dealing with hypervascular liver lesions, and in this situation, I always worry about metastatic disease. Again, typically multiple variable in size, generally associated with a known history of a primary malignancy. One important clue that you can look for for a confident diagnosis of metastatic disease is the presence of a continuous ring of enhancement during the arterial phase. This is characteristic and should not be confused with a discontinuous peripheral enhancement of hepatic hemangiomas. More recently, dual NRGCT has been shown or has been proposed as a powerful tool for the diagnosis of small hepatic metastases that demonstrate increased iodine content compared to hepatic cysts. So in conclusion, focal liver lesions are a common imaging finding and are frequently incidentally found in non-cirrhotic patients. The majority of these lesions are benign and can be confidently characterized as imaging using a standardized imaging approach. It is my pleasure to introduce our next speaker, Professor Yves Meunier from Paris. My name is Yves Meunier and I am from Paris, France, and it will be my pleasure to share with you 10 simple lessons for improving MRI of the upper abdomen. Number one is anticipation. Because you want the best possible security, you need to detect in advance safety issues. Because you want to improve the cooperation with the patient, you need to teach and to train him and especially for breath hold and because you want to ensure a good communication with the technician, you need to clarify protocols in advance. Therefore, the lesson number one is that anticipation improves quality. Lesson number two is clear. Dixon T1 acquisition is the standard T1. It comes with the four images, water images, fat images, in phase, out phase. This patient has a liver cell adenoma with fat. You can see the signal drop on the out phase images. Therefore, always do this Dixon T1 sequence. Because we're talking about fat, you know that there is a signal drop on the out phase images and this is very easy to measure in minus out by twice in with a Roy on each image and then this tells you that this patient has a 27% fat fraction. Lesson number three, the fat fraction is very easy to measure. It is very reproducible. It is an excellent biomarker. It is the reference standard as for today and you should do it. You should measure it in your report. Anytime you have the impression that the in and out images are not quite similar. Things are going the other way around with iron overload. There is a signal drop but the signal drop is on in phase images. So what happens if there is both fat and iron? This is very confusing because you may have the impression that the examination is absolutely normal and if you measure, you will find a fat fraction of zero. So how can we do it? We can do it using a six or better 11 echo sequence and how does it work? This blue line is the normal T1 intensity decay in a normal patient without iron and without fat. If there is iron overload, we observe that the slope is getting down and from the difference, you can guess the importance of the iron overload. What about fat? Beyond this line, you will still be oscillation between out and in phase signal and from the amplitude of the oscillation, you will be able to measure fat. Lesson number four, the combination of fat and iron is a trap on Dixon T1 with a two echo and it requires a multi-echo sequence to be identified. Coming to T2, there are two principal T2 sequences available, the single short fast spin echo also called HAST sequence and the turbo spin echo also called fast spin echo. Look at this patient. This patient has an hemangioma and he has also liver metastasis. Look at the single short fast spin echo. You can see the hemangioma, you can see another one here, but you don't see the metastasis. On the turbo spin echo, you see the hemangioma, but you also see the metastasis. What is the reason for that? The reason is quite simple. If you're looking at the turbo spin echo signal, it increases quite linearly with the increase of T2. This means that even if the T2 increases moderately, there will be an increase in the signal and you will see the images. Conversely, for the single short fast spin echo, the curve is more sigmoid and this sigmoid curves tells you that if you have only a mild increase in T2, there will be no increase in intensity and you don't see the tumor. Lesson number five, TSE is a tumor finder, single short fast spin echo is a fluid finder. Diffusion is very important and in my view, essential in any examination. Look at this patient, he has biliary cyst and liver metastasis. What we do is a four B values diffusion acquisition, B0 or B50, B200, B400 and B800. If you're looking only at the 800 image, you may be confused because the two images, the two lesions have exactly the same signal. But if you are looking at the line, you can see that there is a clear decrease in the signal for the biliary cyst. This is what we call the T2 shine through. Conversely, the signal from the metastasis seems to increase and this is what we call the restriction. This is what is translated in the ADC map. Here it is white because there is no restriction. Here it is dark because there is a restriction. Lesson number six, diffusion improves detection and helps characterization. It is recommended in most protocols. Cholangiopancreatography, the ideal sequence is the 3D acquisition. You have to read it according to MIP and different thicknesses and thin slices. Look at this patient. This patient has a left hepatic duct cholangiocarcinoma. We were quite unsure about the right side. There are two right hepatic ducts and maybe a stenosis here, maybe a stenosis here. Because there was no other contraindication, we went to surgery. It was a very young patient and unfortunately, the surgeon confirmed that the tumor was involving as well the right hepatic ducts and no surgery was unfortunately possible in this patient. You need also to look at the more conventional 2D images. Look at this patient. This patient has a clear cholecystitis, acute cholecystitis, thickened wall, small stones, but you don't see the gallbladder on the MRCP. And the reason is that there is pus within the gallbladder and the pus shortens the T2 and this is why you don't see it on the MRCP images. Lesson number seven, 3D MRCP is the standard but it needs 2D evaluation in addition. Contrast media. Contrast media, you have both extracellular gadolinium chelate. This is the routine contrast media and liver-specific contrast media. The liver-specific contrast media will allow you to have an hepatobiliary phase in addition. However, I would here concentrate on the best arterial phase and the role of delayed phase. This patient has a cirrhosis and we were looking for hepatocellular carcinoma. We were looking for the wash-in and wash-out. Wash-in. What I do is that I perform, in addition to bolus tracking, I perform three arterial acquisitions. Early, middle, late. And as you can see, the wash-in is only unequivocal on the late arterial phase. But you cannot predict it really before you do the acquisitions. If we had done only this one, we would have missed washing on this tumour. Reason number eight, whenever possible, in addition to the bolus tracking, use multiple arterial phases. This is usually very easy on 3T due to the high signal. Now look at the portal and the delayed phase. Portal phase doesn't show the wash-out because we still have some signal, some contrast media in the tumour. But the wash-out is clear on the delayed three minutes images. And therefore, my recommendation is that you should not delete the delayed phase. You should not skip the delayed phase because the wash-out may be seen only on the delayed images. Finally, we would like to shorten the examination. Yes, because the MR examination is lengthy. And when we want to shorten it, we are thinking of getting rid of the longest acquisition. Can we get rid of the turbospineco? Can we replace it with the single-shot fascineco or even with diffusion B0? Yes, probably, but not if we are looking for low-level tumours, low-contrast tumours. But yes, if we are looking for fluid-filled lesions. Can we skip the contrast injection? Probably sometimes if it is a follow-up of a known disease, if it is looking for a characterization of an hemangioma, of a cyst, of an adrenal adenoma, for instance. However, despite abundant literature, there is no consensus today on the abbreviated protocol for solid tumour evaluation. And therefore, the lesson 10 is that for, and not only for the patient, but also for you, the shorter would be the better. However, I am unable to give you a specific recipe, and this is a case-by-case issue. Now, I would like to introduce my colleague and friend, Professor Andrea Larghi, who is going to address the imaging of the colon beyond cancer and polyps. And with that, I would like to thank you very much for your attention, and I will be ready to answer any question you would have about this presentation. Thank you again. Good morning, and welcome to this lecture on imaging of the colon beyond cancer and polyps. There are a lot of diseases beyond cancer and polyps, inflammatory, infectious, and vascular colonic diseases. And I will try to give you an overview of those different entities. Let's start with a case. This is a man, 40-year-old, with a severe diarrhea, diffuse abdominal pain, fever, with a recent history of pneumonia, treated with antibiotics for two weeks, with high white blood cells count. And if we look at the images, there is some very bad signs. Look at the wall of the colon, there is a diffuse thickening of the whole colon, from rectum to sacrum. This is a case of pancolitis, with a diffuse and severe neural thickening, with a marked hypodensity of the submucosa because of edema, with enhancing mucosa because of inflammation. We recognize those wall nodularities, which correspond to the thumb printing observed in old barium enema studies. And of course, there is pedicolonic inflammation and the accordion sign. So those mucosa represent what looks like an accordion and the target sign. There is a list of differential diagnosis in a case like this, but in this case, the diagnosis is a pseudomembranous colitis. Pseudomembranous colitis is a colitis caused by a Clostridium difficile toxin. It is a leading cause of hospital-associated infections in Europe. The diagnosis is based on clinical and laboratory findings with demonstration of the toxin in the stool of the patient. We as radiologists might suggest this disease if we recognize the features I showed you before, of course, in an adequate clinical context. Let's look at another case. This is a lady, 54-year-old. Again, look at the colon, and you see that the descending colon, there is a marked thickening and diffused circumferential thickening of the wall. You see some pedicolic fastening, some fluid in the peritoneal deflection, and also involvement of the right colon, again, circumferential thickening. So this case was erroneously diagnosed as a possible ischemic colitis, and the patient underwent a colonoscopy. And those are the findings that were observed by the colonoscopy. You see the mucosa is whitish, and when the endoscopist tried to make a biopsy of this whitish mucosa, you see that it takes out a piece of the mucosa, a membrane, or better a pseudomembrane. That's the reason why pseudomembranous colitis is called in this way. Well, in this case, this was not related to CD, because pseudomembranous colitis are not always related to CD. You need to know that this is an entity that can be associated to different etiologies. In this case, the lady was a cocaine abuser. I talked in the differential about the tiflitis. What is a tiflitis? A tiflitis is a neutropenic colitis. It is an inflammation of the cecum and sometimes of the terminal ileum in patients with neutropenia, fever, and abdominal pain. So the landmark for the diagnosis is the recognition of the neutropenia. So if you do not have a neutrophil count less than 1,000 cells per square millimeter, don't think about neutropenic colitis. It can be observed either in children or adults, and the features are a circumferential thickening of the colonic wall, which is less prominent than PMC. This is the case of PMC. This is the case of tiflitis. There is less edema compared, of course, with tiflitis. And of course, there is a pericolonic inflammation. There might be ascites, and there might be pneumatosis in the colonic wall, which is not a feature of pseudomembranous colitis. As I told you, neutropenic colitis, in some cases, can involve the terminal ileum. This is a case of involvement of the terminal ileum together with the cecum, together with the ascites. This was a lady who was undergoing a high-dose chemotherapy. But when you look at those findings, those findings are really specific. So if you do not have the adequate clinical contact, you cannot make the diagnosis. This is a case of a patient with a severe edema in the cecum. It might look like PMC or, for example, tiflitis, but if you look at the appendix, this was a case of a rehabilitation of a chronic appendicitis with cecal inflammation. This is another case of a 59-year-old male with a history of HCV-related cirrhosis, previous sigmoid resection for diverticulitis, and the patient presents with abdominal pain, constipation, and rectal bleeding. We see the cirrhotic liver, some ascites, look at the colon, look at the descending colon, look at the thick wall, sigmoid colon. This is the anastomosis and the rectum. I can show you again the rectum, the anastomosis, a lot of edema, but we do not see the hyperdense layer representing flame mucosa like in PMC. So this patient was admitted to the hospital. Three days later, he had a worsening of the hepatic condition. He was referred to us for a TIPS. We performed a TIPS, and after the TIPS, this is the situation. A few days later, where we see the patent TIPS, there is still some ascites, some spraining infarct, and the colon is absolutely normal. You see, this is the anastomosis, the rectum, those are the images, completely normal. What was that? That was a case of portal colopathy, a colitis-like thickening of the colonic wall, which is usually present in the right colon. There are some unusual cases like this one in the left colon. It's an uncommon finding in patients with portal hypertension, and this is only edema and chronic inflammation of the colonic wall. This was a case of a male, a 64-year-old, with a recent surgery for sigmoid carcinoma presenting with abdominal pain. We see, of course, an abnormal left colon, where there is a thickening of the wall. There is a lot of pericolonic inflammation. There is some fluid in the peritoneal reflection, vessels are fatal. What can it be? It can be an inflammatory colitis or an ischemic colitis because of the segmentary involvement because of the left colon. There are, of course, some features in favor of either ischemic or inflammatory colitis. This is a case of inflammatory colitis, where you have this prominent con sign, where you see some lymph nodes that you usually don't see in ischemic colitis. What this patient was diagnosed with is a possible ischemic colitis, and there went a colonoscopy. At the colonoscopy, we see these darkish areas in the mucosa representing ischemia. The patient was, of course, referred to immediate surgery, and there was a segmentary ischemia as a complication of the recent surgery. So ischemic colitis is another entity that you can encounter when you look at the colon. The incidence is not very high, but the mortality is relatively high. It is a typical disease that occurs in elderly individuals with several comorbidities. And please consider it is a non-obscurus ischemia, so it is secondary to diminished blood flow, and that's the reason why we find in this area, in the left colon, it's benefactors on the seagull, which are the watershed areas of the colon. There are different types. We can have a transient reversible ischemic colitis with no sequelae in imaging. We have a chronic colitis with infiltration of scabbing and fibrosis in the pore. We have ischemic colitis, acute fulminant ischemic colitis with transmural necrosis, a perforation, and in most of the cases, a death of the patient. This is a case of a chronic ischemic colitis in an elderly lady. You see the segmentary involvement of the left colon. You see the thick wall, the density, which means a delayed enhancement, which is typical of fibrosis that have caused a complete loss of osteo. In this case, I can show you also the right colon, the sigmoid, which are normal, and I can show you also the images of the chronic ischemia in the left colon because the patient has a bloody diarrhea because of the inflammation in the right colon, and she underwent a total collective. This is a case of end-stage colonic ischemia with perforation and pneumatosis. Pneumatosis in the sigmoid, perforation, a lot of free air. You see air also in the portal venuses. This is an end-stage disease. And this is another case. It is a 50-year-old male in good clinical condition from mild abdominal pain. That's the reason why he was referred for CT, and we see again a lot of air in the wall of the sigmoid. This is the lumen, which is patent, and those are the cystic spaces filled with gas involved in the entire wall of the sigmoid. Is this ischemia? No, it is not. Pneumatosis cystoid intestinalis, so it means cysts filled with gas in the intestine, submucosal and subcutaneous. It's a very rare disease. It's unknown, but it's one of the primary forms of pneumatosis, which should be treated conservatively. And that's the reason why I present this table, where we have a list of the nine causes of intestinal pneumatosis. Pneumatosis does not always mean end-stage ischemia of the colon. And just let me finish up with another case. This is a 37-year-old female undergoing chemotherapy presented with mild abdominal pain, no fever, no neutropenia, and that's the reason why when we look at the images, we exclude the We exclude any other malignant reason for pneumatosis. We consider pneumatosis a relatively good chemotherapy. And after a few weeks, the patient was treated conservatively and the situation was completely resolved. This is my final case. And my final message is that when imaging the colon, please think beyond cancer. Thank you.

lower GI bleeding

computed tomography angiography

imaging techniques

diverticular disease

colonoscopy

patient assessment

Beth Israel Dickens Medical Center

Dr. Olga Brook