Hi, I'm Hediye Baradaran, and I'm going to be talking today about do not miss neurovascular findings in the emergency setting. So the primary objective for this talk is to provide an imaging-rich review of some important emergent neurovascular imaging findings. By far the most common neurovascular emergency we see is acute ischemic stroke, with a majority of CTAs performed for this indication. When imaging the vasculature for suspected acute ischemic stroke, we are primarily looking for any actionable large vessel occlusions, and also secondarily assessing the remainder of the vessels for a potential stroke etiology. Though acute ischemic stroke is the most common indication for neurovascular imaging, we will only briefly touch on this topic since there are others dedicated to this topic on stroke imaging. Before we move on, we will very quickly look at a few examples of large vessel occlusions that may be seen in the setting of an acute infarction. Here is an axial CTA and axial MIP image showing a right M1 occlusion in a patient who is quickly taken for a thrombectomy. Here are a few other examples of M1 occlusions. Large vessel occlusions are probably one of the most important do not miss findings, because if detected early, they can be successfully treated and dramatically change patient outcomes, depending on the degree of ischemia present. Because this is one of the most critical findings in an emergent setting, there are a few other talks dedicated to this topic, so check them out. We're going to start with dissections, which are a large contributor to ischemic strokes in younger populations. They're more commonly seen in females. Carotid dissections are also more common than vertebral artery dissections, and they're most commonly seen in a distal cervical ICA. Just to note that it is extremely rare to see a dissection at the carotid bifurcation. They are usually at least two to three centimeters distal to the bifurcation. So both vertebral and carotid artery dissections are most likely seen close to the skull base, where the arteries are most susceptible to motion in cases of trauma. So for the carotid artery, it's most common in the distal cervical ICA, and for the verte, it's most common in a V3 segment. Dissections can be spontaneous, post-traumatic, or occur in those predisposed from an underlying arteriopathy, such as fibromuscular dysplasia or Ehrler-Danlos. They can present in a number of different ways, which can sometimes make their imaging identification difficult. So here we have a 48-year-old male patient who suffered blunt trauma in an ATV rollover. He had many of the classic imaging findings of dissection. So we see here in the right distal ICA an area of vascular outpouching consistent with a pseudoaneurysm. In the distal left ICA, we see a focal area of significant narrowing, with also a crescentic area of soft tissue density, which was consistent with intramural hematoma. Again on the left, this is more proximal, he had another pseudoaneurysm as well. So again, we can see in the proximal portion of the petri segment of the left ICA, he has again his severe narrowing secondary to this dissection. These are coronal and sagittal reformats. We can see the pseudoaneurysms in the right and left ICAs, respectively. This is a different 48-year-old male who's presenting with right-sided weakness. In this case of a spontaneous dissection, we can actually see the dissection flap as this linear area extending through the lumen. Actually seeing dissection flaps in the setting of cervical dissections is not common, and it's thought to be less than 15% of cases. This is another case in which we see a dissection flap in the distal right ICA. And distal to the dissection flap, we see a free-floating intraluminal thrombus. Here's an MR-based example of a young woman who suffered from quadruple dissections. So on these axial MP-RAGE images, we can see crescentic areas of T1 hyperintensity in the distal left ICA, the distal right ICA, and even in the bilateral V3 segments of the vertebral arteries. All of these are consistent with intramural hematomas in the setting of dissections. The intramural hematomas are leading to stenosis in the bilateral ICAs, and you can see these areas of the residual lumen as these areas of hypointensity. I want to briefly show a few examples that should not be confused with dissections. Here are some examples of patients with eccentric, soft, fiber-fatty plaque narrowing the proximal ICA, some with areas of large ulcerations. Again, all of these are consistent with atherosclerotic plaque, and while many of the plaques do cause severe stenosis and some of them have areas of vascular outpouching that could potentially be confused with a dissection, we know that these are actually just plaques because of the presence of calcification and their location right at the carotid bifurcation. It would be extremely rare to have a focal dissection limited to this location. Similarly, this is an MR image in axial MP-RAGE, and we see an area of crescentic T1 hyperintensity right at the carotid bifurcation. In this case, this represents interplaque hemorrhage, not to be confused with an intramural hematoma in the setting of dissection. Just to briefly review, plaques are commonly seen at the carotid bifurcation in the proximal ICA, whereas dissections are usually seen at least two to three centimeters distal to the bifurcation. Plaques are frequently associated with calcifications, whereas dissections are very rarely associated with calcification unless they're seen concomitantly with plaque. Plaques can have large ulcerations, which may look like a vascular outpatching, but that is not to be confused with a pseudoaneurysm that we can see in dissections. And again, plaque can have intrinsic T1 hyperintensity, which is representative of interplaque hemorrhage. But usually this is a focal finding as opposed to in a dissection where there is longer areas of intramural hematoma throughout the length of the dissection. Here's another differential consideration. This is a 53-year-old male who complained of dizziness. We can see in the distal cervical ICA, we don't see any opacification here. We see a normal right distal cervical ICA, but we don't see any opacification on the left. And again, at the carotid bifurcation here, we can see the bulb here, and we can see these branches, so we know that this is the ECA, but we don't see any contrast here at the proximal left ICA or throughout the left ICA. And instead of thinking of it being an occlusion, we look at the skull base, and here the skull base you can see there's a normal, actually quite a little bit hypertrophied, petrous right ICA, but there's basically no bony canal here. So this is an example of congenital absence of the ICA, which is a pretty rare anomaly. And one of the best ways to differentiate this from a complete vessel occlusion is to look at the bony carotid canal. If the canal is hypoplastic or aplastic, it is likely either congenital absence or hypoplasia of the ICA. Then one last differential consideration. So in these three patients, we can see an area of linear shelf-like low attenuation in the posterolateral aspect of the carotid bulb. And though it may look like a dissection flap, this is not a dissection. This is a carotid web. They're also relatively rare. Though they're not dissections, they actually can be, they are associated with recurrent ischemic stroke. They're most commonly seen in younger female patients and are thought to be a variant of FMD and thought to be related to fibrous intimal hyperplasia. Moving on to another important neurovascular finding in the emergency setting, which can be seen secondary to radiation therapy. The most common vascular complication post-RT is usually accelerated atherosclerosis. One of the dreaded complications is pseudoaneurysm formation from arterial wall thickening from the radiation. So here's an example of a 66-year-old male who had a history of laryngeal squamous cell carcinoma who had had radiation and surgery, and he presented with bleeding from his neck. This is a so-called carotid blowout. So it's pseudoaneurysm related to RT. So I'm going to scroll through these images and you can see here, this is his right ICA, obviously, and this is his hand holding up a piece of gauze to his neck, which he was experiencing bleeding from. And as we're going up through the ICA, we can see this large area of vascular outpouching with focal areas of air around it. The vascular outpouching is extending to the skin surface. You can see that this vascular outpouching is directly connected to the gauze that he's holding up next to it. And this is exactly the site from which he was experiencing bleeding. Here's some sagittal views of the same patient where we see this very large pseudoaneurysm adjacent to surgical clips with, again, small foci of air around it next to the gauze. So this is a carotid blowout. The patient went to angio and he had a coil and onyx occlusion of the pseudoaneurysm, but unfortunately suffered severe anoxic brain injury. So this is a do not miss vascular emergency. Usually they're not this obvious, but you can see subtle areas of irregularity or pseudoaneurysm that should be treated right away to avoid this dreaded complication. So this is an example of a woman who presented with left proptosis and blurry vision. So you can see here there's left-sided proptosis. We're also seeing enlargement asymmetrically of the extraocular muscles on the left. And again, there's marked asymmetric enlargement of the superior left ophthalmic vein. Here on this coronal image, you can see there's early filling or asymmetric filling of the left cavernous sinus. So all of these findings together are consistent with a carotid cavernous fistula. So classic imaging findings are what we just described. Women can have proptosis and sometimes chemosis. They can also have retrograde cortical venous drainage. So there's traumatic and non-traumatic etiologies for a carotid cavernous fistula. And the non-traumatic is something we have to look out for aneurysm. So an aneurysm in the cavernous ICA can create a high flow carotid cavernous fistula. So here's another example. Again, we're seeing proptosis in the right globe with asymmetric enhancement and enlargement of the right superior and inferior ophthalmic veins along with dilatation of other orbital vessels. We can also nicely see early filling of the right aspect of the cavernous sinus on this arterial timed CTA. Together these findings are consistent with a carotid cavernous fistula. And this patient did have an aneurysm, which is not pictured here. So we have similar findings on an MRA of the head. We can see enlargement of the left superior ophthalmic vein. We can see some arterialized flow signal in the left cavernous sinus. And we're also seeing proptosis of the left globe. Again, these findings are consistent with a carotid cavernous fistula. So here's a 36-year-old male with atypical left neck pain. This is not a true neurovascular emergency. It is something that can be seen in the ER. So he had a pretty normal exam except for this focal area of soft tissue thickening and fat stranding surrounding the left proximal ICA. We can see that there is this enhancement on the axial T1 fat-sat post contrast. So this is actually TIPIC, which was previously known as carotid dynea. So TIPIC stands for transient perivascular inflammation of the carotid artery. And there are four major diagnostic criteria. So first, the patient has to have acute pain overlying the carotid artery. And then we see this eccentric perivascular inflammation on imaging. And there basically cannot be any other explanation on imaging. And by definition, it must improve within 14 days either spontaneously or with the treatment of NSAIDs or other anti-inflammatories. OK, moving on. This is a 32-year-old male who presented to the ER with a sore throat and a neck mass. You can see here there's this large flaconous area. And right in the middle of it, there is this focal filling defect within the left internal jugular vein. We're also seeing a sympathetic retrofringal effusion. You can see there's a long tubular area, again, consistent with thrombosis of the left internal jugular vein. On his CT chest, he had multifocal areas of cavitary lung nodules. So together, this is consistent with a post-pharyngitis venous thrombosis, previously known as Lemire. So commonly can be seen, classically can be seen with Fusobacterium necroforum, but can also be seen with other agents like Staph aureus. Classically, the imaging tried is a pharyngitis. Then we see the neck vein thrombosis and the cavitary pulmonary nodules. It's usually seen in pretty young and healthy patients. This is a very important thing for us to recognize because it has a very high mortality if treated, and if untreated, but even if treated, can have a relatively high mortality as well. And for us, it's important to know that we are often the first to recognize this etiology because they can present in kind of nonspecific ways clinically. So here's just another example of a thrombophlebitis. Again, we're seeing a filling defect within the right internal jugular vein with surrounding fat stranding and a little bit of asymmetric enlargement of the sternocleidomastoid muscle. You have this large filling defect here. This is not quite as bad as the last scan. So a couple more examples. So here we have a non-contrast head CT in a young female. She was presenting with a headache. Remember, this is a non-con. And we can see there's markedly increased density within multiple superficial and deep venous structures, including the superior sagittal sinus, vein of galen, internal cerebral veins, and straight sinus. We're actually also seeing an area of low attenuation in the right parietal lobe, which in the setting of extensive venous thrombosis is concerning for venous ischemia. So CTV confirms the presence of a thrombus in the superior sagittal sinus with a classic empty delta sign. So deep cerebral venous thrombosis has a number of contributing risk factors. It's most commonly seen in females. Here's another classic example where we have hyperdensity. Again, this is a non-contrast head CT. We have extensive hyperdensity in the deep and super structures here. And we're also seeing low attenuation and edema within the bilateral thalami, which is classic for venous ischemia. Cerebral venous sinus thrombosis can be tricky to detect on MR. Here's an example of a thrombosis in the right transverse sinus, where we have T1 and T2 symmetry, decreased flow on phase contrast MRV, and non-opacification on the post-contrast SBGR. Remember, they can have variable findings on all of these sequences depending on the timing of a clot. So it's important to use all of the information available when assessing for cerebral venous sinus thrombosis. That's all I have for today, and I thank you so much for your attention on this brief overview of some emergent do-not-miss neurovascular findings. Hi. My name is Nick Koontz. I'm a neuroradiologist and head and neck imager at Indiana University School of Medicine. And for the next 15 minutes, I'll be talking about upper aerodigestive tract emergencies. I have no financial disclosures, but I would like to thank Tabby Kennedy for the kind invitation to speak. So I'd like to break upper aerodigestive tract emergencies into three broad categories. First up is trauma, then infection, and then sort of this wastebasket other camp. So I'm going to first start off by talking about trauma. So traditionally, when you deal with penetrating neck trauma, the neck has been divided into three distinct zones based upon the entry site for the penetrating trauma. So zone one is defined as between the sternal notch and clavicles up to the level of the cricoid cartilage. Zone two is from the cricoid cartilage all the way up to the angle of the mandible. And zone three is defined from the angle of mandible all the way up to the skull base. So whenever you're dealing with patients who have penetrating trauma to the neck, one of the things to be on the lookout is for pharyngoesophageal penetration. Now fortunately, this is quite rare, estimated about 1% to 7% of penetrating trauma. But it's important that you don't miss this diagnosis because it can be deadly, or even a delayed diagnosis can be deadly because these patients can develop mediastinitis, sepsis, and even death. It's been reported that they have up to a 20% mortality. Now CT angiography is really kind of the standard by which we assess these patients in the front line now. And I think you can effectively use it to exclude pharyngeal and esophageal injury. And you do that by looking at the wound tract. And if it's distant from the esophagus and pharynx, you can effectively exclude it, exclude injury. However, if the wound tract is near either of these structures or if there is emphysema along them, you really need to go on to esophagography and or endoscopy. So here we can see that tract, the ballistics fragments from a gunshot wound going through the mandible, going through the floor of mouth, base of tongue, going through the hyoid bone, and then into the supraglottic larynx and hypopharynx. This patient went on to have a trauma protocol esophagram. Now this is a biphasic study. You give a water-soluble contrast material first. If that's negative, then you can follow with barium sulfate. But it's important that the patient be alert and able to participate in this study because you want to avoid aspiration. You need them to cooperate. CT with oral contrast is absolutely not a substitute here. You really need the resolution of the esophagram. So here's that patient. We again see the ballistics fragments tracking from anterior to posterior, going through the hypopharynx. And sure enough, we have a leak from the hypopharynx. You can also have tracheolaryngeal penetration. Also quite rare. Same incidence, about 1% to 7%. Obviously, these patients can have life-threatening airway compromise. Just like when you're dealing with the esophagus and the pharynx, if the wound tract is coming near the trachea or the larynx or if there's unexpected emphysema adjacent to it, you really need to go on with endoscopy and bronchoscopy. You also, on imaging, want to scrutinize the laryngeal cartilage, especially that cricoid cartilage because that's the only circumferential support ring for the trachea and for the larynx. As we look at the patient here, we can see there's massive subcutaneous and deep space emphysema. Look at the anterior upper trachea. We can see that there is deformity as well as hypotenuation from hematoma. Next up is nasal septal hematoma. We're now moving into our blunt trauma. Patients who have blunt trauma to the face, either with or without nasal bone fractures, can develop nasal septal hematomas. That's because of the rich arterial blood supply of the nasal septum. If these go untreated, it can lead to abscess formation and potentially tissue necrosis. On CT, look for iso- or hyponate thickening, oftentimes, not always, but oftentimes, asymmetrically along one side of the nasal septum, as shown here in this case. Next is dental trauma. This is actually quite common, reported about a 30% lifetime incidence. It runs a full spectrum of sort of stunned, concussed teeth to loose teeth to, frankly, a false teeth, and it may be associated with fracture as well. Clinically, these may be quite apparent, but it's easy to overlook on imaging, especially in complex trauma patients. Those loose teeth can, importantly, be aspirated or ingested, so you want to be on the lookout for that as well. Here's a patient with maxillofacial trauma. You see this parasympathetial displaced fracture right here, denoted by the yellow arrow. Make sure to look at the airway. We can see multiple teeth sitting down on the oropharynx, so always, always, always be checking the airway in your trauma patients. Next is laryngotracheal blunt trauma, most common in the setting of motor vehicle collisions. You can get from strangulation-type injuries as well, and this runs a spectrum. It can involve edema and hematomas, out-and-out lacerations or ruptures, and again, be on the lookout for cartilage fractures or avulsions as well. The obvious complications you want to be looking for would be airway compromise, but these patients can have long-term dysphonia, so it's important to identify this and let the treating physicians know about laryngotracheal injury. So you'll oftentimes encounter this sort of on the frontline modality of either cervical spine CT or a trauma CTA, and that should really prompt you to do a dedicated soft tissue neck CT to get a better look at things. You want to scrutinize these in three planes, in both soft tissue and bone reconstructions, and I think emphysema is a big tip-off here. You always want to be on the lookout for airway patency. It can be compromised either due to external compression or it can be narrowed internally from edema or neurohematoma. So here we can see this patient with massive emphysema, and look how deformed that upper trachea is. It's been crumpled by the blunt trauma. Whenever you're doing your detailed search pattern, you obviously want to look at the soft tissues, things like the AE folds and true vocal folds. You want to look at the airway. You want to really scrutinize the anterior laryngeal elements, such as the thyroid and cricoid cartilages. Here we get the tip-off. We've got overlying emphysema, which is overlying the subjacent, non-displaced thyroid cartilage fracture. You also want to screen the posterior laryngeal elements, like the cricoid cartilage, the arytenoid cartilages, and the cricothyroid joints as well. Next broad topic will be infectious emergencies of the upper air digestive tract. I want to start off by talking about something that we see all the time, and that's dental abscesses. This is sort of the result of bad tooth decay, and that can lead to apical or sometimes even intraalveolar abscesses within the bone stock itself. If those puss out into the surrounding soft tissues, that can form soft tissue abscesses. So depending on where it sort of breaks through and pusses out of the bone, that sort of predicts where the abscess will form. So for instance, if you're dealing with a mandibular tooth, if it pusses out above the myelohyoid line, it tends to form an abscess in the sublingual space. If it's a mandibular tooth and pusses out below the myelohyoid line, it tends to present as an abscess within the submandibular space. You have nodes that are within the submandibular space, so if those take up the infection and eventually separate, that can lead to additional submandibular space abscess. And then as this diagram nicely shows, the molar teeth can puss out into the masticator space, forming a masticator space abscess. So here's an example of a dental abscess. We can see on the coronal bone CT, we have pericalucency of this diseased tooth with a carious amputation. Look on the axial contrast enhanced CT, you can see that we have sort of this low-density collection right here with a little bit of thin enhancement overlying it. This is a nice area to use your spectral CT if that's something you have, or a dual-energy CT. I think you can really see that subperiosteal abscess much better by using sort of those tricks playing off the K-edge of iodine. So I think it helps to improve the constant acuity of dental abscesses. Next topic is Ludwigangina, which is the eponym for a floor-of-mouth infection. Now this can be a rapidly progressive, life-threatening process, resulting in airway compromise. And I think it's best remembered by keeping in mind three S's. S for submandibular space and sublingual space, as well as submental VAC. These patients can have mediastinitis in extreme cases, that's kind of where the angina terminology came with. This is usually due to bad dental infection, but as you can see, there are other forms of infection that can cause this as well. This is a patient who had floor-of-mouth necrotizing fasciitis. You can see phlegmon and gas pockets within the sublingual space. You can also see that phlegmon tracking into the submandibular space bilaterally, and the submental neck with all that straining and cellulitis. And then look and just see how large and thick and edematous the tongue is, resulting in airway compromise. This is a patient who developed a transfacial floor-of-mouth abscess. We see this irregular-shaped rim-enhancing collection involving the sublingual space on the right, sort of tracking up along the undersurface of the tongue. It goes all the way back to the base of the tongue. You can see it pussing out into the submandibular space. And note the really marked enlargement and low density of the oral tongue causing airway compromise. So, I showed you a case here of so-called Lugwig angina that's associated with an abscess. Really, to get an abscess in this setting is fairly uncommon. Whenever you see abscesses like this, they're going to require transcervical drainage. All right, I'm going to talk a little bit about this ongoing, probably never-ending debate of intratonsillar versus peritonsillar abscess. And this is a challenging topic because the terminology's variable. It's, as I said, controversial. I think it's quite confusing. And so, there's a couple schools of thought. There's a very vocal school of thought in which they say that an intratonsillar abscess is when you have pus loculating within the tonsillar parenchyma itself. That kind of makes sense. You can see here, denoted in green. And then, they'll say that peritonsillar abscesses are when you have pus that sort of forms a pus pocket in a potential space separating the deep margin of the palatine tonsil from the subjacent superior constrictor muscle. And so, you can see that potential space right here. And that's what they define as a peritonsillar abscess. And that's fine. There are a lot of experienced head and neck radiologists and a lot of surgeons who use that terminology. But there's also a lot of folks who use a slightly different terminology in which they describe peritonsillar abscesses as when the infection, when the pus, when it separates out into the surrounding soft tissues. So, like this diagram here shows when it gets out into the parapharyngeal and masticator spaces, for instance. Further compounding this is sort of the traditional thought that true peritonsillar abscesses are much more common than intratonsillar abscesses. Although the treatment historically has always kind of been the same with incision and drainage. But some newer thoughts have come out. There's been some single institution case series that have shown that intratonsillar abscesses may be more common than previously thought. They may not require as aggressive of management. But again, we don't have a lot of great data on this. And there's certainly a huge variability in practice patterns. I think the most important take-home point that you can take from me describing this is reach out to your surgeons. Use the lingo that they like to use. Because at the end of the day, as a radiologist, you need to be a good communicator. And I think it's also critically important to report those deep extensions of the infection into the surrounding soft tissues, as well as potential complications. You know, things like septic thrombophlebitis or Lemire syndrome, if you like, to name things after dead people, Rick Wiggins. So, here's an example of what nonsupportive tonsillitis looks like. You see thickened, sort of hyperemic palatine tonsils, this tiger stripe appearance. Maybe that's seen a better effect on this spectral CT. But again, you see that tiger stripe pattern of striated hyperemia. This patient does not have an abscess. This is a patient with an intratonsillar abscess. This was confirmed clinically. This patient has a rim-enhancing, low-density pus pocket entirely within the tonsil. This was actually sort of draining out. They saw pus pouring out of it into the oropharynx. This is a peritonsillar abscess, sort of by that definition of the potential space being involved. You see this rim-enhancing fluid collection. You can see that it's shifting the tonsil intramedially. Another example of where spectral CT or dual-energy CT can be quite helpful, really driving up the conspicuity of this lesion. So, I think it's a helpful tool if you have it to turn it on in these cases. This is sort of the other definition of peritonsillar abscess, I guess the one that I was trained to use and still use with my surgeons, in which you see a rim-enhancing fluid collection sort of going between the palatine tonsil through the parapharyngeal fat and into the masticator space as well. So, again, I'm not sure that there is a defined right or wrong way to do this. Just be consistent and make sure you're doing it that the way that you're referring docs understand and you're all on the same page. That's the most important. Okay, next is epiglottitis. This is a true airway emergency in kids. Now, fortunately, this is extraordinarily rare since the Hib vaccine. These kids would show up with fever, stridor, and a sore throat. And as this diagram nicely shows, you can see a thickened edematous epiglottis and arypiglottic folds. On lateral radiographs, you'll see this thumbprint sign or a thumb sign. On the upright lateral radiographs, this thickened epiglottis as well as this thickened arypiglottic fold. Really, CT is not necessary to make this diagnosis. And sort of the classic and vitally important teaching here is that imaging should never, never delay airway protection in these patients. Now, adults can get something that looks similar to this. It's kind of the adult cousin. It's superglottitis. The majority of these cases are uncomplicated and resolve quickly. Obviously, there are patients who don't do well with this and they have compromised airways. But what you see here is diffuse edema of the entire superglottic larynx. Here, we can see a thickened epiglottis as well as a thickened edematous arypiglottic folds. Oftentimes, this will also involve the lingual and palatine tonsils as well. Be on the lookout for complications of abscess and emphysematous epiglottitis as well. All right, I'm going to move on to the last broad category of other. First up is angioedema. This is a rapid onset of edema. It involves the superficial soft tissues in the upper air that just detract. It's typically diffuse, but it can also be asymmetric and focal. Here, we can see edema within the lip, a swollen tongue, as well as edematous arypiglottic folds thought to be a result of overproduction or failure to inactivate things like histamine. Most commonly, this is associated with ACE inhibitors. And critically, you want to be on the lookout for airway compromise. You can have active extravasation. It's uncommon. Most commonly seen in cancer patients. Obvious risks of aspiration and exsanguination. You look for increasing density within the mucosa or submucosal. Sometimes, you'll see hybrid instability within the lumen of the pharynx as well. Typically, this is treated with topical or packing means, but sometimes, these have to be embolized. Then lastly, ingested foreign bodies. This is most common in children, but it can occur in adults. There are some patient populations where it's more commonly seen. Most of the time, these foreign bodies are going to pass spontaneously. There are some things that are at high risk for either perforation or tissue necrosis, things like button batteries, magnets. And importantly, grill brush bristles don't use wired grill brushes, people. It's very dangerous. All right, so here we can see the patient swallowed a razor blade. It's stuck in the hypopharynx. All right, so in summary, upper air digestive tract, it really covers a lot of territory and it's prone to infection and trauma, as I discussed in this brief talk. I think it's critically important as a radiologist you stick with your search pattern. Always, always, always be on the lookout to clear the airway and imaging should never ever delay airway management. Thank you for your attention. Enjoy the rest of this virtual RSNA. Thanks so much. Greetings, everyone. My name is Alan Butt. I'm from the Mayo Clinic in Jacksonville, Florida. And today I'm going to talk about facial and skull base emergencies. I have no disclosures. I do want to thank the program committee, especially Dr. Tabby Kennedy for inviting me to speak. The objectives of this talk are to develop an approach in evaluating a patient with facial swelling. We're going to review emergency pathology involving the face and the skull base. And we'll discuss the potential complications as it relates to orbital cellulitis, sinusitis, and mastoiditis. Let's first take a look at islet edema. Here are two different patients with different histories and some subtleties in radiologic findings, which are very important. What's the difference between the two? Well, it's the orbital septum. The orbital septum serves as a barrier to infection. It's a fibrous membrane extending from the periosteum of the orbit to the tarsal plates of the eyelids and it can be represented on imaging as a line extending from the anterior globe connecting the orbital rims. The patient on our left has edema and fat straining anterior to the orbital septum here. The patient on our right has edema and fat straining not only anterior to the orbital septum but if you look along the medial aspect there's also fat straining posterior to the orbital septum as well. The first case that I showed you was a case of preceptal cellulitis. The cellulitis is localized anterior to the orbital septum. There are two main causes. One is contiguous spread of infection and the other is direct inoculation from trauma or an insect bite. On imaging you'll see perioral fat straining within the preceptal space. Note that the postseptal space is void of any fat straining in both of these cases here. The good thing about preceptal cellulitis is that serious complications are rare. This is in contradistinction to oral cellulitis where the cellulitis involves the postseptal space. It typically occurs due to spread of infection from the perinasal sinuses. On this top case here you can see that there is fat straining and edema of the eyelid or the preceptal space but there's also extension posteriorly to the postseptal space in a patient with acute sinusitis involving the athmoid air cells. The patient on the bottom has right globe proctosis. You can see that there's edema and fat straining within the preceptal space but if you look carefully there's also extension posteriorly where there's fat straining and again this patient has right perinasal sinus disease. The importance of picking up on this finding is that the risk of complications is high and treatment usually involves hospital admission and IV antibiotics with close monitoring of vision. Typically orbital cellulitis is due to extension of disease involving the ethmoid sinuses and why is that? Well the ethmoid sinuses have a lateral wall called the lamina propricia which is a thin osseous wall fenestrated with neurovascular channels so it's easy for infection to go from the ethmoid air cells into the postseptal space into the orbit. Here you have a patient with extensive left perinasal sinus disease and you can see on the right in the soft tissue windows that there's extension of disease into the post septal orbital space where there's subperiosteal abscess formation. What are some other complications of orbital cellulitis? Well let's take a look at this patient. In this case in the top image on the left you can see that there's clearly right orbital cellulitis but you can also see that there's non-opacification of the right superior ophthalmic vein which is dilated and this is consistent with superior ophthalmic vein thrombosis. Take a look at the normal superior ophthalmic vein on the left which opacifies with contrast. If you look intracranially on the bottom image to your left you can see that the cavernous sinuses do not enhance and therefore this patient also has cavernous sinus thrombosis and if you take a look at the MRI you can see that there's this rim enhancing fluid collection within the medial aspect of the right middle cranial fossa consistent with an intracranial abscess. Now let's move on to sinus disease. Here are three different patients with different types of sinus disease one in particular which you do not want to miss. The first case is a case of acute rhinosinus sinus and it's important to remember that the diagnosis is based on history and clinical evaluation. Acute sinusitis is defined as less than four weeks of brilliant nasal discharge or facial pain pressure and fullness or both. Imaging is very non-specific. You may see an air fluid level as in this case with two weeks of facial pain and a nasal discharge but it's also important to remember that you can see fluid levels in patients that are bedridden or have a history of trauma. Imaging may be obtained if there's clinical suspicion for complications so our job is to look for complications in acute sinusitis. In children and adolescents the frontal sinus is traversed by multiple venous channels and therefore this can be a cause of intracranial spread of disease or spread externally into the soft tissues. The patient on our left has extensive frontal sinus disease but you can see that there's dehiscence of the posterior wall of the frontal sinus with the resulting intracranial abscess formation. The second patient here has extensive frontal sinus disease but there's a defect along the anterior wall of the frontal sinus here and there's extension into the frontal soft tissue scalp with a rim enhancing fluid collection and this is consistent with a POTS puffy tumor or subperiosteal abscess. Here's a patient with extensive sinus disease this time involving the sphenoid sinus as well as the ethmoid sinuses but you can see that there's a defect on the roof of the ethmoid air cells with intracranial air. If you do the MRI you can see that there's a pachymeningeal enhancement so this patient has pachymeningitis but if you look on the sagittal post-contrast images you can also see that there's intracranial abscess formation. The T2 weighted image here demonstrates that there's extensive edema and T2 hyperintensity within the brain parenchyma consistent with cerebritis and I'm showing you these set of images to remind ourselves that it's important to use CT to evaluate for bone destruction and MRI to look for intracranial involvement of disease. Next let's move on to chronic rhinosinusitis. Now this disease the diagnosis is based on history and clinical evaluation but imaging can be used to document inflammation or mucosal disease. Our job is also to look for radiology and complications. Let's take a look at this patient with four-month history of left facial pain. You can see that there's severe and complete mucosal thickening within that left maxillary sinus but you also see that there's hyperostosis of the walls so this is consistent with chronic left maxillary sinusitis. Now we're going to look for radiology. Well if you take a look at the tooth you can see that the left most posterior maxillary tooth has disease and therefore this is the cause of the chronic left maxillary sinusitis. Here are two additional patients with chronic sinusitis. It's important to look for radiology. On your left you can see that the sinusitis is due to the disease involving the right maxillary tooth with a defect within the inferior wall of the right maxillary sinus. On your right you can see that a right maxillary tooth is the culprit here. On the bottom right you can see that the tooth has been removed and there's near complete resolution of disease involving the right maxillary sinus. And finally our last case in this set is a case of angioinvasive fungal sinusitis, a do not miss diagnosis. If you have an immunocompromised or diabetic patient you must look for this entity. Imaging findings can be very very subtle. In this patient there's fat stranding involving the right pterygopalatine fossa, pterygomaxillary fissure, and right retromaxillary region. The left side is clear. Two days later you can see that there's persistent fat stranding and infiltration of that right pterygopalatine fossa. This is an ENT emergency so as soon as you make the diagnosis call your ENT surgeon for treatment. Here's a patient who has uncontrolled diabetes that presents with facial swelling. On initial examination on the top left you can see that there's subtle soft tissue infiltrative changes at the level of the right nasolacrimal duct on the coronal. If you're very astute you can see that there's irregularity of the mucosa along the middle and the inferior turbinates. This is soft mucosa and debris from the angioinvasive fungal sinusitis. Unfortunately this was not picked up on the initial exam. The patient presents several days later and had to be debrided. On this right MRI image there's extensive post-surgical changes involving the paranasal sinuses but now take a look. There's no enhancement of the superior medial and inferior rectus muscles of that right orbit. The disease has extended into into the right orbit unfortunately. If you look intracranially there's extensive cerebritis and unfortunately this patient passed away. And this case really highlights the the fact that you must be looking for subtle clues. If you see any suggestion that there may be invasive fungal sinusitis call the ENT for direct visualization. In the case of sinus disease when you have acute sinusitis you want to look for complications. In chronic sinusitis you're going to look for radiology and if you have a case of invasive fungal sinusitis remember to look for your ENT. Next let's move on to mastoid air cell fluid. When you see fluid within the mastoid air cells what does this mean? The first case in this set is a case of acute mastoiditis. It's the most common complication of acute otitis media. It's a mucoperiosteal disease. It's often referred to as otomastoiditis. It's a clinical diagnosis. The patient may have tenderness, swelling, or erythema over the affected side of the mastoid bone. Imaging is very nonspecific. The patient may see partial or complete pacification of the mastoid air cells. Now coalescing mastoiditis is what we're worried about. The mucoperiosteal disease now involves the bone. It's a radiologic diagnosis where there's infiltration and destruction of the bone and complications are much more likely. Here is a patient on your right coalescing mastoiditis where there's reabsorption of the septa of the mastoid air cells. There's also fat stranding and thickening of the soft tissues surrounding the left mastoid. Here's another patient with right-sided coalescing mastoiditis. There's absorption of the septa of the mastoid air cells. There's also destruction and dehiscence of the sigmoid plate. Here's a patient that presents with right face swelling. When you take a look initially at the bone windows there's clearly coalescing mastoiditis. There's destruction of the bone along the anterior aspect. There's also petrous apicitis which we'll look at in detail a little bit later. The soft tissue windows demonstrate a rim-enhancing fluid collection extending into the soft tissue of the right face. This is consistent with an abscess. When you look intracranially there is pachymeningeal enhancement. The patient also has pachymeningitis. Remember to look both extracranially and intracranially when you see coalescing mastoiditis. Here's a patient that presents with otorrhea and face pain. Now initial glance you can see that there's fluid within the right mastoid air cells here. There's fluid within the middle ear cavity as well. But you can also see anterior medially that there's destruction of bone involving the right petrous apex. This is a case of petrous apicitis where there's spread of middle ear or mastoid air cell infection through venous channels involving the petrous apex. Most commonly patients present with otorrhea. Sometimes you can see this triad of petrous apicitis, cranial nerve 6 palsy, retroorbital or facial pain, termed granodeigo syndrome. On imaging you'll see destruction of the bone like you see in this case involving the petrous apex here. You'll see fluid within the middle ear and mastoid air cells. So once you have petrous apicitis you're going to look for complications. Look for abscess and venous sinus thrombosis. This patient unfortunately also had sigmoid sinus thrombosis on the right which extended extra cranially to involve the right internal jugular vein. No normal opacification of the left sigmoid sinus and the internal jugular vein on the left. Here's a patient with right posterior neck pain and fever that clearly had coalescing mastoiditis on the right side but if you look carefully there's also abscess along the mastoid tip and along the posterior belly. The digastric muscle consists of the basal abscess. The patient also had intracranial abscess formation involving both the infratentorial and supratentorial compartments and if you look closely there are foci of non-enhancement within the sinuses consistent with non-occlusive thrombus. Fractures of the temporal bone can also be a cause of fluid in the mastoid air cells. Now fractures were conventionally classified as either transverse where the fracture occurred perpendicular to the long axis of the temporal bone or longitudinal where the fracture occurred parallel to the long axis. Now in reality what ends up happening is most fractures are very complex where there's fractures occurring in multiple planes. Now what we want to do is describe fractures as it relates to patient prognosis and that's where otocapsule violating versus sparing comes into play. Patients with otocapsule violating fractures are more likely to have hearing loss, facial paralysis, and CSF leak. Here's a patient with right temporal bone fracture. If you look carefully there's a fracture violating the otocapsule here on this right image with associated pneumolabyrinth. In conclusion we looked at three sets of patients with some imaging findings that may be subtle for diagnosis. You want to remember that you want to catch these diagnoses before complications arise. And with that I thank you for your attention. Please feel free to email me if there are any questions. Hello my name is Lubda Shah. I'm from the University of Utah and we will be discussing non-traumatic spine emergencies. I have no disclosures. In this talk we will develop a differential diagnosis based on the spinal compartment involved in the imaging features of the lesion. We will review the complementary role of different imaging modalities when evaluating spine pathologies and we will see how in certain scenarios the supercentorial findings can actually help develop a differential diagnosis when evaluating spine pathology. There are various mnemonics you can use when coming up with a differential diagnosis based on the category of disease such as vascular or infectious inflammatory, neoplastic for instance. You can also use the location. In the spine we think about extradural, intradural, extramedullary or intramedullary. You can use the normal anatomic structures in the specific spinal compartments to help come up with the differential diagnosis. For example is it a lesion that's arising from the osseous vertebral bodies? Various imaging clues can help you figure out whether a lesion is in the intradural, extramedullary space. These lesions push the cord away. Intradural extramedullary lesions have a sharp border between the mass and the CSF or contrast in the case of a myelogram. There is widening of the ipsilateral subarachnoid space with intradural extramedullary lesions. Intramedullary lesions, so lesions involving the substance of the cord, may cause cord expansion. There may be reactive edema as in this intramedullary neoplasm. Let's jump into our first clinical scenario. A 40-year-old male with acute low back pain, lower extremity weakness, and incontinence after picking up boxes. The request says rule out cauda equina syndrome. So what is cauda equina syndrome? It's a constellation of symptoms including low back pain, sciatica, saddle anesthesia, there may be bowel and bladder dysfunction. Various etiologies can cause cauda equina syndrome. One very frequently encountered scenario is a disc herniation. In another patient presenting with cauda equina syndrome, the sagittal volumetric T2 weighted sequence and axial T2 weighted sequence demonstrate a disc herniation which severely narrows the fecal sac. At our institution we found a 3D weighted sequence very sensitive in detecting causes of cauda equina syndrome. The radiologist added additional sequences such as contrast as needed. Others have found that CT effacement of greater than 50% also predicts significant spinal canal stenosis on MRI. Other etiologies to consider in the setting of cauda equina syndrome, especially when the patient has red flags, are pathologic fracture. You can see extrinsic compression due to not only retropulsion of bone but also ventral epidural soft tissue. There is leptomeningeal carcinomatosis involving the interdural extramedullary space that can also result in clinical presentation of cauda equina syndrome. Various rare causes of cauda equina syndrome may be encountered. For example, this 45 year old male had progressive lower back pain and lower extremity weakness. This was because of compression myelopathy due to engorged epidural venous plexus, and that was secondary to thrombosis of his IVC and its branch vessels. Interdural hemorrhage, either from vascular malformation or an LP when a patient is coagulopathic, can result in interdural hemorrhage and this patient may present with cauda equina syndrome type symptoms, secondary to irritation of the nerve root. On to our next non-traumatic spine emergency. This 15 year old female presented with acute back pain and paraplegia after abrupt back extension. The yellow arrows point to intramedullary T2 hyperintensity. Closer look, you can see that the hyperintensity involves predominantly the gray matter. It extends along the length of the thoracic cord. After contrast, there is some mild, if any, patchy enhancement in the distal cord. This is an example of surface myelopathy, a long segment myelitis in which patients present with back pain, paresthesias, and paraparesis. The outcome is quite variable with some patients recovering while others facing devastating long-term deficits. The etiology is unknown but felt to be an arterial insult, either due to avulsion of perforating vessels or vasospasm of the anterior spinal artery, or transient ischemia in areas of borderline perforation as a result of prolonged hyperextension. On imaging, you see intramedullary T2 hyperintensity along multiple vertebral segments. In the acute setting, there may be mild cord expansion due to edema. There may be breakdown of the blood cord barrier with enhancement as seen on the right image. While surface myelopathy is not common, cord ischemia is actually a cause of 6% of all acute myelopathies with atheromatosis being the most common cause. The classic appearance is T2 hyperintensity in the ventral cord, particularly involving the anterior horns. This is because the anterior spinal artery supplies the anterior two-thirds of the cord. In this case, there was embolization of atherosclerotic plaque from this descending aorta. It's important to keep in mind that the timing can also affect the imaging appearance. So earlier in ischemia, you may see only anterior horn intramedullary T2 hyperintensity. In later stages, you may see the entire cross-section involved. Often, MRI appearance is mixed. Here is a classic case of aortic aneurysm dissection with ischemia to the lower thoracic cord. You can see some patchy enhancement, edema, and mild cord expansion. Here is a case of a less classic presentation. This patient was just snow shoveling and developed acute onset of low back pain as well as extremity weakness and paresthesias. On imaging, there was intramedullary T2 hyperintensity, predominantly involving the gray matter. The diffusion-weighted sequences showed restricted diffusion. The etiology of this cord infarction was thought to be due to embolism of a small piece of fibrocartilaginous nucleus pulposus, which gains access through a vascularized disc. Often, the clinical presentation can be vague, and the imaging appearance of intramedullary T2 hyperintensity can be very nonspecific. Additional imaging clues such as vertebral body infarction can be helpful. In this post-contrast T1-weighted image, you see lack of enhancement in a section of the vertebral body supplied by the segmental artery. This leads you towards the cord abnormality being a cord infarction. Moving on to our next case, this 28-year-old male presented with stroke-like right-sided symptoms, and he had a CTA head and neck. The CTA brain was negative. On the CTA neck, we see this vascular nidus in the ventral cord. On MRI, there is T2 hyperintensity in the region of that vascular lesion, with cord expansion and edema. The post-contrast images demonstrate enhancement in the area of that vascular malformation seen on the CTA neck. Spinal vascular malformations can be very difficult to understand, but it's easy to categorize them into four different types. The type 1 most common type is the dorsal arteriovenous fistula that presents with the venous hypertension and kind of progressive lower extremity weakness. The type 2, the intramedullary arteriovenous malformation of which this case is an example, the type 3 congenital metameric AVM, and the type 4 perimedullary fistula. Our case is an example of an intramedullary arteriovenous malformation. We saw the nidus on the CTA. These are typically high-flow vascular malformations supplied by the anterior posterior spinal arteries. There's drainage into the coronal venous plexus and then into the extradural space. They tend to be in the cervical and upper thoracic spine. A large proportion of these have an aneurysm associated with them. Here is the catheter angiogram of that case demonstrating the tightly compact arterial vessels. These tend to be younger patients with acute neurologic decline presenting with subarachnoid or parenchymal hemorrhage. Very importantly, these often rebleed 10% within the first month and 40% within the first year. Our next case is a 66-year-old female that presented acutely with low back pain. Her history was very helpful in that she was super therapeutic on Coumadin. The spinal MR demonstrates a heterogeneously T2 hypo-intense T1 iso-intense collection in the spine. The axials are really helpful to delineate that this is epidural in location. It's displacing the fecal sac anterolaterally. This was an example of spontaneous epidural hematoma hematoma most often in the setting of anticoagulation. These spontaneous epidural hematomas most often occur in the cervical-thoracic junction and span over 2-4 vertebral levels. The symptoms depend on the degree of compression of the intrathecal contents. This is another example of a spontaneous epidural hematoma in the dorsal fecal sac. You can see it's a little heterogeneous on T1 and T2 weighted images. The contrast images can be quite confusing because hematomas can demonstrate peripheral enhancement. And this leads us to a very confusing case that caused me much consternation. This 65-year-old female presented with one month of back pain and no systemic symptoms. So you can see the STIR hyper-intense, a little bit hyper-intense T2 collection in the upper thoracic spine. Contrast was given. You can see peripheral enhancement. We did diffusion in imaging. You can see restricted diffusion within this collection. This led us to consider that this might be an abscess, even though she did not have systemic symptoms. Axial T2 weighted images demonstrate intramedullary T2 hyper-intensity in the right lateral cord, which may be due to reactive edema or ischemia from compression. Spontaneous epidural abscesses, often due to hematogenous spread risk factors, include immunosuppression. And that really should make you think twice when a patient has diabetes or chronic renal failure. We often don't put that in that category, but it's important to consider those as immunosuppressed states. And our classic IV drug abusers and alcoholics also have a risk of developing spontaneous epidural abscesses. Staph aureus is a common bug. Spontaneous epidural abscess can be very challenging to diagnose. Clinically, they just present with some back pain. Only a third of them may have fever. Not all of them have elevated inflammatory markers. On imaging, you'll see a dorsal fluid collection. If you give contrast, it will show peripheral enhancement. And while you want to consider epidural abscess, keep in mind that that spontaneous epidural hematoma that I showed earlier can also show peripheral enhancement. You can look to additional clues on imaging. On this example of another case, we have this peripherally enhancing collection. This patient really didn't have any history. He went to a chiropractor and then developed pain after that. So is it traumatic? But what is really helpful is to look at the intraspinous enhancement as well as the disc and vertebral body enhancement. That makes you think, well, maybe this source is hematogenous with the classic discitis osteomyelitis being involved. Look to the parasagittal images when trying to determine whether an epidural collection is infected. There may be septic arthritis with involvement of the retrodural space as well as the intraspinous space. I wanted to share this last case of a non-traumatic emergency because the spine is the etiology for this patient's problem. She had profound positional headaches, could not sit up, and she has all the classic imaging features of spontaneous intracranial hypotension, of a subdural effusion, brain stem sagging, and a filling defect in the superior sagittal sinus due to dural venous sinus thrombosis. CT myelogram revealed that she had a meningeal tear in her lower thoracic spine. Spontaneous intracranial hypotension is often due to meningeal cysts or tears of these cysts, tear of the dura due to osteophytic spur, or there may be a CSF venous fissure. This patient also had a rare complication of intracranial hypotension which is dural venous thrombosis. You can see T1 hyperintensity in the superior sagittal sinus. On the post-contrast, there is a filling defect not only within the superior sagittal sinus but also a cortical vein and this is thought to be either due to slow flow or wall distortion leading to propensity of thrombus or increased blood viscosity. We've gone over various etiologies of non-traumatic spinal emergencies. Cardioacuina syndrome can be caused by various etiologies, a common one being disc pathology. It's important to incorporate clinical information as well as imaging findings in the diagnosis of cortischemia. Advanced techniques such as diffusion-weighted imaging can be helpful. Diffusion imaging can also help tease out spinal infection versus mimics such as a hematoma. And remember that the spine may be the etiology of a non-traumatic brain presentation such as the spontaneous intracranial hypotension that was presented. Thank you very much. I appreciate your time.

neurovascular emergencies

radiological findings

emergency settings

imaging techniques

large vessel occlusions

carotid cavernous fistulas

spinal emergencies

advanced imaging

patient outcomes

emergency clinicians