Hi everyone, my name is Sally Ayessa and I have the pleasure of being your host for this latest free Friday live stream. Although, hot tip, you can actually watch this on replay any day of the week on YouTube for the next few weeks, not just on a Friday, so be sure to tell your friends and colleagues so they can come and watch it too. I am one of the co-conveners for Radiopedia 2024, our upcoming virtual conference.
Remember that access to the conference is included within an all access pass, so you can grab one now on the Radiopedia website or renew it so it is valid by the time that the conference starts in July. As always, access is free if you reside in one of the 125 low and middle income countries listed on our website. If you do want to purchase a conference ticket, which I strongly recommend you do, but I'm biased, there are tiered and concession rates available.
We've got a couple of new things set for the conference this year and we are very very excited to be able to share them with you. First up we have some anatomy review sets across different body systems where speakers will explain key concepts in imaging anatomy and their relevance to disease processes. Our second new content area is the on-call case sets in which we go through important findings in typical and sometimes tricky or not so typical emergency situations. along with tips on what you should include in your reports. You can join me for the chest on call session.
So I look forward to seeing you there. Head over to the conference website to see the full lineup and explore what is on for the week. Now on to this week's lecture. It is my pleasure to be able to introduce the famous Vikas Shah, an abdominal radiologist from the UK.
And you may have seen him around on social media where he goes by the handle, The X-Ray Doctor. Vikas's talk is titled, top 10 pitfalls in abdominal CT. As well as learning about how you can avoid falling into these pitfalls, I think you're going to really enjoy the way that Vikas takes us on a journey around the abdomen.
Just keep watching to see what I mean. Thank you so much, Vikas. Take it away.
Hi, everyone. My name is Vikas Shah. I'm a consultant radiologist in the United Kingdom and I'm on the editorial board of Radiopaedia.
Now anyone who's reported abdominal CT knows that it is fraught with dangers. There are a number of perils, traps, conundrums and hazards ready to trip you up and catch you out. These range from artefacts of contrast enhancement which can mimic true disease, through to normal and variant anatomical processes being mistaken for pathology. Let me be your guide for a journey around the abdomen. I've picked out my top 10 stations to visit, where we will examine the pitfalls that await the unwary.
By the end of this journey, you'll be equipped to navigate all of these danger zones by yourself. We'll begin our journey at gastric diverticular. These are often mistaken for left adrenal lesions, particularly when they're fluid filled.
They arise from the posterior aspect of the fundus of the stomach and can be true or false diverticular and are in fact the least common of all the GI tract diverticular. And you can see them on all different imaging modalities. So here is one that is seen on a barium study. You can see this fluid filled or rather barium filled outpouching from the fundus of the stomach.
Here is one that was seen on MRI as an incidental finding. There's a are a couple of sequences from a cardiac MRI study and you can see here this outpouching which has got the same luminal signal intensity as the remainder of the stomach. This patient went on to have a CT-KUB, so a urinary tract non-contrast CT, which is acquired with the patient lying on their front.
So that's a prone study. Here is the couch anterior to the anterior abdominal wall of the stomach and you can see that the gas within the lumen of the stomach continues into the lumen of the diverticulum. This patient then later had a conventional CT, so a supine CT, where they're lying on their back and now the fluid within the lumen of the CT has continued in to be also within lumen of the diverticulum. So those are useful signs.
So you may see air within the lumen of the diverticulum or fluid or sometimes an air fluid level. Use your multi-planar reformats to make sure that you can identify a hopefully normal separate left adrenal gland and look for that thin channel that indicates it communicates with the lumen. But if you have any difficulties then you can use oral contrast with either fluoroscopy or CT to problem solve.
So here is such an example where there is a structure lying adjacent to the fundus of the stomach. It's got one small bubble of gas here within it. and it's also got some layering high density material.
So then we gave aural contrast and we can see that here we've got the aural contrast within the stomach and it's now also here within the diverticulum and now that Previously noted high density material is in fact low density against the background of the oral contrast so it's probably some food residue within the stomach. And as I said use your multiflamer reformat so we can see here that there is a nice wide channel between the fundus of the stomach and this diverticulum. We'll now move on to our next stop which is the zebra pattern of splenic enhancement.
Now this is that stripey pattern that is sometimes seen on arterial phase studies and it can catch out those people who are just beginning to look at abdominal CT. So here it is, here is an arterial phase study. We know it's arterial because here we see contrast which is very bright within the aorta and there's a stripey pattern of enhancement to the spleen where there are alternating areas of low and high density. But if we go to the portal venous phase, we can see that there is a nice uniform pattern of enhancement of the spleen.
So this is because of the makeup of the spleen and its constituents, red and white pulp. So the red pulp enhances earlier than the white pulp because of greater blood flow. And so on arterial or early portovenous phase studies, you'll see that the red pulp will be hyperdense. And then... and the white pulp is hypodense but this all becomes uniform later on.
This pattern is sometimes also known as Tigroid splenic enhancement because of the stripes on a tiger. So here is another example where we see on the CT this stripey pattern with these alternating bands of low and high density on this arterial phase study we can see the aorta is very bright and you can also see this on MRI so the same patient had an MRI and you can see these high and low signal intensity alternating stripes within the parenchyma of the spleen. So why is this important?
Well it's important to recognize the normal phenomenon of the phase of imaging when you're first starting out with abdominal CT but also to make sure you don't mistake it for disease processes. So one such process is splenic infarction. So in this case we have this low density band that's running from the hilum to the outer surface. It's relatively well defined, there's only one of them. but the remainder of the spleen is relatively smoothly enhancing on this portal venous phase study.
There's no perisplenic free fluid, and so this is a splenic infarction, and you'd be looking for other features in the clinical history, such as a history of pain, features of infarction or ischemia in other organs, such as the kidneys, the bowel, and perhaps echocardiogram findings of thrombi within the chambers of the heart, and that would all go fit together to to indicate a splenic infarction. The other differential diagnosis is a laceration of the spleen. So here is an arterial phase study again we see that bright contrast within the aorta and we see that there is a splenic zebra pattern enhancement but also there is this odd area running down the center of the spleen that looks a little bit unusual. We'll go to our venous phase study and we'll see now a normal uniform enhancement to the splenic parenchyma.
anteriorly and posteriorly but down the middle there looks like there's a split with a jagged low density line running through it and in fact, there are several other Jagged low density lines. So this is splenic trauma with laceration Um a full thickness laceration of the spleen and the other useful sign is you see perisplenic hematoma And if we scroll elsewhere, then we see a bit of high density fluid adjacent to liver. So this is a hemoperitoneum Now clearly in these cases, there'll be a history given of trauma And also you'd be looking for other signs of injury to this quadrant of the abdomen.
So pancreatic tail injuries, renal injuries, perhaps perhaps rib injuries as well. So the next station on our journey is a hepatic Pseudo-lesion. Now this is an unusual pattern of enhancement that is sometimes seen within liver particularly in cases of superior vena cava obstruction And it's important to recognize because it can confuse people and make them think that there is a focal lesion Such as a hemangioma or perhaps even a metastasis when in fact, this is just a phenomenon of vascular enhancement So here is a case.
This is someone who's got a mass within the chest on the right side And then on their ct we see that there is a malignant looking mass invading the right side of the mediastinum completely effacing the superior vena cava and as a result there are numerous collateral venous channels within the chest wall anteriorly and posteriorly and the in fact one thing important thing to note is the contrast has been contrast has been administered via the right arm. So the SVC is completely effaced and as we scroll down to the abdomen then we see that there is an unusual area of enhancement within the left lobe of the liver and there are in fact two areas. There's one here very highly dense area and then next to it slightly softer enhancement and we also notice that there are numerous venous channels adjacent to the surface of the liver and in the anterior abdominal wall as well. and as you keep scrolling you see them here within the anterior abdominal wall converging in the region of the umbilicus.
If we go to the portovenous phase studies we can see that that pattern that area of enhancement is now slightly dissipated it's still slightly hyper dense compared to the background liver but it's nowhere near as abnormal on the previous study. So why are we seeing this? We're seeing this because the blood now needs a route to get back to the right side of the heart now that the SVC is included. So we have recruitment of something known as the third inflow.
So we have supravena cave obstruction. As a result, blood flows into the body wall vein. So that's the internal thoracic vein, the superior and inferior epigastric veins of the intra-abdominal wall. And from then, they anastomose around vessels in the region of the umbilicus, including the parambilical veins.
And the parambilical veins are responsible for that phenomenon in the liver. Now the paramblycal veins are part of what's known as the third inflow. So what's the third inflow?
Well in the liver your two main sources of blood are the hepatic arterial system and the portal venous system. But in fact there is something known as the third inflow of which the chief system are the paramblycal veins but also the cholecystic veins. So they provide an alternative means of blood flow to small parts of the liver.
The paramblycal veins perfuse the liver in two different forms. directly into the parenchyma but also into branches of the portal vein and this accounts for those two different densities of enhancement in the liver in these cases. This anatomy is also responsible for focal fat infiltration and focal fat sparing which we're going to look at in just a little while.
So let's look a bit more at the parambulical veins. The main ones are the superior and inferior veins of sapi and the vein of bureau. The anastomos, as I said with anterior abdominal wall veins around the umbilicus, travel up to the liver and can either directly perfuse the liver or drain into branches of the portal venous system.
So let's look at one more example. Here is someone who's got again a malignant looking mass in the right side of the mediastinum, complete effacement of the supravena cava, recruitment of chest wall vessels and as we get down towards the abdomen, you'll notice again a very abnormal area of bright enhancement in the left lobe here and adjacent to it slightly softer area of hyperdensity. So that's as a result of those two different types of enhancement, one direct perfusion into the liver parenchyma and one as a result of the portal vein drainage.
And as we scroll down we can see these blood vessels in the anterior abdominal wall. Importantly when you go to the portal venous phase images, that area of enhancement doesn't always completely disappear. You might still see a bit of a blush in that area. Now we're seeing this on CT, but you can also see this phenomenon on sulfocolloid scans and also PET-CT studies as well.
And this anatomy is also responsible for the distension of abdominal wall vessels that you see in portal hypertension. So in those cases, the flow is reversed. The flow is from the portal vein into the parambulical veins in the abdominal wall down towards the umbilicus as you see here. We'll stick with the liver as we move on to our next station and we're talking about focal hepatic steatosis.
Now we're all used to looking at diffuse hepatic steatosis which is something of a public health concern and that's usually not a diagnostic dilemma but when you have focal hepatic steatosis sometimes it can mimic a mass and can cause diagnostic problems. So first let's start by looking at diffuse hepatic steatosis. Here on a CT we've got a global reduction in liver density. A good visual indicator is on a portal venous phase CT. If you look at the density of liver and it's less than the spleen then that's a good indicator of diffuse steatosis.
Make sure you do that on a portal venous phase study because on the arterial phase study the spleen enhances early. And here this is uniformly of low density and then we can use our in and opposed face images on mri which can pick up um the fat so if we see a signal drop on the opposed face images like we do here compared to the in phase images then that's a really good indicator that this patient's got diffuse hepatic steatosis And the physiology that's responsible for focal hepatic steatosis is the third inflow that we've just heard about, because the microenvironment in small parts of the liver is altered by flow from these alternative pathways. So that's areas such as the adjacent to the falciform ligament or in segment four anterior to the gallbladder fossa.
And that's where we know we're used to looking for focal fat infiltration and focal fat sparing. Normally, it's not a problem. But as I said, sometimes this area can be, these changes can be more mass-like. The things to look for are that there should be no distortion of the blood vessels or the contour of the liver. And again, it's really useful to have MRI as a problem-solving tool.
So here is an arterial phase study where we've got areas, mixed areas of more normal looking liver parenchyma along with more reduced density liver parenchyma. So it might be that this is all to do with the phase of imaging. So we'll go to the portal venous phase study and then we can again see that there remains this phenomenon of where there's mixed areas of low and high density.
Now there's no distortion of the vasculature here, no abnormality of the contour of the liver. So this is unusual because it could be mistaken for disease. So we'll go to our MRI in an opposed phase images. So here is the in phase and then we go through the opposed phase images and we can see that there is a reduction in signal intensity in so on the opposed phase images but corresponding to those low density areas on the CT indicating that this is focal fat in the liver albeit in a slightly unusual morphology compared to what we normally see which are those small areas in the gallbladder fossil or adjacent to the falciform ligament. For our next stop, we're going to head over to the kidneys and we're going to look at renal parapelvic cysts.
And this is important because this can mimic hydronephrosis and could lead to unnecessary interventions in patients. But fortunately, there are ways in which we can avoid making a mistake and get this diagnosis correct. So here is an example of, first of all, true hydronephrosis. We can see this dilatation of the pelvic calyxal system on the ultrasound study and on this patient's CT we can see that there is distension of the pelvic calyxal system on the right side caused by a necrotic right retroperitoneal nodal mass which is pinching the ureter and we've also got abnormal enhancement of that right kidney compared to the left side.
So those are all signs of acute obstruction. But here we have another case of a kidney with apparent hydronephrosis with these fluid filled spaces at the hilum of the left kidney and on this patient's CT we can see that there is again apparent distension of the pelvical system of that left kidney. But if we go to the post contrast series on the portal venous phase study we see that there's no suspicious renal mass but that doesn't really help us because it still looks like there might be distension of the PC system. One thing to notice though, there is no perinephric fat stranding and the renal cortex is not thinned.
But the delayed phase images really help us because here we see contrast excretion into the calyces and into the pelvis and ureter and they're normal in caliber and in fact they are thinned and stretched around these fluid filled spaces which are in fact left-sided so unilateral parapelvic cysts. These are cysts that extend into the renal sinus fat from the parenchyma and they can be unilateral or bilateral and cause this phenomenon of pseudo-hydro-nephrosis. So this is not real hydro-nephrosis.
Important things to look for are that the cortical thickness is preserved. Remember that you start to lose your cortical thickness with long-standing hydro-nephrosis. And in acute obstruction you'll have perinephric fat stranding and an alteration in the enhancement pattern of the kidney. But you won't see any of that in these cases. And it's really useful to have that trick up your sleeve of delayed phase imaging because you'll see that the collecting system is not distended but is in fact thin, normal calibre, stretched and displaced around these cysts.
So let's look at one more example. This patient presented with acute left-sided renal colic and this CT urinary tract, again acquired prone, you can see the couch here, anterior to the anterior abdominal wall, shows a stone in the proximal left ureter but alongside that it also shows fluid fills. distension, apparent distension of the pelvic helix system bilaterally. So the patient was brought back at a later date for repeat study, by this time the stone has passed but we've still got persistence of the appearance of the PC systems bilaterally. We'll jump to the delayed phase images where we can see that the kidneys have both handled the contrast appropriately and we can see that there is filling of the pelvic heliceal system but that there is no distension and they are thinned.
The calyces are thinned and stretched around these fluidful spaces which are multiple bilateral parapelvic cysts. We're now going to move on to looking at the bowel and specifically talking about submucosal fat. Now traditionally this has been strongly associated with the presence of ulcerative colitis or other forms of inflammatory bowel disease particularly long-standing inflammatory bowel disease and You typically see it more in the colon than you do with the small bowel So here is such an example someone with known long-standing Alterative colitis and you can see here this stripe low density stripe of fat deep to the mucosa of the large bowel the descending colon over on this left side And between this mucosa and the seros and extends all the way down to the rectum here where it's particularly prominent and So as I said this is seen more in UC than it is with Crohn's disease and more often in the left side of the bowel, so the descending colon.
When you see it with Crohn's disease you typically see it in the distal small bowel. But here is someone who had some vague abdominal symptoms but no change in bowel habit, no definite history of inflammatory bowel disease, who also has a little bit of fat in the submucosal space of the large bowel. This was reported and then triggered an endoscopy investigation of this patient to look for underlying inflammatory bowel disease. In fact, the endoscopy was completely normal.
And the reason is that because this is seen as a commonly seen incident of finding in a significant proportion of patients. So whilst we know there is an association with chronic inflammatory bowel disease. and sometimes also graft versus host disease, there was a good study that found that when they examined patients who had no bowel symptoms, 21% of patients had this sign and there was a strong association with obesity. So this should be considered almost as an incident of finding.
And you'd be actually better off reporting the possible diffuse hepatic steatosis in those patients for which at least some management can be instituted for that very important metabolic disease compared to putting them through investigations, unnecessary investigations for the bowel. So one thing to note is it's important to differentiate submucosal fat from submucosal edema that you can sometimes get with bowel inflammation. So here's an example of someone who's got submucosal edema extending from the distal transverse colon all the way down the descending colon down to the sigmoid.
And if you want you can put an ROI on the submucosal space to measure and here you'd find fluid density versus the other case I showed you earlier where you'd find fat density and this is an example of ischemic colitis. But I just want to also make you aware of something which is the utility of that submucosal fat in patients who've got long-standing UC because you know that colorectal carcinoma is a long-term risk of ulcerative colitis. So if you've got someone like this who's got this nice fat um stripe in the submucosal space when you're doing a follow-up ct examine it really carefully because if you see it being lost like here where you have this semi-annular soft tissue density replacement of the submucosal fat at the splenic flexure and then when you go approximately you're back to normal fat distally you're back to normal fat this is highly suspicious for a new adenocarcinoma on the background of long-standing uc and in fact in this case this was proven at endoscopy and with histopathology analysis to be an adenocarcinoma. We'll now move to our next stop which is venous pseudothrombus. Now when you're reporting abdominal CT it's really important to understand the different appearances of contrast enhancement of the organs and of the blood vessels depending on the phase of imaging, depending on where the cannula has been placed, but also the patient's underlying physiology and how that can influence the state of venous enhancement.
And this is to make sure that you can avoid over-calling or under-calling thrombus. So here is an example of a portal venous phase CT where someone's got acute cholecystitis. There's a few chunky stones here within the gallbladder and the gallbladder walls thickened, but also there is low density in the inferior vena cava here and as we pass up then we have this high density which on the coronal images looks like this and this could be reported sometimes as an inferior vena cava thrombus because of this apparent change from the low density to high density but in fact this is a phenomenon of contrast.
The blood that's coming from the lower limbs has not yet been a pacified and therefore has this low density but the blood that's coming in to the renal veins from the kidneys has got contrast within it. It's mixing with the un-epacified blood and therefore you then get this column of higher density blood in the more upper portion, the more cranial portion of the inferior vena cava. And there is in fact a little bit of mixing and swirling here rather than being a definite cutoff. And you see this typically in a more earlier phase of enhancement. So this is a pseudothrombus and there are a few clues to make sure that you don't mistake this for true thrombus.
One is that swirling pattern you see where the blood from the opacified veins such as renal veins mixes with the unopacified blood. Sometimes you see a more laminated appearance. Remember also the true thrombus will have sharper edges and the downstream organs will have expansion or edema.
So think about for example a deep vein thrombosis of the lower limbs. You get swelling of the lower limb and expansion of the tissue spaces. Think about the cause of true thrombus, is there any signs of inflammation such as within the um you get sigmoid diverticulitis leading to portal vein thrombosis or is it underlying cancer or a prothrombotic disorder and think about downstream are there any features of pulmonary embolism. So here is someone with known protein c deficiency who had chest and abdominal symptoms and on the ctpa we can see that there are bilateral filling defects so there are signs of pulmonary embolism. On the abdominal phase imaging we can see that there is a low density filling defect here within the inferior vena cava which is extending into a renal vein branch and we can see the effect therefore on the kidney the right kidney has an abnormal contrast enhancement pattern compared to the left with asymmetric perinephric fat stranding and so this is someone who's developed venous thrombosis And on the coronal imaging you can see that this looks different to the other case where there is a Sharper edge to this thrombus compared to that venous mixing phenomenon we saw on the first study Here is another case someone who had a remote history of endometrial malignancy Presented with chest and abdominal symptoms and we can see that there are multiple masses on the chest x-ray indicating likely metastatic disease on their chest CT they've got bilateral pulmonary emboli as well as multiple pulmonary masses.
And on the abdominal CT, we can see as we scroll down that there is a filling defect within the infravena cava, which fills and expands infravena cava, also extends then into the right ovarian vein, and if we follow this down we can see that the right ovary itself has a very abnormal appearance, likely to be a recurrence of the malignancy. Now how much of this is tumour thrombus and how much is. bland thrombus is difficult to know, there's probably a little bit of both given the fact that there are both pulmonary metastases and pulmonary emboli. We'll move on now from venous pseudothrombus to surgical hemostatic material. Now if there was ever a reason to explain to clinicians why we need good clinical details then this is it because you can easily avoid making mistakes and over calls in your report. by just being given the appropriate and relevant clinical details.
So what is surgical hemostatic material? Well it's bioabsorbable material which is oxidized regenerated cellulose that comes in different forms, sheets and swabs and powder sometimes, that is used by surgeons during difficult procedures to reduce intraoperative blood loss and it's applied to typically to organs that have been resected and the reason it's important is because when you are not familiar with it you could mistake the appearances for an intra-abdominal abscess. So look at this example of someone who had a difficult hysterectomy and on an early post-operative CT because I'd raised inflammatory markers there is this area lying across the pelvis which is fairly well defined, doesn't really have an enhancing margin but it's got lots of gas bubbles centrally amidst this low density and this was reported as extruded fecal matter due to a bowel injury at surgery but in fact one phone call to the surgeon indicated that they had in fact applied surgical hemostatic material to the vaginal apex because there was a lot of intra-abdominal bleeding and in fact this is the surgical hemostatic material.
So what are your diagnostic clues? Well as I said the best clue is a surgeon telling you that they've used it, but other things are looking for a linear array of gas bubbles and no gas fluid levels as you would typically see in an abscess. There won't be any rim enhancement, although in the late phase with a bit of formation of granulation tissue you can get a little bit of rim enhancement, but most cases you won't see any.
They'll take on these geometric shapes because the surgeon will have molded it to whatever shape they wanted to Form within the abdominal cavity and over serial imaging you'll see relatively little change So here is another example where someone's had a partial liver resection and you can see that There is this cavity now within that there are these linear low density strands with some bubbles within them Which is surrounded by this more high density material and we knew in this case that they'd used surgical hemostatic material so these low density strands are the fibers of the material and it's mopped up the blood which is this more high density stuff surrounding it. It's important to know that so you don't over call that as an abscess. Now one thing that's difficult is to absolutely rule out any infection in these regions, so any super added infection.
Something to separate and differentiate out from surgical hemostatic material is a gossip oboma which is sometimes also confused for an abscess so what is a gossip oboma it's a foreign body reaction to a retained surgical swab which is clearly not iatrogenically placed unlike surgical hemostatic material so this is someone who had a recent bowel surgery unwell post-operatively and this ct shows that there is this you walled off collection the pelvis with lots of gas bubbles within and an enhancing margin and these branching high density linear strands within and you can see that on the coronal images as well and this was in fact a retained cotton swab which the body has regarded as a foreign object and then walled off with a forming a collection and that does need to be removed unlike surgical hemostatic material which is left in for the body to absorb so In that last series we learned about how the clinical information is useful. Now the next stop we're looking at is peritoneal tuberculosis and here it's your investigative skills which are really important. You need to investigate the patient's background to see whether or not their demographic data can give you a clue as to whether or not you should consider this as a differential diagnosis when you're looking at abdominal CT. So I'm going to show you two CT studies with patients with almost identical demographic data, both young women and both with abdominal discomfort.
Here's the first one. We've got lots of ascites and then as you scroll down look at this nodular thickening of the omentum and as we scroll down further you see that it takes on a mass-like process as these are nodular masses within the omentum. We still see lots of ascites and then as we scroll down we may see some abnormal thickening of the peritoneum in the pelvis. This is the second case, identical demographic details and again we see ascites and as we scroll down we'll see thickening of the omentum and again we see this abnormal enhancement of the peritoneum particularly when you look lower down the lower abdomen. and towards the iliac fossa as well.
The first one was a case of disseminated ovarian malignancy and this second case, the one that's on the screen right now, is a case of disseminated peritoneal tuberculosis. But there is no way to tell them apart just from the imaging and it's the role of the radiologist to suggest peritoneal tuberculosis as a valid differential diagnosis for then the appropriate investigations to be instituted which is really a biopsy to check for the presence of tuberculosis. So how can you help?
Well you need to think about your patient population and whether or not peritoneal tuberculosis should be considered. So for example, are your patients, do you have a significant amount proportion of patients who are originally from parts of Africa, sub-saharan Africa or parts of Asia? Is there a history of homelessness or alcohol or immunosuppression? And also think about the age.
So peritoneal TB typically affects working age patients, 16 to 60 years. So bearing all those in mind, is there a possibility that your patient could have peritoneal tuberculosis rather than what we typically see report with most cases like that in many parts of the world, which is just disseminated ovarian malignancy? Now, when you're reading about peritoneal tuberculosis, you'll read all about wet, dry and fibrotic forms and how you can.
compartmentalize them and I don't think that's useful really. What I'd rather you look at is what are the clinical features because there's a lot of overlap between these different categories. So look for ascites, it may be diffuse or it may be loculated. Thickening of the mesentery and the omentum which may be fine or it may be nodular and more lumpy and mass-like in appearance and also sometimes enlarged low density nodes. Now typically these will be peripancreatic, portohepatous, mesenteric, not typically retroperitoneal.
So here's one more example and this was proven peritoneal tuberculosis. So as we scroll down we see that we've got this streaky increased nodularity, increased density nodularity of the omentum and we've got some ascites which appears to be loculated here on the right side of the abdomen. we keep scrolling and then we see that the small bowel mesentery has got a very nodular appearance to it lots of small lines and dots that we can see and again small pockets of fluid scattered throughout the lower abdomen and pelvis there's a little bit more here in the pelvis and then also this uh nodular appearance uh to the peritoneum you shouldn't be able to really draw a line over the peritoneum you should be able to see that clearly so that's a sign of peritoneal involvement by tuberculosis We're going to go back to the spleen for the final stop on our journey to look at splenosis. Now, this isn't very common, but it can cause some confusion, particularly when you're looking at staging or surveillance CT studies for patients with known malignancy and you come across some peritoneal or a mental nodular soft tissue lesions and you might think that they're metastases. Now, at the very outset, let's be clear with our terminology.
So we're not talking about splenonculi, which are supernumerary spleens or accessory splenic tissue. So this is an example of a splenunculus. We have this rounded focus adjacent to the normal spleen and the imaging characteristics on the arterial and portal venous phase studies are identical to the normal spleen and the blood supply to these islands of tissue will be from the splenic artery. These are splenunculi. splenosis is something different.
splenosis is when you've had previous splenic trauma or surgery and small islands of splenic tissue can auto implant throughout the abdominal cavity or sometimes even within the chest if there's been diaphragmatic trauma and they will take blood supply from other adjacent organs but not from the splenic artery. So here is a small nodule of tissue as we scroll down this patient's abdomen then we see that deep to the abdominal wall there's another small nodule there further here another small nodule and the largest bit of tissues here in the pelvis anterior to the rectum and just superior to the seminal vesicles so their blood supply will be from other arteries so look for that history of prior trauma surgery the these islands of tissue will auto implant and parasitize blood supply so it won't be from the splenic artery but they'll have the same imaging characteristics as the normal spleen If there is any confusion and clarity is required then there are a couple of technetium labelled nuclear medicine imaging studies that can be acquired. One is with autologous heat damage red blood cells and the other is with sulphur colloids.
So here is an example where the autologous heat damage red blood cells were very handy. I'm not showing you this patient CT but it showed no normal spleen, no spleen in the left upper quadrant and lots of rounded soft tissue density structures throughout the abdomen and pelvis and we can see that there's no uptake in the left upper quadrant and there are all of these different islands of tissue do have uptake indicating that they are islands of splenosis. Here is someone who had previous trauma the chest x-ray shows a soft tissue density structure in the left lower chest and their CT shows lots of pleurally based soft tissue lesions and they were also seen within the abdomen and pelvis. So they had a sulfur colloid study and that indicates that there is trace uptake within the chest in a paravertebral location and also throughout the abdomen, indicating that those islands of tissue were due to splenosis. Okay, so here we are, we've reached the final stop on our travels across the minefield that is Abdominal CT.
We've explored 10 different areas that often trip people up. Having visited these 10 stations with me, you'll now be familiar with these traps and pitfalls, and you'll be far better prepared the next time you report an Abdominal CT to avoid these hazards. Unfortunately, our journey ends here, and I must say goodbye.
See you all soon. Bye-bye. Thank you so much, Vikas. There were so many useful tips and tricks in that talk, and I love the way that you took us on a journey across the abdomen.
Vikas, we'll be back for Radiopedia 2024 with a brand new talk on rectal cancer. as well as showing us some abdominal on-call cases, which as we said before, is a new feature at this year's conference. That's all for us now.
Remember to head over to Radiopaedia to register for the conference and we will see you back here in a few weeks for the next Friday live stream. Bye for now.