to share some interesting bowel-related cases for you today. So, case one, 50-year-old female with pelvic pain. So what do we do with a female with pelvic pain? Usually we start with an ultrasound. So I'm going to show you a few select ultrasound images labeled left adnexa, sagittal and transverse views, a gray scale and a colored opular image. I'll let you take a look at that for a few seconds before we move on. So what do we do in somebody with an adnexal finding on ultrasound that we can't fully characterize just based on the ultrasound alone? Oftentimes we'll go on to an MRI, which is what we did here. So a few images from the MRI, pre- and post-contrast T1 fat-saturated images on the left and a T2-weighted image on the right here. I will take you through a few cuts of the T2-weighted image here. It's important to look at all the slices together. So I'm showing you the adnexal finding again. And then the finding was made on the MRI, but because of a little bit of disbelief from the referring physicians, a CT was ordered just for more anatomic delineation. So I'm going to show you that CT next. Coronal and axial images from an IV and oral contrast-enhanced CT of the abdomen and pelvis. Again, select images through the pelvis, multiple contiguous images here in the axial plane and in the coronal plane. Okay, so our first question, and there's just going to be one question for each case here. I'll try to show you three questions. What is the diagnosis? A, hydrosalpinx or pyosalpinx? B, cystic ovarian neoplasm? C, Meckel's diverticulum? D, appendiceal mucinous neoplasm? Or E, small bowel obstruction? And I'm going to take you back to the images so you can see what's the clue in this case. So on the ultrasound, you can see there's a tubular structure, kind of a tubular structure. Certainly, what's a tubular structure in the left adnexa? First thing you're going to be thinking about is a hydrosalpinx. There's definitely some complexity here, some kind of laminated-looking avascular material. There's some complex ascites or fluid adjacent to the structure as well. So definitely pyosalpinx was a thought. On the MR, because of the level of complexity in the ultrasound finding, we wanted to see if we were dealing with a mass or is this truly just a pyosalpinx. Pre- and post-contrast images, there's some mixed T1 and T2 signal intensity material within this tubular structure in the left adnexa. The wall's enhancing, and there's some complex material here. There's a little bit of T1 hyperintensity layering here as well as T2 mixed signal in the fluid adjacent to this tubular structure. And the key here is that it's blind-ending, it's tubular, and you follow the stalk of this finding. And there it is going all the way up into the right lower quadrant. So if you can identify where that structure's coming from, and you take a look at this portion of bowel here and recognize that it's the cecum, then this has to be a blind-ending tubular structure extending from the cecal tip in somebody with an appendiceal mass of some sort. And on the CT again, here you can see the rim calcifications, which are harder to appreciate on the MRI, but that's the rim calcification and the dilated fluid attenuation structure arising, again, from the cecal tip here. Here's the stalk on the CT. Should tell you that you're dealing with an appendiceal mass. So in this case, this was an appendiceal mucinous neoplasm masquerading as hydrosalpinx or adnexal mass, and these are epithelial tumors that produce mucin and may result in pseudomyxoma peritonei. It's a spectrum of neoplasia from benign entities to outright adenocarcinoma. Trying to differentiate where you are in terms of the level of neoplasia can be difficult by imaging alone, but certainly the presence of pseudomyxoma peritonei would make you worry about a higher-grade lesion. And the treatment is appendectomy, surgical debulking, plus-minus intraperitoneal chemotherapy. So, great. Case 2, 30-year-old male with a remote history of trauma. Previously treated for a chronic pericardial effusion. Now with shortness of breath, tachycardia palpitations, and abdominal distension. So, shortness of breath, tachycardia palpitations. Usually we start with a chest X-ray. I'll let you take a look at that chest X-ray for a few seconds. Definitely not normal. Again, we're in the bowel section. So for this finding in the chest, as well as for the abdominal distension, they went on to a CT of the chest abdomen and pelvis. I'm going to show you the scout images from that CT first. And the answer is right on the scout, actually, but I'm going to also show you the axial and coronal images through the chest, the PE portion of the study, the CTPA portion of the study, just to show you the mediastinum and soft tissue and lung windows. And then I'll show you a coronal view of the abdominal portion of the study, as well as ask you the second question for this case. So the question is, what happened here? A, intrathoracic herniation of the stomach. B, bronchial leak with pneumomediastinum. C, esophageal leak with pneumomediastinum. Or D, colon perforated in the pericardium. Or E, infectious pericarditis. And I'm obviously ignoring the biggest abnormality in the abdominal CT here, but relevant to the diagnosis. So let's take a look at the images here. If you look at the CT images here, and you can see it in the CT scout image as well, you definitely see an air fluid level in the pericardial sac. It's pushing the heart posteriorly here. And in terms of other structures that are in the pericardium, you can see this upside-down U-shaped tubular structure here. Tracing that back to see what portion of the bowel it connects to, it's connected to the transverse colon. So this is the transverse colon in the wrong place in the pericardial sac, with an air fluid level. And somebody that just is having some cardiac symptoms as well as an obvious big fat attenuation intra-abdominal finding. So this is a colon herniated into the pericardial sac. And somebody with a prior history of chronic pericardial effusion that necessitated surgical treatment. So this is somebody with an intrapericardial diaphragmatic herniation of transverse colon, secondary to a large liposarcoma. Basically, the previous procedure that he had was a pericardial window. And there are a couple different approaches to performing pericardial windows. They can be done anteriorly, either percutaneously or surgically through the pleural side of the pericardium. Or what many surgeons seem to prefer is a pericardial-peritoneal window, where they open the window inferiorly into the peritoneum. So there's a hole in the pericardium to drain whatever pericardial fluid, chronic pericardial fluid, is present into the peritoneum. And a potential hole for herniation. Usually the left lobe of the liver protects the window from any kind of a herniation. But in this particular case, it's rare to have a complication of intrapericardial bowel herniation. And it can be secondary to these pericardial windows. It can be from a congenital defect in the transverse septum of the pericardium. It can be from trauma, from prior procedures like a coronary artery bypass graft or subxiphoid epicardial pacer insertions. In this particular case, it's secondary to a large mass that's pushing the colon and all the intra-abdominal contents towards the right as well as superiorly. And the reason why they seem to prefer this subxiphoid approach is it seems to have a lower complication rate and infection rate compared to external drainage or other anterior approaches. And it's important to surgically repair these to prevent incarceration, strangulation, or cardiac tamponade. In this case, the colon already perforated into the pericardium, but they were able to do a subtotal colectomy or a partial colectomy as well as to remove what ended up being a well-differentiated liposarcoma, which in this case actually arose from the mesentery rather than the retroperitoneum. And this is a companion case from a CT colonography following an incomplete colonoscopy. This may be a colonoscopy complication where the colon is actually herniating through a diaphragmatic defect. Whether it was related to the colonoscopy or not, I don't know if the GI folks will ever fess up, but certainly possible and has been described in the past. And my last case is a 26-year-old female with abdominal pain. I'm going to show you some images from the MR enterography. TT-weighted images on the left, T1 post-contrast images on the right. And I'll show you the same images in the axial plane. All right. And then just for kicks, I'm just going to show you a CT following a procedure for this finding. Coronal and axial images. All right. So my last question is, what is the diagnosis? And I'm showing you a steady-state free-possession coronal image from the MRE here on the left. A, adenocarcinoma? B, lymphoma? C, small bowel mets? D, polyposis syndrome? Or E, scleroderma? You can see multiple feeling defects in the distal small bowel, as well as interception on the original MR enterography here. You can see the intercepted portion of the bowel in the upper left quadrant. So this was a polyposis syndrome. In particular, this was Putz-Jager syndrome. When you have a polyposis syndrome, there's a whole spectrum of different polyposis syndromes that can be answers here. But in this particular case, it's in the small bowel. So that should narrow down your polyposis to either Putz-Jager's or familial adenomatous polyposis. Putz-Jager's is basically an autosomal dominant germline mutation in tumor. Most of them are associated with STK11 gene, a variable penetrant. Some of them are spontaneous mutations. And these are non-neoplastic hematomatous polyps sparing the mouth and the esophagus. They can result in interceptions and give you intermittent abdominal pain from interceptions. And are typically associated with mycocutaneous pigmentation, oral, nasal, axillary extremities, genitalia. The important finding here, though, is that although the hematomatous polyps don't really have elevated neoplastic potential, there are certainly associated malignancies 18 times greater than the average risk of malignancies in other organs. Not just GI tract, but also breast, pancreas, ovaries, uterus, and cervix, as well as testes and lung. And here, screening is recommended for those malignancies, the other associated malignancies. And just a real quick companion case here is a solitary hematomatous polyp in the terminal ileum, which is telescoping through the – it was telescoping or intercepting through the ileocecal valve. And this one's near and dear to my heart because this is my own hematomatous polyp. I do not have the STK11 mutation, so this is presumably a sporadic solitary hematomatous polyp. So get your screening at 45. Thank you. Hello, my name is Shannon Sheedy, and I'm from Mayo Clinic Rochester. Thank you to Dr. Jane Wing for the invitation to speak. I wish I could be there in person, but hope that those of you who are there are enjoying the conference. I have only a few short minutes today, so this will be a bit of a whirlwind. I'll be providing a case-based review of biliary imaging, showing interesting cases with hopefully some good teaching points thrown in. Starting off with immune-mediated and inflammatory conditions, on the left we have an example of PSC with multiple typically short structures and often involving both the intra- and extrahepatic bile ducts. The intervening segments may be normal or slightly dilated, resulting in a characteristic beaded appearance. On post-contrast images, we see duct wall thickening and enhancement in keeping with inflammation. When cirrhosis is present, atrophy of the left lobe can be a clue to the PSC etiology compared to other etiologies of cirrhosis where the left lobe is usually hypertrophied. Up to 70 to 80% of PSC cases are associated with IBD, especially ulcerative colitis. The only cure available at present is liver transplant. However, PSC can recur in the allograft. On the right in PBC, there is autoimmune destruction limited to the intra-hepatic bile ducts. PBC is not associated with IBD, but is strongly associated with other autoimmune diseases, especially Sjogren's syndrome and autoimmune thyroiditis. PBC has a very strong female predominance and is usually diagnosed through blood tests and liver biopsy versus through imaging. However, the classic imaging finding is seen on this T2-weighted image where you see the parenchymal lace-like fibrosis and the periportal low signal halosign. Successful medical therapy now often precludes progression to cirrhosis in many of these PBC patients. They do not have the same rates of malignancy as PSC patients. The risk of cholangiocarcinoma in PSC patients is about 15%. Occasionally, however, cholangiocarcinoma can occur de novo in patients without PSC. The CT and MRCP in this patient with right upper quadrant pain and jaundice showed a stricture with enhancing soft tissue resulting in bile duct obstruction and was concerning for cholangiocarcinoma. However, there were no background changes or a history of PSC. Both biopsy and C199 were negative. And when radiology re-reviewed the imaging, we actually suggested that because of the smooth, tapered appearance of the stricture that IgG4-related disease should be considered. The serum IgG4 level was not elevated, but there was very faint IgG4 staining at histopathology. And with a steroid trial, the patient had significant improvement of the stricture, as is the hallmark of IgG4-related disease. IgG4-related sclerosing cholangitis can be indistinguishable both clinically and on imaging from PSC or cholangiocarcinoma. However, some potential clues to the IgG4 diagnosis include isolated extrahepatic duct involvement, as well as longer, smooth and symmetric strictures with funneling and, of course, finding other organs of involvement. Three interesting cases here. On the left, a patient with an outside diagnosis of PSC presented with mental status changes. MRCP appearance was in keeping with the outside diagnosis of PSC. However, the ER doctor noticed this rash on his palms and soles and the patient was ultimately diagnosed with secondary syphilis. He had complete resolution of the biliary imaging findings following treatment with penicillin. Remember also, in HIV-positive patients, AIDS cholangiopathy can also be a mimic of PSC on imaging. The young patient in the middle presented with abdominal bloating after traveling to Ethiopia. CT shows hypo-enhancing, ill-defined subcapsular areas and linear periportal changes, some of which converge toward the hepatic column. She was found to have marked peripheral eosinophilia and was ultimately diagnosed with fasciola hepatica caused by liver flukes. During the parenchymal phase of this infection, the immature flukes bore through the small bowel into the peritoneal cavity and then penetrate through the hepatic capsule to reach the parenchyma. In the biliary phase, they migrate to the biliary tree and their eggs and waste result in ductal inflammation and obstruction. The patient on the right first presented 15 years ago with right upper quadrant pain and jaundice and has suffered from recurrent bouts of cholangitis ever since. This patient is from China and has a diagnosis of recurrent pyogenic cholangitis. This is a diagnosis of exclusion seen primarily in Southeast Asians and may be associated with biliary parasites. The left lobe is most commonly affected and as in this patient, imaging typically shows focal stricture or strictures with upstream dilatation and hepatical lathiasis, and there's often associated parenchymal atrophy. Corollis disease is an autosomal recessive disease due to a congenital malformation of the precursors of the intrahepatic bile ducts. It appears as fusiform or saccular and sometimes cystic dilatation of the intrahepatic ducts with a normal extrahepatic duct and is segmental more often than it is diffuse as in this case. The classic imaging finding is the central dot sign. The dot corresponds to a central enhancing portal vein surrounded by the dilated bile ducts. Complications include intraductal stones, cholangitis, and abscesses, and these patients are at risk for developing cirrhosis over time as well as HCC and cholangiocarcinoma. Corollis disease is considered type 5 of the choledocal cysts but really is the only type with a ductal plate abnormality and we now know it is a different disease. Type 1 cysts with focal dilatation of the extrahepatic bile duct is the most common type, and types 2 and 3, saccular dilatation of the extrahepatic duct and a choledocal seal are quite rare. The patient here on the left was initially misdiagnosed with Corollis disease. However, these cystic areas do not communicate with the bile ducts and these are biliary hematomas composed of abnormal disorganized clusters of dilated ducts. They're usually tiny, fairly uniform in appearance, and can be mistaken for cysts, cystic metastases, or microabscesses, especially when there's a thin enhancing rim present at CT or MR. Autosomal dominant polycystic liver disease is thought to result from progressive dilatation of the disorganized ducts in biliary hematomas. These cysts are typically larger, of varying size, and they replace the hepatic parenchyma. The most common complications include infection, compression of adjacent structures, bleeding, or cyst rupture. Peribiliary cysts are mostly in a higher distribution along the ducts. The cysts can be hard to make out on CT, but they'll be seen on both sides of the portal veins as opposed to dilated ducts. They can be acquired, such as with chronic liver disease, or congenital, such as with polycystic disease. Cholangiocarcinoma is found most commonly in individuals with underlying biliary disease. Periductal infiltrate of cholangiocarcinoma accounts for approximately 60% of all cases, and it often occurs at or near the hepatic confluence. The initial ultrasound of this patient, with right upper quadrant pain, dark urine, and jaundice, discovered hypoechoic hyaluronidase. Subsequent MRCP and ERCP confirmed an obstructing hyaluronidase. Because of the concerning radiologic appearance, the patient was presumed to have cholangiocarcinoma despite negative cytology and CA-19-9. Because it involved beyond the second order ducts bilaterally, the patient was considered unresectable and went on to liver transplant. Unfortunately, biopsy of the mass from the explanted liver showed lymphoma. Other infiltrating ductal cholangiocarcinoma malignant mimics to be aware of include pancreatic cancer, gallbladder malignancy, and, of course, metastatic disease. The least commonly encountered subtype of cholangiocarcinoma is the intraductal subtype, accounting for about 10% of all cholangiocarcinoma. This subtype is also unique in that it has a relatively indolent course and relatively good long-term clinical prognosis. The CT and MR of this patient with known PSC and cirrhosis showed a regular unstructured bile ducts. The subtle filling defect in the dilated right hepatic duct was not identified at this time. An ultrasound several months later showed a regularity in wall thickening of the extrahepatic bile duct, and the hyperechoic mass in the right intrahepatic duct was erroneously attributed to sludge material. MRI two years later shows interval growth, and biopsy at this time revealed an intraductal cholangiocarcinoma. An ultrasound in this patient with right upper quadripane showed mild intrahepatic duct dilatation and what was thought to be echogenic biliary sludge. A CT at the same time shows the bile duct dilatation but also noticed the enhancing material in the extrahepatic bile duct. At ERCP, they discovered thick mucus as well as a carpeted villus polyp in the bile duct which was biopsied and was found to be noninvasive intraductal papillary biliary neoplasm, or IPNB. IPNB is a premalignant biliary epithelial tumor thought to be the counterpart of the pancreatic IPMN. However, it has a higher malignant potential and more variable mucin secretion than the pancreatic IPMN. When an actual mass is visualized, it may be multi-cystic or solid with a polyploid or superficial spreading morphology and will commonly have both up and downstream duct dilatation which is a clue to the diagnosis. Although a different entity, the mucinous cystic neoplasm of the liver, formerly referred to as biliary cystadenoma, can be mistaken for a complex cystic IPNB. This multi-cystic mass is characterized by the presence of ovarian-like stroma which is absent in IPNBs and thus this is found almost exclusively in females. The distinction can usually be made on imaging by the biliary ductal communication of the IPNB. However, as in this case, the MCN occasionally can erode and protrude into the bile duct. Whereas IPNB is considered pre-malignant, the MCN is only at low risk for stepwise progression to invasive carcinoma. Well, we had a whirlwind case-based tour today of the biliary tract. We saw examples of inflammatory disease including PSC, PBC, and IgG4-related sclerosing cholangitis. We saw interesting cases of infectious disease involving the biliary tract including a case of syphilis diagnosed out of the ER, fasciola hepatica in a patient who traveled to Ethiopia, and recurrent pyogenic cholangitis in a patient from China. We showed some examples of congenital and acquired cystic diseases of the biliary system including Corolles disease, autosomal-dominant polycystic disease, and biliary cysts. And lastly, we talked a little bit about cholangiocarcinoma, shared some potential mimics including lymphoma, and lastly, we touched on the introductal papillary neoplasm of the biliary tree. Thank you for your attention today, and I hope you enjoyed the tour. Hi, my name is Elena Korngold. I'm the Section Chief of Body Imaging at Oregon Health and Science University in Portland, Oregon. Sorry not to be able to meet with everyone in person in Chicago this year, but I hope you're having a wonderful time at the conference. I'm going to be talking about the peritoneum today and illustrating some important findings on cases. And so for our first case, whoever said that a picture speaks a thousand words has never seen a stack of pictures the way that we do. I want to start with just showing you this is an image of the pelvis. This is the bladder. And I'm going to go through the images on this patient from top to bottom. So this is a particular kind of study that is not a typical study, and we'll talk about what it is in a moment. This is a non-IV contrast CT of the abdomen and pelvis, and you can see that the liver and spleen are not opacified. The vessels are not opacified. The stomach up here is also not opacified. There's no bowel contrast. However, there is clearly contrast in this patient. And so the question is, where is this contrast? We can see that it is outlining liver, and you can see it laterally along the left abdomen as well. It is extending around the lateral aspect of the left colon here. We call that our pericolic gutter. And then as you go down further in the abdomen, you can see that it is outlining non-dilated loops of small bowel. Their mesentery is not bright with this contrast, and here you can see the omentum that's coming over. This is also, there's contrast outlining it, but not within it. And then in the retroperitoneum, you're not seeing that contrast either. And so as we go down, you can see pretty clearly that this contrast is all within the peritoneal cavity. And coming down into the pelvis, you can see that it starts to kind of come centrally with sparing laterally along the lateral pelvis, and sparing anteriorly as well in front of this bright contrast. And so the question is, what is this contrast, and why is it there? Again, as we start at the beginning, we can talk about the fact that this is the bladder, right? So this contrast didn't come from the bladder, and this contrast didn't come from the bowel. So where did it come from? I can show you three images demonstrating the same findings on the same patient. You've got this incredibly bright contrast in the peritoneal cavity that is sparing the mesentery here. You can also see it spares retroperitoneally, and then extending posterior to the rectum and sigmoid. It also extends above the bladder, but not in front of or below the bladder. So this is the peritoneal cavity, and you can see here I put an arrow. This is our peritoneal cavity. This was our omentum, that fat that floats within it anteriorly. That's separate from the mesentery that's supplying this small bowel. And you can also see here that this left colon and right colon are also separate, and not within it, but actually it's coming up and over, and these are retroperitoneal structures. This down here, and we'll come back to it in a second, is the anterior peritoneal reflection. This is the inferior-most portion of the peritoneal cavity, posterior to the bladder and anterior to the rectum, and this is an important landmark that we'll talk about in a minute. And it's important to note as we look at all of this that the peritoneal cavity actually doesn't come down too far into the pelvis. It tends to sit up higher in the pelvis and within the abdomen. It spares anterior, posterior, and lateral. So why do we do this study? It was done as a peritoneogram, and it was looking for, you can see it was actually too bright, the contrast, to see that there's a peritoneal dialysis catheter in this patient. And if you look up higher, you can see that it was coming through the abdominal wall, and there was spillage of peritoneal dialysate, or contrast, through the entry point of the catheter. And that's what this study was done to evaluate this peritoneogram. This is an image showing what that peritoneal dialysis catheter looks like, but when you look at it in real time, you can see that it spirals like that, so it can, and it lays low in the pelvis, in the bottom of the peritoneal cavity, and is used to infuse the dialysate for patients with end-stage renal disease. So what is a CT peritoneogram? Well, it's done in patients who have peritoneal dialysis catheters, have end-stage renal disease. What are the indications? So it's either difficulty with fluid exchange, recurrent peritonitis, or as in this situation, it's an abdominal wall fluid bulge, or edema, and no one can figure out where it's coming from. And what was the issue with this patient? This patient had an abdominal wall fluid accumulation due to a catheter leak, and fluid coming through the abdominal wall. And what can this teach us at the peritoneum? So we know, as we said before, the peritoneal cavity lies mostly above the pelvis, and it is filling the sort of central abdomen. You can see it around the liver. There's actually fat that's outside of the peritoneum that's in front of the peritoneum called the properitoneal fat. This patient has more of it than some. That's extraperitoneal. And I thought this was a good illustration just showing that it kind of comes above the bladder and then down and hooks right in front of the rectum. And this is all intraperitoneal, while this is all extraperitoneal. So how can we use that information to assess images? So for case two, we're gonna take what we know and apply it. This was our trauma activation. That's how they come across in our hospital. Usually there's no other information that goes with it. And so on our bone windows on this trauma activation patient you can see that there are multiple pelvic fractures. The pubic ramus and then the inferior pubic bone, and in the sacrum. So on this same patient, you can see as we come up from the pelvis, we're not seeing the pelvic fractures the same way, but you can actually see that there's fluid anterior and lateral to the bladder. And this is sort of low in the pelvis, right? So we can see that there's this fluid in the front of the bladder and around towards the pelvic sidewalls. And so the question is what happened to this patient, right? Fluid in the abdomen post-trauma is always worrisome. And in the setting of pelvic fractures, we worry about bladder injury. And so as we're coming up, you can see that there is this fluid coming up and around the bladder, but it's not involving the loops of bowel in the same way that we saw previously. You can see that the small bowel is not supported by fluid. So in this same patient, they went ahead and they did a CT cystogram and that's when they put a Foley catheter in the bladder and give positive contrast. You can see that they haven't given IV contrast for this. It's a non-IV contrast exam. And you can see that there is fluid that is matching that bladder contrast to the side in front of, and then around on the other side, the lateral wall of the bladder. You can see it's extending. We almost call this the molar tooth sign where it looks like it comes up and around like a molar tooth with the roots on either side. Here's a good example of it. And so what happened with this patient? This patient had an extra peritoneal bladder rupture. This is actually 85%, the majority of severe bladder injuries. And it's usually due to pelvic fractures or penetrating injury in the setting of trauma, direct penetrating injury to the bladder itself. When it is extra peritoneal, again, this is not in the peritoneal cavity, the treatment is with indwelling Foley catheter and they allow it to heal. It usually tamponades off itself because there isn't a lot of space in the extra peritoneal tissues. And so this is an example in the setting of severe pelvic fractures of an extra peritoneal bladder injury. Here's another example of an extra peritoneal bladder injury. You can see that it's coming into that pro-peritoneal area below the rectus and that same molar tooth sign where it comes around the bladder, the front and the sides. And on this lateral view, you can see again, here is the contrast in the bladder and the contrast is coming up in front of the bladder in that sort of pre-peritoneal region. This is the peritoneum. It's almost an inverse of what we saw before. This is peritoneum, this is pre-peritoneal and this is that posterior where you can see that it's not in that same area that we would have seen before. So this is just looking, there's some almost inverses of each other. This was the intra-peritoneal where higher up in the pelvis, you could see it sort of sparing the lateral aspects of the pelvis and further down, you barely see any at all except for this posterior area between the bladder and the rectum. There was intra-peritoneal contrast, but then on the extra-peritoneal as we come further down, you're actually seeing the contrast filling the spaces that were previously spared. This is all extra-peritoneal contrast in that pre-peritoneal tissue and also laterally around the bladder. So this is what intra-peritoneal looks like. So it's higher up and it spares the anterior lateral aspect of the pelvis and the extra-peritoneal bladder rupture tends to fill those same areas that were spared. So for case two, this is another patient with bladder injury, but this is a very different pattern. And what do we see here as we come down? Again, we're seeing contrast in and around the loops of small bowel. And so again, this is a case of intra-peritoneal bladder rupture doing what that peritoneogram did before. And this patient doesn't have pelvic fracture in the same way. We can see that there's fluid. The contrast is in and around loops of small bowel, intra-peritoneal, and it's coming up the very top of the bladder is the defect, filling that peritoneal cavity in and around the loops of bowel. So this is an intra-peritoneal bladder rupture, which is only about 15% of cases. And it's usually actually a result of direct blow to a distended bladder in the setting of trauma. And the treatment has to be surgical repair. If you put a Foley catheter in, that will not solve this problem. It will not heal the same way. So again, just comparing intra-peritoneal, this is an intra-peritoneal contrast where you've got it coming down into the posterior bladder in the top of the bladder, but sparing the anterior bladder and surrounding loops of small bowel, as opposed to an extra-peritoneal rupture, which really doesn't involve the small bowel or the peritoneum at all. And it's just tracking extra-peritoneally in front of the bladder where it was completely spared before. And the last case we're gonna talk about, which is near and dear to my heart, is the anterior peritoneal reflection. That's referring to the anterior aspect of the rectum here and where the peritoneal reflection comes between the seminal vesicles and the anterior rectum. So this is a T2 sagittal exam of an MRI without Fatsat. This is a T2 axial oblique without Fatsat. And we do these for all of our rectal exams. And you can see that it's this line that comes up from the seminal vesicles to the mid to superior rectum. And on the axial, it forms the seagull appearance. That's the anterior peritoneal reflection. And that's our landmark we look for when we're assessing whether there is involvement of the anterior peritoneal reflection of rectal cancer. And again, this is just that contrast showing that same area right here, right? This is the peritoneal reflection, and this is that peritoneal reflection right here. And so this is a patient with a rectal cancer. It was a high to mid rectal cancer. This is the sagittal T2 again. And you can see that it's in the area that we'd expect the peritoneal reflection to be. And on the axials, you can actually see that that seagull is getting sucked in and involved with rectal tumor that has gone beyond the wall of the rectum. And so that's really important. This area, we call the mesorectum, and it's gone beyond the mesorectum, but involving the peritoneum itself. So it's gone intraperitoneally. And you can see here that gull wing is getting pulled in by the tumor. And that's important for us because it's actually an important part of staging. And so I'm not gonna go too much into detail, but for the lower rectum, it's completely extraperitoneal. And as you come up, the posterior portion of the rectum remains extraperitoneal. But as you come up, actually at the anterior peritoneal reflection, you have peritoneal covering of the upper to mid rectum. And so because of that, if it involves the anterior peritoneal reflection, it's called a T4A tumor. So that is the T4 is extension beyond the mesorectum. It means that it's perforated through the bowel wall, and then it's gone beyond the mesorectum, which contains the rectum, into the peritoneum. And so that actually changes the staging completely. And this is just a good diagram of what we're looking at here. So here's a rectum, and T1, T2, and T3 tumor is all within the mesorectum, which is the area that contains the rectum. But once you go and you involve the, this is that gull wing look, the anterior peritoneal reflection, it becomes a T4 tumor, which is the most advanced kind of tumor. So it's important to note and important to remember when we evaluate. So thank you very much. I hope these were helpful for evaluating the peritoneal cavity and looking at the different reflections. And I hope you have a good day. Okay, good morning, everyone. I'm going to be presenting a few pancreas cases today. I'm going to start with my first case. This is a 48-year-old woman with abdominal pain and steatorrhea. She was diagnosed with chronic calcific pancreatitis around 20 years ago. And here we have axial and coronal CT images in soft tissue and bone windows. I'm going to let you look at these images for a few seconds. My question is, what's the diagnosis here? Is this hereditary pancreatitis from a gene mutation? Is this main duct IPMN, alcoholic chronic pancreatitis, or a densely calcified neuroendocrine tumor? In the interest of time, I'm going to move quickly, if you don't mind. So the answer is hereditary pancreatitis here. So for comparison's sake, I have imaging from another patient who has idiopathic chronic pancreatitis in the bottom row. And we have our patient with hereditary pancreatitis in the top row. Both of them have obstructing interductal calculus, upstream ductal dilation, and surrounding parenchymal atrophy. So what are the findings that help us suggest that this patient may have hereditary pancreatitis? There are two things here. One, the patient has hereditary pancreatitis The stone is pretty large in size. In these patients, it tends to be larger than 50 millimeters in diameter. And another important finding is they tend to be centrally loosened, giving a bullseye appearance. And the clinical relevance of this is that when you say that somebody has hereditary pancreatitis, they have a better chance of having a technical success at endotherapy. Our gastroenterology colleagues talk about how these are pretty soft stones, and sometimes they almost are like toothpaste in consistency. But the more important relevance is that they are very prone for pancreatic cancer. There's a nearly 50 to 70-fold increase in incidence of pancreatic cancer, which means that starting at a particular age, they'll have to be screened for pancreatic cancer, and you may have to do genetic counseling for the patient's skin. Moving on to our next case, this is a 86-year-old man who, for a week, has a history of intermittent shortness of breath and decreased energy. We have CT images at the level of pancreas, unenhanced, and post-contrast phases. Again, I'm going to let you look through the images for a few seconds before revealing the diagnosis. Okay, so the answer is pancreatic lymphoma. The key imaging findings here that suggest that this patient has pancreatic lymphoma are there's diffuse marked enlargement of the pancreas. The head and neck are spared, but the rest of the pancreas is pretty bulky. And it's also very homogeneous, both in the unenhanced and post-contrast phases. The peripancreatic vessels, including sphenic artery and sphenic vein, are encased, but they still remain patent, and there are a few enlarged retroperitoneal lymph nodes. So the constellation of these findings suggests that this is pancreatic lymphoma. When you have a sausage appearance, just like sausages are all of different kinds, pancreatic sausages and their etiologies are also pretty variable. The most classic example is IgG4-related autoimmune pancreatitis, where you see the sausage appearance of pancreas. You see a thin, actually a rind of T2 hypointense capsularone that shows enhancement in the delayed phase. But there are other entities that can mimic autoimmune pancreatitis. The most dreaded of all is pancreatic adenocarcinoma. When you have a mass that is large enough to involve the entire body and tail and give you a sausage appearance, that's pretty advanced. Sometimes you may even see an enhancing capsularone, as in this patient. These patients usually have extensive regional vascular involvement, which is way beyond what you'd expect for autoimmune pancreatitis. And often they have a very bad prognosis. And this patient actually died in three months after the CT scan was done. Autoimmune pancreatitis is not only from IgG4. There are other entities that can do that. Here we have an example of a patient who had checkpoint inhibitor-related autoimmune pancreatitis. He had renal cell carcinoma, post-nephrectomy, he developed extensive retroperitoneal lymphadenopathy that responded very well to the therapy with nivolumab. But his pancreas, which was initially normal, later on got inflamed, and you can see extensive FDG ability. And a few months later, it actually decreased in size. The length is less, you see there's loss of the lobularity. These findings are suggestive of autoimmune pancreatitis related to the checkpoint inhibitor therapy. Here we have another patient with granulomatosis with polyangiitis. Some incidental findings in pancreas when he was being imaged for his pulmonary symptoms. Here again, you can see that there is increased bulk of the pancreas in the body and tail, a little bit of stranding around, loss of lobularity. He did not have any elevated serum lipase or amylase levels. And with therapy over a period of time, the pancreas became progressively atrophic. And finally, we have one more patient who has, again, a sausage-shaped appearance to the pancreatic body and tail, but this is just plain old, simple interstitial pancreatitis. This patient had acute and chronic pancreatitis. There is an obstructing calculus in the pancreatic duct in the proximal body. And you can see the enlarged hypo-enhancing pancreas with a little bit of surrounding fat stranding. Over a period of time with therapy, the body and tail was more normal in caliber, but you do see progression of the calcific pancreatitis. Next patient is a 48-year-old woman with incidental pancreatic cystic lesions and several punctate calcifications in the pancreas. These were all seen incidentally when the patient was getting worked up for trauma. I have CT images here on the left, unenhanced and post-contrast phases. And on the right is a MRCP image. I'm going to let you look through these images again for a few seconds. My question is, what's the diagnosis here? Multifocal branched duct IPMNs, asthma or cystic transformation, serious cystadenoma, or is this pancreatic amyloidosis? So the answer here is asthma or cystic transformation, or as it was previously called as asthma cell cystadenoma. This patient underwent endoscopic ultrasound that showed some cystic lesions without any solid components or thick separations. There was a little bit of debris here and there. The aspirate did not reveal any mutations, but the presumed diagnosis was branched duct IPMNs. Patient underwent distal pancreatectomy, and they saw these multiple cystic lesions which were lined by bland asthma reptilium, and there was no communication to the main pancreatic duct. So asthma or cystic transformation is an interesting entity. It's commonly seen in women, and the age group is slightly less than what you'd expect for branched duct IPMNs. It can be either inunulocular or multilocular. I don't think there's a way to preoperatively diagnose this if it is unilocular, but when it is multilocular, we do have a shot at making a diagnosis preoperatively, and that's really important. The features that we can see are multiple cysts, typically more than five. They tend to be clustered more in the periphery than around the pancreatic duct. You do not see a communication with the main pancreatic duct, and they often tend to have these punctate calcifications, and the clinical relevance is that you're going to avoid a surgery, and then they also don't need any long-term imaging follow-up. Moving on to the next case, this is a 52-year-old man with acute necrotizing pancreatitis from alcohol abuse. His initial CT scan presentation was without contrast, and we see some peripancreatic fat stranding. Four days later, he had a contrast-enhanced MRI that showed an area of necrosis in the proximal pancreatic body. There was an associated adjacent acute necrotic collection containing some hemorrhagic components, and six weeks later, he presented with increasing abdominal pain and had a CT scan. On the top row, you see the contrast-enhanced CT images, axial and coronal. He also had a MRCP at the same time. And my question is, in addition to this walled-off necrotic collection, what do you see there? Is there thrombosis of the main portal vein? Do you have finger-like extensions of this collection extending through the hepatodermal ligament into the liver? Or do you see any fist-less communication either with the portal vein or with the biliary tree? So the answer is pancreatoportal fistula. Here you can see that the walled-off necrotic collection is T2 hyper-intense with all the fluid signal, and you see the same kind of fluid signal in a tubular branching structure in the configuration of main portal vein. The red arrow points to the common bile duct in its branches, which are normal in caliber. So the key imaging findings that help us in making this diagnosis are presence of fluid attenuation or fluid signal intensity in the main portal vein, which is continuous and contiguous with a pancreatic fluid collection. Or you see a filling defect in the portal vein which has similar attenuation or similar fluid signal, similar signal intensity as the adjacent contiguous pancreatic collection. The clinical relevance is that when you see an occlusive or a near-occlusive filling defect and especially the setting of sepsis, these patients have a very high mortality. On the contrary, if the filling defect is subocclusive, and these patients tend to do very well, the survival is much better, and they also have long-term patients with a main portal vein. I'm going to show one more case, and I'm going to stop after that. This is a 17-year-old girl with intermittent upper abdominal discomfort, nausea and vomiting since a year and a half. She never had a history of acute pancreatitis or elevated serum lipase levels. Initially, a right upper quadrant ultrasound was done that showed a cystic lesion in the pancreatic head. She later on underwent an endoscopic ultrasound exam that showed some debris in the cyst, no solid components. The fluid aspirate did not reveal any elevated amylase, CEA, and there were no gene mutations on the aspirate. There's one more finding that I'm going to withhold for a few seconds. The patient also underwent an MRI, and we have the T2-weighted images, T1 pre-contrast, post-contrast, and 20-minute delayed hepatobiliary phase images. And my question is, what is this, a branched-type AMN, pseudocyst, ciliated foregut cyst, or a type 2 colitical cyst? Okay. So the answer is ciliated foregut cyst of pancreas. Now, among these entities, it's not a type 2 colitical cyst because it does not communicate with the biliary tree. We don't see any contrast extension on the hepatobiliary phase into the cyst. Branched-type AMN is very uncommon at this age group unless you have a gene mutation in something called SKIL. And the diagnosis was made preoperatively. This patient did not undergo surgery. The key finding was that this patient had, in the fluid aspirate, the patient had detached ciliary tufts. Either you see these, or you see a ciliated epithelium on the fluid aspirate. That's what leads us to the diagnosis. And the clinical relevance is that you basically avoid a major surgery or long-term follow-up. So that brings me to the end of my presentation. Great, so I have a few minutes to present my cases, which are liver cases with a little bit of a biliary flavor to them. Again, I'm Jorge Soto, and I'm at Boston University. Okay, the first case is a 62-year-old female with increasing right upper quadrant pain over three months. I'm gonna show a few images. This is the MRCP. This is the ERCP. And we have a few images from the cross-sectional MR study, T2-weighted with fat suppression, then the diffusion-weighted images with the ADC map, and then the arterial phase of the multi-phase contrast enhanced sequence, and the subtraction of the same image. So take a look, and the question is, what is the diagnosis? And you have a few options there. It is the intraductal type of cholendrocarcinoma. So notice that this is a purely intraductal lesion with relatively normal bile ducts elsewhere, which makes it not the IPMN that Dr. Shidi showed initially. The lesion is completely obstructing, and abruptly, the segment of the left hepatic duct. And the key feature that doesn't make it a stone or a group of stones, sludge, or parasites is that it enhances quite avidly with contrast, and it does have restricted diffusion. So it's a solid intraductal mass, and the morphologic classification of cholendrocarcinoma, there are several types, one of which is focal dilatation within an intraductal papillary mass. And again, the absence of diffused dilatation tells us it's not producing mucin. It is not IPMN. And this is an image of the pathology specimen, clearly showing the papillary mass and the normal biliary epithelium surrounding it. The next case is a young male who was involved in a motor vehicle accident presented with abdominal pain and tenderness, was stable hemodynamically, and we performed a multi-trauma CT, and I'm showing one image. And this is just hours after the injury. So obviously there's a liver injury, but the question is, what is the next step to confirm a suspected bile leak? Is it paracentesis, HIDA scan, ERCP, MR with hepatobiliary contrast agent, or follow the trend of serum bilirubin levels? And I think diagnosis could be confirmed with several of these options, but the question is, in practice, what would you do next? The most cost-effective way to make this diagnosis is with a HIDA scan. Yes, we can do MR with hepatobiliary agents, but in a trauma patient, and it's really not very practical. Plus, HIDA is just easier and cheaper, so advantage of a biliary leak is that you do have a little bit of time, so it's not something that has to be diagnosed immediately after the injury. It can wait until the following morning for the HIDA scan to be done. So this is the image of the HIDA scan, and we see the photopenic area, which is the liver injury, and then the free leak into the peritoneal cavity. The next question is, what is the recommendation for therapy for this patient? Is it multiple paracenteses, operative repair, conservative management, or ERCP with a stent placement? Remember, this is a free leak. There's a little bit different if it's a contained biloma within the liver. The answer is ERCP and temporary stent placement. So by placing the stent, the flow of bile is diverted away from the area of the injury, and that decreases the output of the leak, and eventually it heals, and then the plastic stent can be removed. We have patient number three here, 59-year-old male patient with cirrhosis and elevated liver enzymes, and I'm showing a few images from an MRI, T2 weighted on the top, two images, T1 with contrast, and then, again, an ERCP image. So the question here is, what is the diagnosis? Is it biliary hematomas, cholangiocarcinoma, peribiliary cysts, asymptomatic cholangitis, or HCC and high-lever lymphadenopathy with biliary obstruction? So this is a very good example of the peribiliary cysts. I think the history of being a cirrhotic does help, even though the morphology may not be that clear about cirrhosis, but the findings are there is cirrhosis. There's apparent central dilatation, but the key is when you put together the MR and the ERCP, notice that there's some scalloping of the bile ducts, and the bile ducts are not, in fact, dilated. They're just being compressed by the peribiliary cysts, which we know occur in cirrhosis. This entity was first described in 1984, and on pathology, it represents cirrhosis that are obstructed small periductal glands. And I have, oh, this is CT of a different patient, clearly cirrhotic, and again, that central apparent dilatation, but with a cystic morphology is the key finding to indicate that this is a peribiliary cyst. And I have one minute, one and a half, for the last case, which is short. This is an alcoholic, 47-year-old male patient who had this CT examination, so take a look. The question will be, this patient has diffused fatty infiltration, and what else? Is it nofocal lesion, focal fatty sparing, simple hepatic cyst, focal nodular hyperplasia, or hepatic adenoma? Take a look. So, again, these are the questions. This is a, I think it's a cool case because it is a simple hepatic cyst. And what's happening here is that on the non-contrast phase, so here's the IVC, the patient has a diffused, fatty liver background, and the focal lesion is right here, and it completely almost disappears in the arterial and the portal venous phase as the liver enhances. As the liver enhances, the lesion itself is not enhancing at all, and it is a hyperdense, slightly hyperdense simple cyst relative to the liver background. I can prove it because we did an MRI for a different reason, and that is the same lesion, so it's a simple hepatic cyst. And the point of this last case is to really, when you look at focal lesions, you have to consider in the liver what the density of the background liver is when you determine significance and when you come up with a diagnosis. Thank you very much.

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