Hello everyone. On behalf of the RS&A Educational Committee and our TRAC Chair, Dr. Ricardo Restrepo, we welcome you to the case-based review of CT. My name is Amish Doshi and I'll be presenting on adult neuro-CT. We have some additional fantastic speakers and topics. We'll be reviewing cases in adult small airway CT, adult hepatobiliary tract CT, and adult emergency CT. Our first case is a 32-year-old with eye swelling. Images from a orbital CT demonstrate proptosis of the left eye. There is some dilatation of a structure within the posterior left orbit. If we look at the coronal images, this structure is located within the superior left orbit, just superior lateral to the optic nerve and inferior to the superior rectus, consistent with a superior ophthalmic vein, which is dilated compared to the contralateral side. MRI further confirms these findings. You can see a dilated superior ophthalmic vein on post-contrast images that enhances. When we look at the level of the cavernous sinus, we can see enlargement of the left cavernous sinus, and we can also see some periorbital soft tissue thickening and enhancement, suggesting some inflammation. This is consistent with a carotid cavernous fistula, which is defined as an abnormal connection between the cavernous carotid artery and the cavernous sinus. On imaging, we saw prominence of the superior ophthalmic vein, proptosis, stranding of the internal horonal fat, and prominence of cavernous sinus. There's two types of dural AV fistulas in this location, direct and indirect. Direct implies a direct connection between the cavernous carotid artery and the cavernous sinus, whereas indirect is a connection between branches of the internal carotid artery and the cavernous sinus. Direct can be due to trauma or a ruptured aneurysm and typically results into a high flow fistula. Indirect, because they are meningeal branches to the cavernous sinus, they are typically a slow flow lesion. The cause is usually unknown, but can be associated with pregnancy, sinus disease, and cavernous sinus thrombosis. Digital subtraction angiography is the gold standard in evaluating these cases, both for diagnosis and for treatment. This is an example of a direct CC fistula. There's injection on this angiogram of the internal carotid artery. In the arterial phase, you can see immediate opacification of the cavernous sinus at the level of the cavernous carotid artery and immediate opacification of the superior ophthalmic vein, both on the lateral image and on the AP image here. This is consistent with a high flow lesion. This is an example of an indirect carotid cavernous fistula. You can see opacification and filling of distal branches and slow filling of the superior ophthalmic vein as well as the cavernous sinus. On delayed images through the capillary phase, you can even see more robust filling of the superior ophthalmic vein, clearer visualization in this slower flow lesion when compared to a direct carotid cavernous fistula. Other considerations include an orbital varix. You can see in this example here a dilated vein in the orbit here that enhances. If we do Valsalva, this can actually enlarge, which helps with the diagnosis of an orbital varix. Dilated superior ophthalmic veins are another consideration. These can be seen bilaterally in patients with increased intracranial pressure or orbital pressure. This has been reported in intubated patients and can resolve after extubation. Superior ophthalmic vein or cavernous sinus thrombosis can also result in an enlarged superior ophthalmic vein. Generally, what we will see is non-opacification of the vein or the sinus due to occlusion from the thrombus. MRV or CTV can be helpful in identifying a filling defect. Next case is a 65-year-old female with altered mental status, vertical gaze palsy and memory impairment. On the CT images, you can see hypodensity along the medial thalami here as well as here. MRI further demonstrates this abnormality where you can see hyperintensity along the medial thalami on the T2 and flare images and clear diffusion restriction on the diffusion-weighted ADC maps. This is due to an artery or persian infarct. It's an uncommon cause of stroke. Typically, thalamic and midbrain perforators arise from the distal basilar and proximal posterior cerebral arteries. In the variant artery or persian, we see a single vessel arising from the P1 segment of the posterior cerebral artery supplying those regions. Occlusion of this vessel results in infarction of the paramedian thalami and rostral midbrain. The clinical triad that we can see is altered mental status, vertical gaze palsy and memory impairment. We generally see an MRI diffusion abnormality in the paramedian thalami as we saw in this case. The literature has also reported this V sign where there's flare or diffusion changes within the rostral midbrain, which has approximately 70% sensitivity to an artery or persian infarct. Other considerations include deep cerebral vein thrombosis, secondary occlusion of the internal cerebral veins, vein of galen or straight sinus. You can see engorgement or edeminous changes in the thalami. Hemorrhagic changes can be seen secondary to venous infarction on this gradient image. And the MRV can be helpful in evaluating for occlusion of these vessels. You can compare that to the normal MRV where there's good flow within the internal cerebral veins, vein of galen and straight sinus. Dural AV fistulas are uncommon, but a consideration. This is an example of a patient who has hypodensity along the bilateral thalami, some diffusion changes, T2 hyperintensity and diffuse enhancement. An angiogram demonstrates a connection between external carotid artery branches and the straight sinus consistent with the fistula. This is rarely reported in the literature. Bilateral thalamic gliomas can have a similar appearance, but there's enlargement of the thalami. Generally, there's no enhancement or limited restricted diffusion. Again, a very rare case. This is a 58 year old male with altered mental status and seizures. You can see that there is an area of hypodensity here in the right temporal lobe. Hyperdensity along what appears to probably be the MCA branch, but also could represent hemorrhage. So this could be either hemorrhage or a dense MCA sign. You can see that there is hypodensity also here along the insular cortex with relative sparing of the basal ganglia. Similar findings on MRI. However, there are also hyper intense signal changes along the single gyrus and the temporal lobe. We can see that here and here, as well as the hippocampus. This is a bit unusual for MCA infarction, and we can also see a very kind of hazy appearance on the diffusion-weighted images with very variable appearance of diffusion restriction and facilitated diffusion with areas of hyper intensity and areas of hypo intensity on the ADC maps correlating to the areas of diffusion restriction. This is consistent with the herpes encephalitis, the most common etiology being HSV-1. It accounts for 20% of all encephalitis cases with common presenting symptoms including altered mental status, seizure, and fever. Most common radiographic findings include a hyper intense signal on MR or hypodensity on CT in the limbic, temporal, orbitofrontal, and insular regions. Hemorrhagic changes can be seen in the setting of herpes encephalitis, and generally this spares the putamen and basal ganglia. This is an important distinction between MCA infarction. On diffusion-weighted imaging, we generally see patchy restrictive diffusion changes. Other considerations for this case include MCA infarction. As in this example here, you can see that this adheres to the vascular territories. It does involve the basal ganglia, and in particular, this example has some hemorrhage. On MRI, you'll see more clear restricted diffusion in the early stages. Limbic encephalitis is another potential diagnosis where there's involvement in the temporal lobes and the limbic system. This can be autoimmune, and it's usually non-hemorrhagic but can involve the basal ganglia. Status epilepticus is included in the differential here and involvement in the temporal lobes. You can see signal changes as well as diffusion changes. On follow-up imaging, usually days to weeks, you'll see resolution of these signal changes. 47-year-old female with seizures. You can see multiple calcified lesions in the bilateral cerebral hemispheres. There's an area of hypodensity, suggesting edema, and probably another lesion here along the medial right frontal lobe. As we went over those imaging findings, the differential considerations include metastatic disease, neurosis and psychosis, and calcified vascular lesions. On MRI, we see multiple lesions with associated edema. There's multiple enhancing foci. This is most consistent with metastatic disease. This was consistent with metastatic colon adenocarcinoma. This patient had multiple metastatic lesions to the liver, several nodules within the lung consistent with metastatic disease, and the calcified lesions within the brain. Calcified brain metastasis can occur in various types of adenocarcinoma, including lung, breast, and colon. It can be secondary to radiation therapy, as well as seen in the setting of sarcoma metastasis. Other considerations include neurosis or psychosis, which is a parasitic infection with four stages, with the healed stage resulting in multiple small calcified lesions within the brain. Cavernous malformations can also result in hyperdense lesions within the brain, generally secondary to hemorrhagic components. These can calcified. MRI is usually helpful in elucidating this etiology with multiple lesions seen on susceptibility-weighted imaging. Our next case is a 68-year-old male with dysarthria and weakness. Initial CT exam demonstrates hypodensity within the right basal ganglia compared to the contralateral region. A two-hour follow-up shows hyperdensity within that right basal ganglia region, which resolves at 24 hours post-initial scan. What this patient actually had done was a mechanical thrombectomy. He had an occlusion within the distal ICA. The clot was received, and you can see the patency of the vessels after clot retrieval. This is consistent with contrast staining of the infarct bed. This can occur after mechanical thrombectomy and results in hyperdensity in the infarcted region on CT. It may be difficult to distinguish contrast staining from hemorrhage. Follow-up CT can be used, but can take up to 24 to 48 hours to demonstrate resolution of the contrast staining. Dual-energy CT has been shown to be beneficial in this circumstance. In this example from the literature, dual-energy gives you an iodine image and a virtual non-contrast image. You can see hyperdensity in the sylvian fissure, which is hyperdense on iodine, but not on the virtual non-contrast image. This resolves on follow-up and is consistent with contrast staining. Here's an example of a hemorrhage, which you don't see on the iodine image, but you do see on the virtual non-contrast image. On follow-up, you can see evolution of that hemorrhage. Dual-energy can be quite helpful. MRI can be helpful. It's seen as iso-intensity on gradient in T2 with contrast staining versus hypo-intensity with hemorrhage. Our last case is a 34-year-old female with headaches. Two images from a non-contrast head CT demonstrate what appears to be a lesion within the right frontal lobe. However, on sagittal images, you see a non-conforming abnormality within the sagittal images that has this vague hyperdensity. This is a result of a CT ring artifact. It's important to note that these can be mistaken for lesions. This is secondary to a misalignment or miscalibration of the CT detector. And it's an error in reading by the detector at each of the angular positions, which results in that circular or ring artifact. And with that, I thank you. I'm delighted to introduce our next speaker, Dr. Daniela Martin. Thank you. Hi, good afternoon, and thank you for joining us. It is my pleasure to talk to you today about adult small airway disease, which I will be referring to from now on as bronchiolitis for simplicity. Over the next three slides, I will briefly define bronchiolitis and describe the classification system that we will be using today. Then we'll start with cases which will help us review the most common type of each bronchiolitis, point out direct and indirect signs on CT. We will touch on clues that can help us think of specific diagnosis. I picked three cases of bronchiolitis that are often under-recognized, and we will end with two common entities that can be confused with bronchiolitis. Bronchiolitis is a really broad term, but it's used to describe a spectrum of diseases that involves the bronchioles and small conductive airways. These are usually less than two millimeters in size and have no cartilage. There are many ways to classify bronchiolitis, and today I chose the histopathologic classification because there is really good correlation with the abnormalities that we see on CT with the histology. And that can help us develop a more specific differential diagnosis. So for cellular types of bronchiolitis, on CT we tend to see more direct signs. And for the constrictive type of bronchiolitis, we tend to see more indirect signs, and we'll discuss that as we go through our cases. We don't normally see bronchioles on CT because of their size. Now, the histopathologic finding in cellular bronchiolitis is the presence of inflammatory cells, whether they are acute or chronic or both, in the wall or in the lumen of the bronchiole. And this causes abnormal increased soft tissue density in and around the bronchiole and thickening of its wall, which allows us to see them on CT. And this is what we call the direct signs of bronchiolitis. They can manifest as solid type nodules such as centrilobular, dream bud, pure white shaped, or more centrilobular, ground glass nodules. We will start with a couple of cases that highlight the solid type of nodules. The first case is someone that presented with cough and shortness of breath. And we immediately see on this image a lot of long nodules, so we should be asking ourselves, what is the distribution of these nodules? MIB images can help us determine the distribution of long nodules, from random to perilymphatic to airway centered. So here we can see that they are all sort of clustered around the bronchovascular structures, which is suggestive of airway centered. And also we see almost a black line where the fissures are supposed to be, which argues against them being perilymphatic. We also know that the nodules are not homogeneous and come in different sizes, like these larger ones in the right lower lobe, and some medium and smaller nodules that are scattered in our lobes. And if we try to determine their distribution in the axial plane, we know that they are clustering segments or subsegments, but without an anterior to posterior gradient, which can be helpful to differentiate it from other very common type of bronchiolitis. This was a case of infectious bronchiolitis, which is by far the most common type that we see. It can be caused by many organisms, and the findings can be nonspecific on CT, but sometimes we can find clues that might help us narrow the differential diagnosis. Right middle lobe and lingular bronchiectasis, very suggestive of a typical mycobacterial infection. We see this with airway centered nodules, different sizes, sometimes cavitary, and sometimes with ground glass like here in the right lower lobe. Second case, classic findings of tuberculosis with a cavity and airway centered nodules. So these are really good examples of specific pathogens we can suggest based on the distribution on the image. Nodule size is nonspecific. There was a study done in immunosuppressed patients with infections that said that if all the nodules were less than 1 cm in size, the most likely etiology was viral. This is not always the case, like everything in medicine, so I think a good take-home point is that if you see nodules of different sizes, think of infection and aspiration, and I'm talking about airway centered nodules, of course. And speaking of aspiration, I said that I was going to show cases that are often under-recognized, and this is one of them. For aspiration, the first clue often is the history, very commonly seen in trauma. Classic findings are airway centered nodules. They can be different sizes, sometimes solid, sometimes a little bit more ground glass. We can have consolidations, and sometimes they can be seen along the bronchovascular structures. The distribution, especially with altermental status, tends to be classically dependent, like in this case, but sometimes aspiration can present as unilateral nodules, particularly if the patient always sleeps on one side. So we need to keep aspiration in the back of our heads because it is the second most common type of cellular bronchiolitis. It is often misdiagnosed with infection or even metastasis. The clues are there if you look for them. So, classic history, someone with trauma, stroke, seizures, bed reading, they all aspirate. And then on the image, you have someone with hiatal hernias, head and neck cancer and radiation, disorders of the esophagus. This patient, for example, here, had an esophagectomy for esophageal cancer, and he has a pretty normal-looking conduit pointed by the arrow. So if you're following up these patients to look for metastasis, you almost always will see a little bit of aspiration, like here. In the circle, we see these airway-centered nodules, a little bit of ground glass appearance to them. This is not metastasis, this is aspiration. So let's keep going, and now we will focus on patients with predominantly ground glass nodules. This patient presented with progressive dyspnea and never smoked. We start by asking ourselves the same question, what is the distribution of the nodules? So, they are evenly distributed, they spare the pleural surfaces, so they are centrilobular. The borders are very hard to see, which is very common with ground glass nodules. They are all about the same size, and they occupy the entire surface of the lung in this image. It is good practice whenever we have patients with chronic dyspnea to add expiratory images. And here we can see that these areas stayed dark in expiration, suggesting this is air trapping. So all of these findings together are very suggestive of hypersensitivity pneumonitis as a cause. In this patient, it was related to a parrot pet that they had. Centrilobular ground glass nodules are another direct sign of cellular bronchiolitis and reflect prebronchiolar inflammation. While virtually any type of bronchiolitis can have GGOs, a take-home point is that infection rarely presents as pure centrilobular ground glass nodules. If you have a case like that, hypersensitivity pneumonitis and respiratory bronchiolitis are the two most common entities that cause this imaging pattern. Imaging-wise, they may be hard to distinguish, but we may find some clues. For example, HP tends to be diffused, while RB is a smoking-related lung disease, so it tends to be overload-predominant, and we may also see emphysema. AP patients tend to have subacute or chronic symptoms, while RB patients are asymptomatic. And with HP, exposures are only found about half the time. So if you don't have that history but suspect HP, you should suggest that diagnosis. I chose the case of vaping presenting as a hypersensitivity-like reaction because this is one of the imaging patterns that have been recently describing patients that vape. Patients present with acute or subacute symptoms. And as radiologists, we can include this diagnosis in the differential, and remember that an HP pattern can also be seen with smoking substances like synthetic marijuana. Moving from cellular to constrictive bronchiolitis. These patients have concentric fibrosis and scarring that cause circumferential luminal narrowing that might result in complete luminal obliteration. So what we see on CT is not the bronchioles like in cellular bronchiolitis, but the result, which is distal air trapping caused by narrowing of the small airways. This patient had acute myelodysplastic leukemia, a bone marrow transplant, and presented with two weeks of dyspnea. The CT looks almost normal, but note that if I narrow the windows, we can appreciate that the lung parenchyma is not homogeneous. We regularly include expiratory images in patients with bone marrow transplant because GVHD in the lungs manifests as constrictive bronchiolitis with air trapping, as we can appreciate better in the expiratory phase. Note that the vessels are smaller in the areas of air trapping because of hypoxia-related vasoconstriction. Constrictive bronchiolitis is unfortunately another common complication of lung transplant, seen in about half the cases in five years. Constrictive bronchiolitis is a type of chronic rejection. It can be hard to diagnose on transbronchial biopsy because of how patchy it is. So you may hear the term bronchiolitis obliteral syndromes from the clinicians when it has not been proven by biopsy, but they use surrogate markers such as PFTs or even imaging. Prognosis is unfortunately poor. Deep neck is our under-recognized and misdiagnosed case. Radiologists make this diagnosis at presentation only about a third of the times. Like this 69-year-old woman that was presented in our tumor board for management of a biopsy-proven neuroendocrine tumor. The imaging is classic of a pulmonary carcinoid in the right upper lobe, with a well-defined elongated nodule associated to a narrowing. But see in this mid-image there were many smaller long nodules, which raised the question of metastasis. Deep neck can be suggested if you see all the typical imaging findings. These patients have a proliferation of neuroendocrine cells, which on CT manifest as small long nodules, usually lower lobe predominant, and larger nodules that can have classic features of carcinoid. There is often a varying degree of constricted bronchiolitis caused by several mechanisms that I won't go into details today, but manifest as air trapping, with or without nodular bronchial wall thickening. So if you see a patient with carcinoid and multiple long nodules, consider a deep neck. The demographics can also help you because they are very characteristic, almost always women in their 60s, and often with a history of chronic cough and misdiagnosed with asthma. And now we will finish with two common mimics of bronchiolitis, starting with tumor embolism. This can be often confused with bronchiolitis at initial presentation because the bronchioles are next to the arteries, and when tumor starts growing in these small vessels, it looks like dream, but it has been described with RCC, HCC, and other cancers. Since these patients are usually followed for their malignancies, the clues are that they don't wax and wane and continue to enlarge without treatment. It may continue to grow to the point that the vessel starts getting distended, so whenever you see these branching opacities that have some nodularity to it, like pointed by these arrows, that's a great look for macroscopic tumor embolism. And our last pitfall is excipient lung, which is a groundless opacity of vascular origin. This patient with a history of sarcoma presented with progressive shortness of breath and new pulmonary hypertension. Imenin showed new tiny centrilobular ground-glass nodules that were diffused. We already say that this is not a good look for infection. Because of the new pulmonary hypertension, excipient lung and pulmonary tumor thrombotic microangiopathy were considered. Biopsy confirmed granulomas related to the injection of talk. This is often a delayed diagnosis that is proven with biopsy, and the pulmonary hypertension is a fantastic clue in this case. And that's a wrap. Thank you very much for your time. This is my contact information in case you have any questions or comments. These are my references. I'll leave this here for a second. And now, please welcome our next speaker, Dr. Perry Pickhart, also from the University of Wisconsin, who will talk about adult hepatobiliary tract CT. Thank you and greetings. I want to continue this excellent session by showing a number of adult hepatobiliary cases on CT. I have no relevant disclosures. Here are my generic disclosures. OK, case one. This is a 58-year-old man presenting with abdominal pain. I'm going to show you these transverse and coronal stacked images here. And you can see fairly obvious finding of a thick-walled complex cyst in the right hepatic lobe. But I would also direct your attention to the adjacent duodenum here. And there's a bit of a connection that I'm pointing at here. Perhaps better seen on coronal here on this image here. And I'll go back and forth a little bit. OK, and that's all I will show you. Here are some key final images in composite. What do you think is the most likely diagnosis? Is this a fishbone perforation, amoebic abscess, bleeding hepatic adenoma? Or is this hydatid disease? Give you a second to think about it. This is a fishbone perforation. And they all start to look the same once you've seen this before. This gentleman was actually from the Gambia, which is the smallest country in mainland Africa. As you can see, it's surrounded by Senegal. Why do I tell you this? West African cuisine includes this tasty baked fish, whole fish. And it's wonderful, but you have to be very careful about the bones that are involved here. And just to show this one last time, again, you can see this fishbone that's perforated the duodenum and punctured the liver capsule, resulting in hepatic abscess. Here's a case I saw. This was someone from northern Wisconsin enjoying a Friday night fish fry. And this is a fairly complex looking aggressive mass that may have been mistaken for an aggressive malignancy, perhaps. But again, in the center, you can see this curvilinear density, which is the key to the diagnosis, and some eccentric adjacent thickening of this jejunal loop where this fishbone actually perforated. And here's the specimen radiograph following surgical resection of this inflammatory mass. These all start to look the same. This is an excellent article out of South Korea just showing a number of fishbones that it perforated. And again, they all start looking similar. OK, next case is an unfortunate 54-year-old woman presenting to the ED with abdominal pain and hypotension. This, I'll show you some soft tissue windows on the left and more of a wider lung window on the right. And you can see the abnormalities on both quite clearly. This patient was doing very poorly, had no relevant prior history. I'm going to go lower on the left sequence here. We're getting into colon. If you follow the colon down, you can see some associated findings here in the mesentery. And then I'm going to stop at the sacral level right here adjacent to the uterus. OK, what do you think is going on here in this hypotensive, obviously symptomatic patient with no prior history? Is this clostridium septicum infection with occult sequel cancer? Is this benign pneumatosis with portal venous gas, spontaneous tumor necrosis, or ischemic colitis with portal venous gas? A little more uncommon, but this is, in fact, clostridium septicum. A little bit about clostridial infections. This is a rare form of clostridial infection with septicum accounting for about 1% of cases. However, about 85% of clostridium septicum cases involve malignancy, most commonly the cecum, and it's most commonly an infection with cecum, and it's most commonly an occult malignancy at presentation. My friend and colleague, Cookie and Company, published a couple of cases of clostridium septicum that presented with aortitis. You can see gas forming infection within the aortic wall here in this patient with an occult sequel cancer, as well as this patient. Don't mind the autosomal dominant polycystic disease, but another occult sequel cancer. So fairly similar in many respects to the case I showed you. All right, case three of five, I will add. 51-year-old woman presenting with right upper quadrant pain. I'll give you the bonus of a T2-weighted MR series as well, but focusing first on the CT and remembering our category here of hepatobiliary. Looking at the gallbladder, you can see some scattered calcified stones here, and then an adjacent abnormality as well, which by the time we got to MR here, you can see that that has gotten bigger relative to the adjacent gallbladder with stones in it. You can see the surrounding pericolycystic inflammatory changes on both MR and on CT with some infiltration adjacent to that pericolycystic fat. Okay, what do you think this is? And here are some representative images. Do you think this is gangrenous cholecystitis? Is this a duplicated gallbladder with associated cholecystitis? Is this a kind of cockle infection, E. granulosis, parasitic infection? Or is this intraductal papillary neoplasma of the biliary tree, or IPNB? This is, in fact, a gallbladder duplication, and there is acute cholecystitis, as you can see. I'll just show you this coronal MR sequence, again, T2-weighted. And here you can see that one gallbladder looks a little more hydropic than it did on CT, perhaps from secondary occlusion related to the inflammation of this inflamed gallbladder with gallstones. And it appears that these come together and form a common cystic duct prior to joining up with the extra hepatic duct. Here are a few more cases I've seen of gallbladder duplication. They start to look quite similar when not inflamed. Of course, someone has gone and categorized these and split them into all these categories. I think the case in question is probably one of these V or Y-shaped with a common cystic duct as it joins the common hepatic duct. I think the main differential here is gangrenous cholecystitis. Here are some cases, a little different in that these pericholecystic collections are a lot more in terms of inflammatory changes, and you can see communication with the gallbladder due to the pericholecystic abscess from gangrenous cholecystitis. But some similarities certainly are there. Okay, case four. This is a complex case. Actually, it was a neighbor of mine who visited our local community hospital after minor trauma, but was experiencing vague abdominal pain, which may or may not have predated this minor trauma event. Of course, remember the category again. We're seeing these obvious findings at the lung base, but as we go beneath the diaphragm, the abnormalities continue. And I think this, I'll stop right here. This is a fairly pertinent level to make the overall diagnosis. But going on, you can see there are further abnormalities in this perihepatic or peripheral location of the liver. Okay, with that, show you a couple of additional images, coronal and sagittal images of that abdominal thoracic process. What do you think's going on here? Is this pulmonary sequestration, post-traumatic biolomas, dropped gallstones, or is this another parasitic infection with fasciola hepatica in this case? Give you a second to think about it. Remember the category that I'm dealing with, which makes dropped gallstones much more likely than pulmonary sequestration. The key image again here was that the patient has undergone prior cholecystectomy, let me just cruise through those images again. You can see the thoracodominal communication of these dropped gallstones through probably a preexisting channel here. And you can see adjacent perihepatic stones. And the key to the diagnosis is that the gallbladder is missing. I'll also show you a hepatobiliary phase MR performed with Eovist that shows both renal and normal hepatic excretion. But now you can see these inflammatory looking stones have now involved the adjacent colon. It was colon cancer was considered, of course, lung cancer and liver cancer or metastatic disease were all considered. This patient was basically told to put his affairs in order, but this proved to be a benign process. Here's another example from Malincroft that we've shown at prior meetings. This patient after laparoscopic cholecystectomy has an indurated lap port site that was due to this laminated gallstone that was inciting the response. This, of course, serves as a nidus for infection. Note, we are at the level of cholecystectomy again. So there's that dropped gallstone. And just to round it out, a case we've also shown in the past, fasciola is a parasitic infection that has a complex life cycle, but tends to extend from the hepatic capsule towards the biliary tree. And you can usually see the pathway it's taken along the way to get to the biliary tree. All right, final case. This is a 23-year-old presenting to the emergency department with back pain. I think you'll see why. There's this thick-walled massive cystic collection occupying the right hepatic lobe. And you can see extension through the liver into the body wall here surrounding ribs and likely causing pain. Notice that there's also some extra hepatic findings that are key to the diagnosis. I'll show you the coronal images in a second here in association with the scout image shown here. So the scout has some pertinent findings and nicely shown as well on the coronal CT. And then we're getting into this dominant collection, which I've already shown you. So do you think this represents enterohemorrhagic E. coli, the O157H7 variety with colitis leading to liver involvement? Is this metastatic colon cancer, mucinous due to the low attenuation? I've also given you an ultrasound image here, thick-walled cyst with fluid-fluid levels. Is this amoebiasis from Entamoeba histolytica or is this an infected hepatic cyst, pre-existing cyst? This is amoebic dysentery. And you can see the colitis from amoebic dysentery is where the process begins. And then portal spread to the liver with hepatic abscess that then caused the patient's back pain. And this patient had recently moved from Mexico to Wisconsin. This was amoebic dysentery. So this was successfully drained and the patient actually did quite well. With that, I thank you for your attention. And I would now, it gives me a pleasure to introduce our next and final speaker of the session who will be talking about adult emergency CT. Dr. Douglas Katz hails from the NYU Department of Radiology and is a good friend of mine. So take it away, Doug. Greetings everyone to the final component of our RSNA 2020 virtual case-based review session. I'm gonna be showing two brief cases of the acute admin as initially was imaged with CT in young individuals. And I'm the final speaker. So I wanna thank our other participants in this presentation. And I'll conclude the session before questions with these two related, challenging, interesting, recent cases of the acute admin from my institution. I'm gonna ask and answer a few questions. I should say I have no disclosures other than to disclose that I've been challenged for over 30 years by imaging of the acute admin pelvis remains a strong interest academically and in real practice. I wanna thank Dr. Edward Lee from Boston Children's who organized this session was kind enough to ask me back who didn't initially know I was gonna show pediatric cases but he knows dabble in pediatric imaging, do a lot more adult cross-sectional imaging with various modalities. So our first case is an adolescent male with acute right lower quadrant pain. There's no prior history. And as many of you, most of you know, we do a lot of ultrasound for the acute admin pelvis in pediatrics, but in this instance, the clinicians wanted a CT. And so CT is done with oral and IV contrast. And here are three representative images through the pelvis from that examination. Let you look at the pictures. I think the findings are fairly apparent, but exactly what is the diagnosis, a lot less apparent. And so here's a representative coronal image from that scan, which you look at that. So what's your best diagnosis based on the history? It said there's no other prior imaging or relevant history. Is this epiploic appendagitis or mental infarction? Is this some sort of pelvic fat torsion infarction but neither of a mental nor epiploic appendage origin? Is this some sort of unusual presentation of a liposarcoma or you just, you have no idea. And more importantly, I think we really need to emphasize management. How do we think this patient should be managed? Is this a conservative management? Is this someone who should go to optimal colonoscopy? Should the patient be admitted to surgery, observed but not operated on, but kept an eye on? Or is this someone who should go emergently to surgery? Or again, I have no idea. So here's, I won't read the whole thing, but here's a rather long, for me, I like to have short impressions, long impression for this particular patient's CT that I interpreted prospectively. And the bold portions, I included considerations such as an unusual large ear of epiploic appendagitis. So this is not a typical location for that. It's much more common along the descending colon, very, very unusual to have one this big in this location abutting the sigmoid colon. It was at the lower aspect of some ileal loops as well. Is this an area of unusual spontaneous fat necrosis slash torsion or something else? And I said at the end that if this patient's managed conservatively and you need additional imaging to follow it up in the near future, do either non-contrast MR or repeat CT. You could do that without contrast. So I've never seen this before, and what I do with really weird cases I've never seen before, I show them around. So I asked some of my more, even more experienced pediatric radiology attendings, have they seen this before? And some other folks at the main campus and at our, the campus that I work at, and body imaging, have you seen this? And basically nobody said anything other than what I had to say. So my best guess, I don't have path proof on this, my best guess is this was an unusual primary focus of fat necrosis, maybe associated torsion. It's not clearly an epiploic appendage, but we're kind of managing it that way or the way you would manage a uncomplicated focus of a mental infarction. And in fact, the patient was managed conservatively and sure enough, coincidentally, a few months later, here's a repeat representative entry of the pelvis on a CT done for unrelated reasons, and it looks like other more common foci of fat necrosis that are evolving, they get smaller, they have a rim, they may even calcify over time. And there are some weird other locations that you can see this phenomenon in the abdomen above me on the usual epiploic appendagitis in a mental infarction. And those include processes such as a perigastric appendagitis, I showed a case of that last year at the case-based review that I was involved in. And also, you can have infarction of fat in the thalassoid ligament region of the liver. So those are some weird locations, and there are other weird locations that are reported in the literature as well. So here's kind of a related case, this is my second and last case, the 10-year-old boy with one day of abdominal pain, and again, whatever reason, they opted to do a CT, coral and ivy contrast, there were no radiographs or ultrasound, no prior imaging, again, would be really helpful if we had prior imaging, we don't have that here. And these were called unremarkable, and it's understandable why. Here are some representative images in the axial plane. And again, I probably would have called these negative, honestly, myself, unless somebody told me exactly where to look. And I had, in particular, a comparison exam, which I don't have. And so here are representative coronal images through this examination. And again, I think the findings are very subtle, particularly subtle if you don't have the particular images that show areas of interest, if you're just looking at the whole skin, and nobody tells you exactly where to look. So based on what I've shown you, and I'm sort of hinting a little bit here as to what is going on, but would you call this negative, you agree with the official interpretation? In retrospect, is there a mild colitis or mild enteritis? Is there, in retrospect, early a mental infarction? Or E, I'm even more confused than ever, Dr. Katz is really torturing me, I don't know what to do with these cases. Well, and again, more importantly, what about management? How do we think this patient should be managed? Conservatively, should they undergo optical colonoscopy, admitted to surgery but observed, not go to the OR, or should they go to the OR? Or again, I still truly have no idea. So interestingly, the patient had continued and slightly worsening pain. And so two days later, an MR was done as an MR enterography protocol. And I've shown you the areas of interest, and I think it's a bit more apparent now in the coronal plane and even more so on the axial plane as to what the diagnosis is. And so based on the FOP MR, what do you think the diagnosis and the management should be? Should this be diagnosis of mental infarct, managed conservatively, or mental infarct go to surgery, epipleic appendagitis managed conservatively, or epipleic appendagitis managed surgically? Or I completely give up, I surrender. So in retrospect, there's some subtle swelling of this region of fat, and it is asymmetric, although it's not that dissimilar from the fat sitting immediately superior to the mid trans colon. It's a little bit more prominent, a little bit more edematous, totally understandable why this was missed. And again, I would have missed it too. And so these findings, now that we have the sequence of events with the CTMR, are in fact diagnostic of mental infarction. This is clearly the subtlest case I've ever seen and I have seen multiple examples of this in both adults and to a lesser extent in children. The only realistic differential here is epipleic appendagitis. It's more common in general, but it's a lot less common on the right, as already alluded to, compared with the left, just where the epipleic appendages live compared with the momentum that is prominent and tends to infarct occurs. Again, rare in children, but it happens. I used to think epipleic appendagitis didn't happen at all in kids, and then I saw a couple of examples in conferences and in the literature. So that's even rarer than a mental infarction, but a mental infarction quite uncommon in children. And we'll show a couple of references and discuss those briefly here. The imaging findings are basically the same as adults. In adults, it's uncommon, but increasingly reported prospectively over the years. It's not exactly clear what's causing it unless there's associated torsion. There are a variety of associations, obesity in particular, trauma, recent surgery, or prior surgery where free up ligaments, disattachments, reports of association with strenuous activity, and even amusingly, to some extent, associating with, quote, tight pants. Why the right-sided predominance? Presumably the blood supply is more tenuous or it's a bit more prominent normally, and just anatomically has a predisposition to thrombosin, very occasionally tors. Patients generally present with pretty significant acute pain. No one ever comes to an ER at any age saying, Dr. ER clinician, I have a mental infarction, right? I mean, it's just not a diagnosis anybody's gonna suggest, and nor are clinicians going to suggest it either for the most part. It really is, the burden is almost exclusively on us to make this. And so we've seen inflammatory mass with associated fluid, ill-defined somewhat, in between the rectus sheath, immediately anterior, and typically the hepatic flexure, the transverse colon, immediately posterior to it, and the parumbical region extending off to the right, again, much more common than left, although left does happen. The adjacent bowel's almost always normal. If you've seen associated swirl, that's diagnostic for associated torsion, and those patients probably do go to the OR, should go to the OR. There is some overlap with epipleic appendagitis, but again, this is usually much larger, larger than five centimeter, and again, much more common for epipleic appendagitis to occur on the left. With follow-up, as with our first case, we typically see either complete resolution or over the next weeks to months, a smaller, better-defined denser rim, as with our case, for the first case. And there may be associated development of calcification. So here are the two papers. This is from Ramon et al., 19 children. It's a report from 11 years ago now. Immune age was about nine, and not surprisingly, a substantial minority had right lower quadrant pain, because this tends to be in the sort of mid-ab, and so we need to image for appendicitis. That's gonna be, of course, the most common diagnosis, cholecystitis, very unusual in children, but it happens. And in this particular series, the sensitivity to ultrasound was not good. It was only 64%, compared with 90% for CT. In a more recent publication of 30 patients, McCusker et al., who had a mental infarction, they all underwent ultrasound, and ultrasound did much better. Similar kind of age, mean, and range. Almost all these kids were very overweight, and ultrasound did much, much better in this series. Presumably more experienced, better technology, et cetera. They knew maybe to look for this more often. Again, although fairly unusual. 26 of the 30, they made the diagnosis based on ultrasound. Not sure I would have achieved that level of success in my practice, but, you know, good for them. So this is generally managed conservatively. It's usually self-resolving, like the even more common epiploic appendicitis surgery, if there's torsion surgery, if there is a lack of improvement. A lot of these cases in the older literature did undergo surgery, because nobody knew about this diagnosis, or thinking about it, or there wasn't imaging. More recently, not so much. And there's some other rare things that can occur with a mental infarction. You can have super infection, again, torsion, things that might push for more aggressive management. So with that, 11 and a half minutes, I thank you all for your attention. Thank Dr. Ed Lee and the RSNA for allowing myself and my colleagues to present. Here's my little guy. He's four and a half now, he still wants to be a doctor, and we haven't convinced him not to be. So again, hope everybody is enjoying so far the virtual RSNA, whether you're seeing it live or several months down the road. Again, appreciate everybody's patience.

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