So by the end of this session, you should be able to describe the ultrasound findings of common pediatric abdominal emergencies. You should also be able to identify pitfalls that may result in incorrect or missed diagnoses. And then you should be able to demonstrate how we can use ultrasound technique as well as our knowledge of key anatomic landmarks to work through some challenging cases. So our first case is a 10-month-old with abdominal pain. You can see a target appearance of bowel in the right lower quadrant. It measures greater than 2.5 centimeters. There is a prominent fat core centrally, which is thicker than the outer bowel wall. And in longitudinal image, it looks like a pseudokidney. And so this is an ileocolic interception. So that first case shows really classic features of ileocolic interception, which we use to differentiate it from small bowel interception. In real life, though, we often come across cases that are very borderline, and so it's very difficult to confidently categorize something as small bowel versus ileocolic interception using those features. So here's one of those cases. So this is a nine-year-old with abdominal distension. This is, again, a target appearance in the right lower quadrant. The diameter was barely 2.5 centimeters, maybe like 2.2, 2.3. We see a prominent fat core centrally, but again, it's kind of barely thicker than the outer abdominal wall. And this was 10 centimeters long, so it was going from the right lower quadrant all the way to the left. In cases like this, I think it's really helpful to look for the terminal ileum inserting into the ileocecal valve. Because if you can see that, and you can see that it's normal, you've essentially excluded an ileocolic interception. Unfortunately, in this case, the radiologist wasn't able to do that, and so they went to CT, and you're basically gonna do the same thing. So you show a normal terminal ileum inserting into the ileocecal valve. So we know that this is now a small bowel interception, and this was due to a mechaldiverticulum lead point. So a teaching point here is look for that terminal ileum on tough cases. If you see it going into that ileocecal valve, it's very helpful. So to look for that terminal ileum, because I think not a lot of people do this, I start with a high-frequency transducer in the right upper quadrant so that you can see the tip of the liver. Slowly pull that transducer down the body wall. You keep the lateral body wall in your field of view so that you know you're following the ascending colon. So eventually, if you're doing this slowly enough, you'll see the TI going into the cecum. And this is an important landmark, because now you know, well, if I go a little bit lower, you'll see the appendix coming off as well. So it's very handy to do. I recommend putting it in your ultrasound protocols. So small bowel interceptions, they're often transient, but there can be some with concerning features that would warrant further evaluation. That includes length greater than three centimeters, particularly if it's persistent, any signs of obstruction or a lead point. In addition, we should consider, some of these can be associated with underlying pathologies like Henoch-Schonlein purpura, celiac disease, so it's important to look for other clues as well, bowel wall thickening, other organ abnormalities, and then the patient's history and presentation. So our next case is a pediatric patient with abdominal pain and emesis, and we see this blind-ending tubular structure. This is compatible with the appendix. It measured at large, greater than six to seven millimeters. You can see it's very hyperemic. There's a lot of echogenic fat around it. We also have a shadowing appendicolith, and these are classic findings of acute appendicitis. Now again, with the interceptions, often in our practice, you run across a lot of equivocal cases, and those are usually the tough ones where you don't have all of these findings and they aren't as classically shown as they are here. And so you have to be able to differentiate those from cases that may mimic appendicitis, so I'm gonna go over a few companion cases. So case A, here we have an appendix. This was borderline enlarged, you know, in that seven-millimeter range, which is always tough. It was non-compressible. You can see it's hyperemic, but there was no peri-appendiceal inflammatory change. In addition, when we look at the hypoechoic laminopropriates thickened greater than 0.1 centimeters, and this was actually a case of lymphoid hyperplasia. Nope, showed the answer for this one too early. All right, well, this was another case where we did see echogenic fat, it was focal, it was just deep to the anterior abdominal wall in the right lower quadrant. And these will also be palpable, these will be tender to palpation also, so they can fool some people. But we can see a normal appendix here, and so it was an omental infarct. Case C, we see this is, oh, let me show you here. This is the appendix here. Again, borderline around seven millimeters. Had some mild hyperemia, there's echogenic fat around it. However, when we look at the cecum, when we look at the terminal ilium, there's marked inflammatory changes, you know, bowel wall thickening and hyperemia. And so this is actually a case of inflammatory bowel disease with secondary involvement of the appendix. And the key here is that these inflammatory changes at the cecum and terminal ilium are very disproportionate to what we see in the appendix. This is a case I read recently, a 14-year-old with abdominal pain, fever, and emesis. So the technologist noted this complex fluid collection in the right lower quadrant. You can also see it's contiguous with this irregular tubular structure here. There's echogenic fat, there's some free fluid. Because of this on the worksheet, it said perforated appendicitis. However, the curious thing about this is we could see this tubular structure so clearly, but we could never really confidently connect it to the cecum. You always wanna try to visualize the entire appendix when you can. But what we did see, which you can see here on the cines, is it comes very, very, very close to the ovary. And so we raised suspicion for a tubo-ovarian abscess, and that's what they found at surgery. And I included this case because of the season that we're in, actually. So this is a pediatric patient, fever, right lower quadrant pain. They did a right lower quadrant ultrasound. Again, this borderline case, right? Maybe about seven millimeters, maybe partially compressible. The tech had raised possible echogenic, little bit of echogenic fat and some free fluid. This patient also had a cough, though, and so they got a chest X-ray. And you can see these interstitial opacities. This ended up being pulmonary edema. And so when I went into the chart, the patient actually had a history of COVID, I think, several weeks before that. And so we raised suspicion, actually, for MIS-C. Further workup was done, and that was what the diagnosis was. So the patient had left ventricular dysfunction, elevated inflammatory markers, BNP. So this is something to keep in mind now that we're in respiratory season. Other things that you can see on ultrasound, echogenic kidneys, these are from different patients with MIS-C, gallbladder wall thickening and hyperemia, hepatosplenomegaly. I've seen cases where they have just lymphadenopathy throughout the abdomen. So it's something to keep in mind. And over the height of the pandemic, we actually saw several cases that mimicked, of MIS-C that mimicked appendicitis. And if you look in the literature, you'll see that some people actually got taken to surgery. So a summary of some of these tips and tricks for appendicitis and ileocolic interception. Identify a normal insertion of the terminal ileum into the cecum. I think it's very helpful to differentiate, number one, the terminal ileum from the appendix, because you'll see a lot of people, when they're scanning, will confuse the two. And it helps differentiate ileocolic from small bowel interceptions. As well, image the entire appendix from the base to the tip, so you can be confident that you're looking at the actual appendix. When you're following the bowel, look at the extent of the bowel changes. Inflammatory changes. Look for inflammatory changes in other organs so that you can differentiate a primary acute appendicitis from secondary involvement of the appendix in a more generalized inflammatory process. And then again, look in the chart and consider how the patient is presenting and their history. So here we have a 28-day-old with emesis. After feeding, we see the pylorus. It's thickened. The muscle wall is greater than three millimeters. The channel is elongated, greater than 1.6 millimeters. No fluid was seen going through this. And these are, again, classic for hypertrophic pyloric stenosis. Here I have pictures from two different patients, a four-month-old and a five-month-old, again being evaluated for pyloric stenosis. The technologists in their worksheet called these normal, because you can see there's a thin wall, thin wall, and they saw it opening up and they saw fluid going through. But when we look at this more closely, what you should notice is that it's almost immediately adjacent to the upper abdominal aorta. We can see the IVC. This was pretty high up, also close to where the hepatic veins were draining in. We don't see the pancreas anywhere. We don't see the gallbladder anywhere. And this is a common pitfall. These were both actually GE junction. So this is a common pitfall, something to be aware of. A couple of other tips for when you're reviewing these or if you're scanning these yourself. An over-distended stomach will push the pylorus posteriorly, so it'll be a little bit harder to find. Sometimes the technologists will also give fluid for the kid to drink to see if things pass through the pylorus. I'd recommend not doing that before you find the pylorus, because that action of feeding introduces air into the stomach, and it can sometimes obscure visualization of the pylorus and make it more difficult. All right, so this is a five-week-old concern for pyloric stenosis. Instead of pyloric stenosis, we see there's reversal of the SMA and SMV relationship. Here we also see there's swirling of the bowel, swirling of the vessels. And if you look at this CINI, you see this beaking of the duodenum right here, and then you get that swirl. So this is a whirlpool sign. This is a case of midgut malrotation and volvulus. A lot of institutions now are using ultrasound as their first-line modality for evaluating this. Things that we look for are reversal of the normal SMA and SMV relationship. So under normal circumstances, this is normal. The SMV should be to the anatomic right of an axis drawn between the aorta and the SMA. The other thing we look for is intraperitoneal D3, anterior to the SMA. Again, in normal position, the D3 should be passing posterior to the SMA. And then, like we showed here, a whirlpool sign. And it's important to differentiate the whirlpool sign from normal counterclockwise swirling of jejunal SMV branches, and with that, you won't see swirling of the bowel. All right, the last two cases I have are a little bit more, I found them a little bit more challenging. So this was a two-year-old with abdominal pain. The radiologist reading this noticed this. We weren't sure if it was a target appearance or if this was a whirlpool appearance in the paraumbilical region. We looked at that terminal ilium, and it looked normal inserting into the cecum, so we knew it wasn't an ileocolic interception. We felt pretty confident that the SMA and SMV relationship was normal, though I didn't show the image here because it wasn't a great image. So they ended up taking the kid eventually to upper GI, which was normal. But when we went back, and when you look at the cines, you can see there's this tight swirl of bowel and vessels in the paraumbilical region, and this ended up being a segmental volvulus. So segmental volvulus are actually unrelated to malrotation, typically seen in the neonatal period, but rarely they can be seen in young infants. They can be associated with intestinal atresias, peritoneal cysts, other bowel abnormalities. The whirlpool tends to be smaller and lower down in the abdomen, so when people are looking for that relationship of the SMA and SMV, we usually tell them to try to go down as low as you can to see if you can see a whirlpool lower down. All right, this is the last case I'm gonna show. This one was really complicated and tough when we read it. The patient actually came in a few days in a row. We diagnosed them with an ileocolic interception. They did go to air enema. There was an interception, an ileocolic interception that was reduced, but afterwards we had this persistent interception appearance in the lower abdomen, and you can see there's some trapped fluid in there. And when we look at the CINI, you can see, I'll come up here, there we go. There's the interception, but it's also like swirling. It was a very odd appearance, and what we ended up saying was that this was a small bowel interception that also evolved, so this was a pretty complex case because it was a ileocolic interception with an associated small bowel interception that had evolved on itself, and this patient had a history of HSP vasculitis. So some take-home points. Completely image the structure of interest. Be really critical of just limited still images. Remember to identify your key anatomic landmarks. Look for other findings that may lead you to alternative diagnoses, and look in the chart, and as much as it pains me to say this, if you can't figure it out in ultrasound, and it's a complicated case like this, and you need that diagnosis, if it's appropriate, please move on to additional cross-sectional imaging like CT or MRI. All right, thank you. Hello, everyone. So we're gonna be talking about acute ultrasound of pelvic pain. As you all know, ultrasound's often the initial modality that we use for patients presenting with acute pain, and so we're gonna talk about some common and uncommon acute GYN pathology. So our first case, this is a 31-year-old coming in with left lower quadrant pain and nausea. Here we have a transvaginal image of the left ovary, and you can see this large, septated lesion, measures over nine centimeters in diameter, and on spectral Doppler, there is a sliver of ovarian parenchyma at the side with normal arterial flow, and as we commonly see from the ED, the indication is to rule out torsion. So the first thing you have to ask is how do you identify a nexal torsion? And two of the big things that we look for are ovarian size and echo texture. So this is a more classic example of a patient with left ovarian torsion where we have an enlarged ovary, heterogeneous central stroma that's edematous, pushing the follicles out to the periphery, and you see this thick echogenic rim around some of the follicles. We also assess ovarian position. So this is a patient with a large, known right ovarian dermoid, and as we sweep through the midline pelvis going from right to left, you can see that the bulk of this lesion is actually to the midline and to the left of the uterus. So it's on the wrong side. So even though I can't see any normal ovarian parenchyma, I know just based on the position that it's not sitting where it should be and that this ovary is torsed. Doppler flow is not as helpful as you'd think it would be. So absent flow is, of course, concerning for torsion, but the presence of flow does not exclude torsion. It tells you that the ovary may be viable, whether it's normal flow or high-resistance flow. And then finally, there is the whirlpool sign that we see when we identify the twisted vascular pedicle or the meso-salpines, and this is our most specific finding of adnexal torsion. Now, I say adnexal torsion because usually the ovary and the fallopian tube twist together, and so adnexal is a little bit more encompassing of a term. Here it is on grayscale. We see an abnormal and large heterogeneous ovary, and then the twisted vascular pedicle adjacent to it. On colored Doppler, same thing, twisted vascular pedicle leading into the abnormal ovary. So getting back to our index case, what can we say? You know, is our report gonna say torsion not excluded? Can we be a little bit more precise? Can we give our clinicians a little bit more information? And actually, if you go back to the transabdominal images, you get a better look of where things are. So here on the transverse view, here's the uterus, and then anterior and to the right is where our left ovarian lesion is. On the sagittal view, again, here's uterus, here's bladder, and the ovary is out here sort of in center field, and so that abnormal position is what tells us that this lesion is torsed or this ovary is torsed. So the presence of a lead point can limit your assessment of ovarian size and ovarian echo texture. Use whatever tools you have to assess ovarian position, and a lot of times, if you have a large enough lesion, that includes looking at the transabdominal images and not just the TV. Our next case, this is a 34-year-old with right pelvic pain following egg retrieval. Now, my wife's an OBGYN, so I hear her voice reminding me that torsion's a clinical diagnosis, but this is a challenging clinical scenario. These patients often have pain, nausea, bloating, and discomfort following their retrieval. Their ovaries are going to be enlarged. They're going to be heterogeneous after retrieving all of the different follicles. So it's tough to use the typical things that we do to assess for torsion. Here, when you look at the right ovary, it measures six centimeters in diameter, and it's important to note that this is a transabdominal image. Transvaginally, we see the left ovary, which is enlarged, but about half the volume of the right, and we saw this transvaginally. We saw the right ovary only transabdominally. There is some flow on spectral Doppler, but the fact that we couldn't see it transvaginally is concerning. Remember that these ovaries, you know, they undergo a lot of hormonal stimulation. They're enlarged, they're edematous, but they tend to sit lower in the pelvis. So the fact that we have to hunt a little bit higher up in and of itself is concerning and was really one of the only clues that this ovary was torsed for this patient. Here's another case, a 27-year-old with right lower quadrant pain, a lesion that looks very similar to what we saw earlier, septated adnexal cyst, measures over seven centimeters in diameter. There is some flow in the normal ovarian parenchyma at the periphery, and then we're measuring the right ovary here. And so the patient came in with right lower quadrant pain, and the radiologist read this as a septated left ovarian lesion, recommend GYN follow-up, no evidence of torsion. So in the emergency department, they consulted GYN. Patient was having significant enough pain that they underwent diagnostic laparoscopy, and the patient had right adnexal torsion. So what did we miss? If you look at one of the synate clips, there's our whirlpool sign. So ovarian lesion, twisted vascular pedicle. And if we take a closer look at what we were calling a right ovary, it's actually more tubular, and you can just make out some alternating hyperechoic, hypoechoic layers. And so there's a very good chance this is just a decompressed loop of bowel. So when something doesn't quite add up, and in this case, it's the fact that there's right lower quadrant pain, and the large mass is on the left side, start asking questions. Maybe the ED wrote the wrong side on the indication. Maybe the sonographer mislabeled the images. Or in this setting, maybe we misidentified what we were thinking was a normal right ovary when in fact it was something else. Okay, our next case, this is a 17-year-old coming in with left lower quadrant pain. We have transabdominal images here, and you can see the ovary here was normal in size. Adjacent to the ovary is this tubular elongated structure that's fluid-filled. There is normal vascularity to the left ovary. And again, when we look at color doppler in the adnexa, we see our whirlpool sign. So this is an isolated fallopian tube torsion. It occurs more often in women who have preexisting tubal abnormalities or tubal ligation. You want to look for dilation of the fallopian tube or a large paratubal cyst. And the key finding is the combination of a normal ovary in conjunction with this swirling vasculature. So you know that there's some degree of torsion, but the fact that the ovary itself is normal, normal in size, normal in echo texture, tells you that that's not involved and it's isolated to the fallopian tube. Here's a companion case where we have a large paratubal cyst. Adjacent to that is normal ovarian parenchyma. More inferiorly, again, normal left ovary here anteriorly, and this was the vascular twist. And this looks very much like it could be part of the ovary, and so you want to use your syn eclipse to go through, and you'll see that this was in fact separate, not something to be measured as part of the ovarian parenchyma. And this was a torsive paratubal cyst. So although it's less common, remember that torsion is not limited to just the ovary. Okay, our next case, this is a 47-year-old presenting with pelvic pain and fever. So here we have a transvaginal image of the right ovary, and adjacent to the ovary is this hyperemic structure in the adnexa. When we look with our syn eclipse on grayscale, you can see that it's tubular, somewhat echogenic, thick-walled, and if you look, the signature is very different than the adjacent loops of bowel, right? This is sort of more typical of gut signature with the outer wall and alternating layers. This does not look like that. And when you look with color doppler, there's associated hyperemia. So we have what looks like an inflamed tubular structure in the adnexa. I know it's not appendix just because of the absence of gut signature that I would expect to see with bowel, and so this was, in the clinical context, an acute salpingitis. So pelvic inflammatory disease is an ascending infection that can be acute, it can be chronic, it can be subclinical. And when I say subclinical, I mean, for example, women that come in with infertility and tubal factor infertility may have no known history of PID, but the presumption is that at some point, they had inflammation that led to tubal factor infertility. It can be unilateral, it can be bilateral, and there's a broad spectrum of clinical and imaging findings. So it starts with endometritis, spreads to the tube with salpingitis, pile salpings, oophoritis, and then full-blown tubal ovarian abscess with or without peritonitis to go with it. Here's an example of bilateral TOAs. So in the right adnexa, we're seeing low-level echoes within the fallopian tube. We're not seeing normal anatomic landmarks and normal contours of the ovary adjacent to it. In the left adnexa, we have a large complex collection, thick septations. On CT, you can see bilateral TOAs. Here's a companion case. So this patient also came in with left lower quadrant pain, and here we have a dilated tubular structure. You can see part of the endosalpingial folds that are thickened. We see some low-level echoes within. And there's also this left ovarian lesion that has low-level echoes, as well as a more echogenic, solid-appearing component. There was no Doppler flow associated with this. The patient had no infectious signs or symptoms, and their history was actually more typical of that of someone with endometriosis. So they opted for follow-up. And six weeks later, as these blood products have evolved, you can see this looks more like a typical endometrioma with diffused low-level echoes and no internal vascularity. So if you're trying to decide blood versus pus, and when we see low-level echoes in the tube, that's kind of what we're thinking about. The clinical suspicion for PID is what's gonna drive your management. You're gonna think about things like endometriosis, you're gonna think about things like ectopic pregnancy, and you're gonna think about piosalpings, but it's really how the patient is presented clinically that's gonna decide what they're gonna do. Here's sort of the counterpoint to that. Classic endometrioma, low-level echoes, no vascularity, posterior acoustic enhancement. Here it is on CT. Two days later, the patient came back with worsening pain, and you can see now it's replaced with echogenic material, it's expanded, it's increased in size compared to the prior CT, and we can see inflammation around it. So this looks very much like an endometrioma that's acutely bled, but the patient came in with infectious symptoms, and so when they went into the OR, because their pain and white count were getting worse, they found pergolent material and evidence of pelvic inflammatory disease. So superinfection of benign pathology or superinfection of preexisting lesions does happen and is something to be aware of. Along those same lines, this is our last case. It's a 41-year-old with prior hysterectomy presenting with pelvic pain and sepsis. So her hysterectomy was a year ago for grade one endometrioid adenocarcinoma, and she opted for ovarian preservation because she was young. So here you can see the right ovary is normal. The left ovary has been replaced by a predominantly solid-appearing mass, flow on spectral doppler, maybe a little bit of complex fluid, but again, predominantly solid mass, and so this was read out as recurrent metastatic disease, no evidence of infection to explain sepsis. The patient's had a hysterectomy, and ascending gynecologic infection didn't quite make sense, and this looks very much just like tumor. Of course, her sepsis was not improving. They operated to get a better sense of what this was. The pathology came back as recurrent metastatic disease, but again, they found pergolent material at the time of surgery, and so this was superinfected. So be cognizant of atypical spread of infection, and that could be transmural spread from adjacent loops of bowel. That could be hematogenous seeding. In this case, the cultures were positive for enteric pathogens, and so the thought is that there was something from the adjacent colon that had spread to this tumor and caused superinfection. Okay, so our take-home points. Pay close attention to ovarian position. Use whatever you need to try and determine what that is, and whether that means getting additional imaging or not. Question the information that's presented to you when the imaging findings don't add up to what the clinical information is. Remember that torsion is not just limited to the ovary, and always keep infection or superinfection of preexisting structures in your differential when the clinical scenario calls for it. Thank you very much. It's great to see everyone. Again, I'd just like to start off by thanking Dr. Rubens for organizing the session, the fellow speakers, and of course, all of you for coming. So what I want to share with you today are three very commonplace and three clinically important scenarios that we see in the acute setting with MSK ultrasound. So without further ado, we'll move on to the first case, and we're gonna take a deep dive into each of these scenarios. So in this very first case, this was a 26-year-old woman who had come to the eMERGE with right shoulder pain, and the clinical query from the eMERGE doc is, is there a rotator cuff tear? So what we're looking at is a transaxial or short-axis image through the long head of biceps tendon here in the bicepital groove, and I'd say we have the transducer in this orientation parked halfway between the supraspinatus and the pectoralis major. And so the question here is, as you look at this image, is there this cleft here that we can see, is this a split tear or not? Now, of course, ultrasound is a very dynamic modality, so we're going to take a look at the CINI here. And on this CINI, we are staying in short axis, and what I'm doing is dragging the transducer from very, very high up at the level of the supraspinatus and bringing it down through the rotator cuff interval along the bicepital groove all the way down to pectoralis major. And as this descends, we can see the long head of biceps tendon here. But as we get down to about this level here, again, we see what looks like a cleft in the long head of biceps tendon. Or is it? Maybe this is another structure. So if we follow this structure down inferiorly, we can see it blending in with the fibers of pectoralis major. So now the transducer is down at about this level here, and we can see that the pectoralis major has come into view. Now if we go all the way back up superiorly, we can see this is the supraspinatus tendon here. It's not a very lovely picture of the supraspinatus just because the way that the arm is positioned, but as we go inferiorly again, we can begin to see that this structure arises from the supraspinatus, and it just carries on here, and again, blending in with the fibers of pec major. So the question is, is this a longitudinal split tear? It doesn't look like that's the case, and what this is is a normal variant. This is the supraspinatus aponeurotic expansion, and this is a very, very common variant that you see in about half of the patients that you image, and this is a beautiful cadaveric dissection here showing the expansion as a connective tissue extending from the supraspinatus tendon here all the way down to the pectoralis major, and so I've color-coded it in blue here, and you can see where the long head of biceps tendon is sitting in relationship to this. So this expansion always courses anterior and lateral to the long head of biceps tendon, and it can have different morphologies as well. It can be flat and thin or, as in the case that we just saw, can have a cord-like or oval appearance, and this is a nice MR correlate here just on this arthrogram here. You can see the aponeurotic expansion just sitting anterior to the long head of biceps, so important not to mistake this for a longitudinal split tear. Again, we see this in about 50% of patients. Case 2. This was a 50-year-old patient who had presented with severe lateral elbow pain, worsening over the last two weeks. Clinically, there's weakness and pain to resisted supination and wrist extension, so the transducer is oriented in this longitudinal plane here, and this is a very typical image that the sonographer is going to present, and there's nothing wrong with this image here. We can see a lot of important bony landmarks. There's the lateral huma apicondyle, the capitulum, and the radial head, and we can see the common extensor origin. So the question here is that on this image, is the common extensor origin normal? And I would argue that this, yeah, it doesn't look too bad. There's a normal fibular architecture, maybe a little heterogeneous, but not that bad. We don't really see a tear at all developing on this image, but again, ultrasound is not a static modality, so we're going to take a look at a sine loop here through this area, and the way that the transducer is positioned, we're going to start off posteriorly, but we're going to slide the transducer anteriorly, and as we do this, I'm just going to get up to the very beginning of the clip here. Again, the common extensor origin posteriorly doesn't look bad. As we slide that transducer anteriorly, though, you'll begin to see that the appearance does begin to change, and this portion of the common extensor origin now looks very equiporeal and heterogeneous. There's a certain partial tearing along the deep surface, and so is the CEO normal? Well, about half of it is, and the other half doesn't look normal at all, and if we need any further proof of this, we can turn on the color, and there's a lot of hyperemia through the CEO origin, so definitely not normal, and so of course this is the common extensor tendinosis and tearing, also referred to as lateral epicondylitis or tennis elbow, and by far and away is the most common cause of lateral elbow pain that we see referred, and of course these cases are secondary to repetitive stress, leading to micro tear formation and degeneration, and the real take-home point here is that sometimes this condition will only affect one specific part of the common extensor origin, and that explains why it looks very normal in half of the tendon, and it looks completely abnormal in the other portion. Now to really understand this well, we have to unpack the anatomy just a little bit more, and so what I've done here is level by level just demonstrate here what the common extensor origin looks like. This is a posterior slice, this is the mid portion of the CEO, and this is the anterior portion of the CEO. We also have to remember that the CEO is comprised of four muscles. The most posterior muscle is the ECU or the extensor carpi ulnaris, and then we have the extensor digitorum communis. The extensor digiti minimi, the EDM, is not illustrated here because it lies deep to these muscles, and the fourth muscle of the CEO is the extensor carpi radialis brevis. So in this position here with the transducer very posterior, when you're imaging the CEO really all you're looking at is the extensor carpi ulnaris. If we shift the transducer slightly anteriorly, we come into the mid portion of the CEO, and now we see a multi-layered CEO where we have the EDC superficially, and the middle layer is formed by ECRB and the EDM, and the deep layer here you'll see is the radial collateral ligament and the anterior ligament, which are not part of the common extensor origin, but they're closely related, these structures. And again, this is the typical static ultrasound image that the sonographer will present, and there's nothing wrong with this image, but if we stop here, we haven't imaged the entire common extensor origin. So you want to take the transducer and continue to push anteriorly here, and it's only when you get to this stage that we see the ECRB tendon in its bulk. And so this is really, really important to image this portion of the tendon in order to avoid misdiagnosis. We've seen lots of cases of rip-toring common extensor tendinosis and tearing that looks completely normal at this mid-level here. Okay, this is the third scenario. This is a 52-year-old patient who presented with acute onset, very severe pain localized to the ulnar wrist, and this night she has slightly elevated CRP, leukocytosis, and a low-grade fever. There may have been some sort of minor direct trauma to this area about one to two weeks ago, and so on this photograph that I took, you can see that there's a mild hyperemia around the vulnar ulnar wrist, and the eMERGE doc is concerned about things like cellulitis, maybe even an abscess that feels a little bit fluctuant to touch, or maybe even an occult fracture, given the history of possible trauma a couple weeks ago. So what is the diagnosis based on the following ultrasound? So I'll show you another CINI here, and this particular ultrasound is oriented in the satural plane here, so we're just over the pisiform here. This is how it's oriented. So the pisiform is this structure here, and we can see that there's a tendon coming down to insert onto the pisiform, and of course this is the flexor carpi ulnaris, but what's interesting about this is that there's this sort of clumpy echogenic material here related to the FCU. So what is this? So what's the diagnosis here? This is calcium apatite deposition disease, or CAD, and more specifically of the FCU, and we typically will see this around the hips and very commonly around the shoulders as well. This is some calcium that was pulled out of this particular shoulder. It also goes by the name of hydroxyapatite deposition disease, or HAD, but this is really a historic misnomer. There's no hydroxyapatite crystals in these types of calcification. There's a subset also referred to as calcific acute periarthritis, and the reason for understanding this condition is that this is a very, very frequent and, I would say, unexpected cause of acute pain presentation to the eMERGE. Clinically, it can mimic a lot of other conditions all around the body, not just in the shoulder or the wrist, and it's never on the eMERGE physician's radar, from my experience, and the labs, when they're drawn, often normal, but sometimes, as in this case, they can be a little bit out of whack. Now, it's important from an ultrasound perspective to think about the different phases of CAD because the ultrasound appearance changes, so depending on which phase this is in, you may see something different. In the pre-calcific phase, this is where the tendon is undergoing degeneration and metaplasia into fiber cartilage. In the formative phase, the chondrocytes begin to deposit carbonate apatite crystals, and if you were to do an ultrasound in this formative phase, you get very strong acoustic shadowing artifact here. You can see the cortex of the bone here is completely obscured, and if you were to put a needle into this, it feels like a pebble, and so this is physically hard calcification. Sometimes, this calcification will begin to resorb, and this resorptive phase is very intense clinically because it's inflammatory, and you get infiltrates of leukocytes and lymphocytes and giant cells, but importantly, on ultrasound, if you were to image during this phase, it begins to liquefy, and as a result of this, you get less acoustic shadowing artifact. We can see the cortex of the bone again, and then we move on to the reparative phase after that, and so again, it depends on which phase you're imaging in. As I said, this can occur in a lot of different parts of the body. This was a case recently that we saw a patient presented with severe neck pain, difficulty swallowing. The clinical suspicion was retropharyngeal abscess, maybe discitis, but here you can see that there's a huge deposit of calcium in the longest coli. This is another patient presenting with severe, severe pain, such severe left hip pain. In fact, the eMERGE doc thought maybe this was a pathologic fracture, but what this is is a big clump of calcification in the origin of the direct head of the rectus ephemeris arising from the anterior inferior iliac spine, and this is the corresponding CT scan here, nicely demonstrating that clump of calcification, and in this case, this was another recent case of a carpenter who had come in with severe hand pain. You can see how the first web space there is just completely swollen and red. On the x-ray here, we can see that there is lots of calcification in the first carpometacarpal articulation, and then all of this mineralization in that first interosseous space, and on the CT scan here, what's very interesting about this is that we see this plume of calcium extending into the first dorsal interosseous muscle, and this is a very interesting thing that CAD sometimes does, is it will expand into the muscle or can even erode into bone. So what I hope that you've taken away from this talk is, number one, do not mistake supraspinatus aponeurotic expansion for a LHB split tear, but always confirm its course going from the supraspinatus tendon to the pectoralis major tendon. Number two, when examining the common extensor origin, always be sure you examine the full width of the CEO, and you do this by pushing that transducer all the way anteriorly to avoid missing ECRB pathology. And number three, think about calcium appetite deposition disease in any patient presenting with acute pain to the ED. We've been surprised by this condition time and time again. And with that, thank you very much for your attention. All right, moving on to the very first case, a young male, 35 year old, presenting with abdominal pain. And we were asked to evaluate the mesenteric arteries as suspected etiology for a patient's symptoms. So what are we seeing here? We are looking at the celiac artery, nicely labeled here, and this is the aorta, but this does not obviously look like a normal celiac artery. There are a lot of things wrong here. Number one, the angulation is wrong. Typically the celiac artery faces downwards. The caliber or the lumen of this artery is very abnormal. There's severe narrowing here, suggestive of stenosis, and then there is a dilatation, which suggests a post-stenotic dilatation. So obviously we're going to go ahead with a color doppler. So let's see, as part of the protocol, we do evaluate the celiac artery in the inspiratory as well as expiratory phase. So what are we seeing in the expiration phase? We are seeing again the upwards deflection or the angulation of the celiac artery, really elevated velocities, up to 455 centimeter per second, as compared to the inspiration phase, where the angulation looks like it's a little bit different. It seems to be deflecting downwards rather than upwards, and the velocities have come down to almost 260 centimeter per second. So definitely the respiratory phase is making a difference in the velocities and the narrowing of the celiac artery. Just to confirm that hemodynamically significant stenosis, we are going to go more distally downstream and look at the main hepatic artery, and we are demonstrating this delayed upstroke, also called as a tortoise parvus waveform. So it suggests that yes, there is a proximal significant stenosis, and also downstream from the proximal celiac artery, we can see that there is a tortoise parvus, a lot of turbulence, and spectral broadening. Again, all of them signifying and suggesting that there is a tight stenosis here, which is getting affected by the respiratory phase. So yes, the diagnosis is median arcuate ligament syndrome. Very nicely demonstrated on the CT, as you can see here, it's a J shape or a hook shape, which is very characteristic for median arcuate ligament syndrome, and you can actually see this median arcuate ligament coming here and compressing on the proximal portion of the celiac artery. So what is this median arcuate ligament? It is a fibrous arch that connects a diaphragmatic crura on either side of the aorta. Patients typically present with weight loss, postprandial pain with emesis, and abdominal bruit. And the physiology is, again, the mesentric ischemia that is caused from compression of the celiac artery, or from postprandial steel via the collaterals from the superior mesentric to the celiac bed, when there is a really, really tight stenosis. So the diagnosis of median arcuate ligament syndrome is made on ultrasound based on the maximum expiratory peak velocity of greater than 350 centimeter per second, and the deflection angle. So that's what contributes to the J shape or the hook shape that we were looking at on CT. But yes, we can see that on ultrasound as well. And these two are considered the most reliable indicators. The management is usually surgical, because this is not an atherosclerotic. It is not an inflammatory process. So you usually require a surgical decompression of this median arcuate ligament, and that would be the treatment of choice in symptomatic patients. So here is a short animation to show you exactly what happens in median arcuate ligament syndrome. So that's the celiac artery. And during expiration, typically, the ligament will not do anything to the celiac artery, or very mildly touch it and not cause compression. However, in the median arcuate ligament syndrome, it will compress it during expiration, and usually it comes back to normal or reduces the velocity during the inspiration phase. But sometimes, in severe cases of median arcuate ligament syndrome, be aware and be cognizant that the velocities may not come back to normal inspiration, and you may have to stand up the patient. So in erect position, you may actually see a further drop in velocities, and that will help you confirm the diagnosis. So let's look at this case. Is this, again, a median arcuate ligament syndrome? So if we follow the criteria that I just mentioned, inspiration 208, expiration 237, so not really a significant increase in velocities. So can we just blindly call it that, no, this is not median arcuate ligament? Well, just wait and watch. So what are we seeing here is this downward deflection of the celiac artery as expected in inspiration. However, in expiration, I'm not really seeing the distal portion of the celiac artery. I don't know where this is going. It almost seems like it's trying to curve upwards, but the sonographer is not really showing me, and I'm not sure what the angle is correct or not. So I go in the room, and I put the probe, and voila. What do you see? You see this nice J-shape of the celiac artery, which is deflected upwards. And of course, you try to interrogate distal to the point of narrowing, you will get a very elevated velocity. So another thing to remember here is that the maximum velocity is usually at the stenosis or just distal to the stenosis, not proximal. So if you're trying to interrogate the proximal portion, you will always get a much reduced velocity than what actually it is. So this indeed was a median arcuate ligament syndrome, which was giving false negative results earlier. Sometimes, and some institutions would also do CT in the inspiration and the expiratory phase. So again, beautifully demonstrating the median arcuate ligament syndrome in the expiration phase with the J-shape and narrowing from the median arcuate ligament, which was very normal-looking in the inspiration phase and corresponding findings on the Doppler, just as I mentioned. All right, let's look at this case. Is this median arcuate ligament syndrome? So celiac artery, a little bit of narrowing, a little bit of aliasing here, and now we're going to try and get the velocity. So we're getting 256 during inspiration, and during expiration, what happens? It drops down to 200 centimeter per second. So no median arcuate ligament syndrome? Wait a minute. What are we really doing wrong over here? The aliasing is here, and we all know aliasing is at the spot where the velocity is higher, right? There's a lot of turbulence there. That's what causes the aliasing. So your spectrum should be obtained here, not here. Plus, we are expecting this is, if you're suspecting a median arcuate ligament syndrome, we know that this is not where the compression is going to be. So this is not going to be the area of stenosis. So we correct that, put the pulse a little bit distal in the area of aliasing, and of course the velocity is up more than 39 centimeter per second. So yes, again, correctly diagnosed as median arcuate ligament syndrome. So be very careful with this entity because the stenosis may not be at the very origin as we suspect in atherosclerosis. And there have been so many times I have sent my technologists, my sonographers back to the room to go further into the celiac artery and interrogate there. And so much so that I made it a protocol that you will do the origin and you will also do two centimeter distal of the celiac artery so that you do not miss this post-genotic elevated velocities. So again, beautifully demonstrated on the B-flow image and the power Doppler, the narrowing and the post-genotic dilatation. So if you see this with the deflection, your mind should automatically start thinking towards median arcuate ligament syndrome. Let's look at another case, 22 year old female complaining of abdominal pain. So again, asked to evaluate the mesentric arteries. And, oops, all the images showed up. Great. So this is the aorta and this was the celiac artery origin we were trying to interrogate, but we are hardly getting any flow, no detectable flow here. A little bit distal to it, with expiration and inspiration, there was flow but no difference in the expiration phase. We keep going further, going into the hepatic artery where there was some reversal and steel happening and some tortoise porous waveform and also the splenic artery. Why are we doing all this? Because they are all coming from the celiac trunk. So the changes have to be seen in the hepatic artery and the splenic artery as well, if they are really a stenosis. So yes, that confirms that there is a stenosis at the celiac artery. And then we did a CT to confirm that and yes, of course, there is a very tight stenosis. But what is really happening here? This is not really fitting in the category of median arcuate ligament syndrome. Really young patient, not really seeing any atherosclerotic plaque. So to complete the exam, we move forward and evaluate the superior mesentric artery. So what are we seeing here? Again, abnormal looking superior mesentric artery, somewhat irregular caliber. So it's not a nice normal caliber that we expect to see. And on color, the proximal velocities are looking pretty okay at 150. But you go a little bit more distal, aliasing 450 centimeter per second. And then you go a little bit further, there was some reversal happening and then more distally, some tortoise porous and spectral broadening and turbulence you are seeing. So yes, there's definitely an area of stenosis, not necessarily at the proximal origin of the SMA as you would expect in the atherosclerotic situation. So this patient also had a replaced hepatic artery, which again showed a tortoise porous, again confirming that there is a proximal stenosis of the SMA. And then to complete the protocol again, the inferior mesentric artery also demonstrating slightly elevated velocities. So clearly this is not showing any evidence for atherosclerosis. It's not fitting in the category of median arcuate ligament syndrome. So what is this? Multiple arterial involvement, young patient. So we think of fibromuscular dysplasia. Yes, we have seen FMDs in renal arteries, not so much in mesentric arteries, but it does happen. So it's a non-inflammatory, non-atherosclerotic process seen in young patients, most commonly in the renal arteries. But you can see it in the mesentric arteries as well, so you should keep that in mind. The diagnosis does need a high index of suspicion and the management is usually surgical. And this is a nice example of renal arterial FMD with a nice beaded appearance treated with angioplasty. So FMD is the dysplastic arterial wall with overgrowth of smooth muscle and fibrous tissue, which leads to the narrowing, leading to the string of beads appearance. And on Doppler you would see the high-velocity turbulent flow with distal flow changes. Next case, 45 year old with acute abdominal pain. Okay, what are we seeing here? You're seeing an irregular dilated SMA and there is a flap. So clearly it's a dissection with both the true lumen and the false lumen being opacified. And that's what we are seeing on the ultrasound as well. There's a dissection flap and there are two lumens, but both of them are filling with color with no significant change in velocity. So this is clearly a case of SMA dissection. Let's look at another case, another patient with acute abdominal pain with a flap but a non-opacified false lumen. So if you assume this is a false lumen, this was not filling with color. So this was slightly different from the case we just saw. And I'll show you in a second why that's important. So in this patient we also then went ahead and did a CT, which is almost essential, and you saw extensive dissection with thrombosed false lumen. As you can see here, this is the SMA involving the branches as well, seen in these static images. But we also saw something extra and that was the hepatic arterial involvement. So the hepatic artery also demonstrated some dissection happening here. So this was not an isolated SMA involvement, it was hepatic arterial involvement as well. And this was a case of segmental arterial medial lysis. This is a very uncommon condition but a very high mortality, almost up to 50%, and involves the medium-sized branches of SMA. And the patients sometimes present with spontaneous intra-abdominal hemorrhages, which is what can be fatal. So you have to be extra aware of this entity, and if you see dissection involving the SMA or the hepatic artery, look at all the vessels. Patients usually present with fusiform aneurysms, tenosies, dissections, and occlusions, and you do not want them to reach the state of spontaneous intra-abdominal hemorrhage. This is also a non-atherosclerotic and non-inflammatory condition, so it's often confused with fibromuscular dysplasia. Isolated SMA dissection is rare, as I said, but it's more common than the celiac and the hepatic arteries, and these are some of the causes of SMA dissection, of which segmental arterial medial lysis is one of the commonest. And this is why we need to do a CT on all these cases of SMA dissection to make sure how to assess further management, because if both the true and the false lumen are patent, you're usually doing a more conservative management. But if the false lumen is thrombosed and the true lumen is showing some ulcer-like projections, it needs an emergent revascularization. And that's why most of these dissection cases that you will see on ultrasound should undergo a CT angiogram, not just a CT, CT angiogram, so that you can identify these ulcer-like projections. Last few cases, this is a 65-year-old female with abdominal pain, hypervolumic shock, and there's a no-brainer that this is clearly an abdominal aortic aneurysm with some plaque. And the color is, obviously, there's a lot of turbulent flow. This is not all thrombosed, but what we are really seeing here is that there is some color bleeding going outside of the abdominal aorta. So this was initially discarded as, or disregarded as, just an artifact of the color Doppler. But what we should be really aware of the secondary signs of abdominal aortic aneurysm rupture, because in ultrasound we are usually not thinking on those lines and we're always going to CT for identifying or diagnosing rupture. But any sign of retroperitoneal hematoma fluid or when the OOO, when the abdominal aortic aneurysm is much larger than five or six centimeters, that increases the risk of rupture. So if you see any secondary sign, such as retroperitoneal hematoma, on ultrasound you should immediately ask for a CT. As you can see here, this was a ruptured AAA. Another very, very giant AAA. This is, I've never seen this big abdominal aortic aneurysm. Luckily it was still intact, but these are the kind of patients we should immediately go to the OR for repair. And you should also be able to identify cases of impending rupture, because that's where you will be really protecting these patients and saving patients' lives. So penetrating ulcer is something very subtle, but you should keep an eye out on those, because that means this patient has a high risk for rupture. And also fluid immediately around the abdominal aorta, especially when it's aneurysmal, because that could suggest that the patient has contained rupture and this could blow up any time and be fatal. So some take-home key points. In younger patients, consider median arcuate ligament syndrome as a cause of celiac artery stenosis. Focus on the area of narrowing, which may not always be at the origin. So find that area of focal aliasing and put your pulse there to find your maximum velocity. Look for other arteries involved in SMA dissection for the segmental arterio-medial lysis, because you don't want these patients to bleed and have severe intra-abdominal hemorrhage. And look for signs of impending AAA rupture.

pediatric abdominal emergencies

ultrasound techniques

diagnostic pitfalls

anatomical landmarks

adnexal torsion

pelvic inflammatory disease

MSK ultrasound

appendicitis diagnosis

ileocolic interception