Good morning everybody. It's my pleasure to welcome you here at this very first emerging radiology refresher course at this 109th edition of the RSNA. And this is session S1 CER 01 on imaging in neurotrauma. My name is Koen Radnibur. My friends call me Hans, so you can call me Hans. No problem. I'm an emerging radiologist in the University Hospital of Brussels. We are affiliated with the Dutch-speaking Free University of Brussels in Belgium. So this morning we gathered three talks on this topic of this session. It's an essential session. Dr. Div Yakunda will cover skull-based trauma. Dr. Carlotta Andreu Arraza will talk about traumatic emergencies of the soft tiffus of the neck. And I will start the session with a lecture on the essentials of traumatic brain injury. So again, thank you also to the organization for inviting us. My lecture will be about traumatic brain injury, brain, blood, and bones. So we talk about, I do a short introduction and a short review of the primary traumatic brain injuries. We talk about extra and interaxial hemorrhage and tips for a primary review. In the United States, we have about 1.5 million Americans who survive a traumatic brain injury. It leads to about 223,000 hospitalizations a year and about 3% mortality. And you can imagine this creates a high general and economic burden on patients, families, and society. The definition of traumatic brain injury is an evolving process with biochemical changes that may result in progression of primary lesions or eventually lead to secondary injury. It can be part of an isolated trauma or part of a polytrauma, as you can imagine. And of course, you can have blunt or penetrating trauma. The primary neurological damage is actually the physical destruction of tissue that occurs at the moment of the impact. So the moment that the brain hits the skull gives you this primary neurological damage. Often we see this as hemorrhage in the extra or interaxial space, can lead to brainstem injury or CSF leaks. This primary neurological damage can go further into secondary neurological damage, worsening of the primary neurological damage, and it's due to multiple mechanisms. So you can have a worsening of the hemorrhage. So during the primary damage, there's a rupture of the microfasciculature. This creates local hemorrhage. It can go on. But you also have the crush of your brain cells leading to ischemia, so cell death. You get cerebral edema, ischemia, and this can eventually lead to a higher pressure in the skull and to herniation. What's our role for imaging? Detect, of course, the treatable lesions before secondary neurological damage occurs. So we have to be very careful in looking for these. We do some triage. We can do prognostication. There's more on MRI. We don't go into this topic. And we do follow-up, of course. What do we use? In the primary setting, we use CT scan. We know why, because it's quick, it's available. A few condom indications, so patients have to be able to lie flat. ICU patients, so the intensive care patients, we can easily follow them up. And we use it in the super acute follow-up phase. We use MRI because it has a higher sensitivity and specificity. Mainly we use it when we have normal CT and unexplainable symptoms. We use it in pediatrics, mainly in the follow-up, early phase, long-time follow-up of adult patients. We use, of course, specific sequence for this. But you have the safety constraints, especially patients coming in with a lot of materials around them, or in the ICU, or they are not stable enough to get into the MRI. So I will do a short review of the primary somatic brain injury, the extra and interaxial hemorrhage, and tips for primary review. So as I said, we'll have hemorrhage in the extra axial space or the interaxial space, the extra axial space. We talk about the epidural space, the subdural space, subacular spaces, which are closely related to the interventricular space. We can have CSF leaks. And interaxial is the pancremic contusion, intercerebral hematoma, and the traumatic axonal injury, and of course, brainstem injuries. So the epidural space is a space lying under the skull bone, above the dura mater. This is the top space here. We can move it here. These hematomas often happen under a fracture. So in 91% of the case, we'll find a fracture line. These are often arterial ruptures. The middle meninsul arteria might be ruptured, or branches of this. And they don't cross shooter lines normally. So normally, it can happen. So this is a typical epidural hematoma, a very clear one from textbooks. It's a convex, lens-shaped hematoma. And what has to be described, they can be very small, but if you see a swirl sign, so this is hyperdensities in this hyperdense clot, this is a sign of active exorcization. It's something you have to mention. So mention this in your report. This is a sign for neurosurgeons to go further, quicker after terpenation. And here's the fracture line. They can be venous. So if you find them in the posterior fossa, the middle cranial fossa, or paracetatol, like in this case, this is probably a venous epidural hematoma. They are closely related to the venous sinuses. And in this case, here's the fracture. Sometimes it's very difficult to find the fractures in this area. As you'll always suggest, to create some VR images, volume rendering. So in this case, at the right side, we had a fracture at the left. These are all smooth suture lines. In this case, here, you see the left side, this impression fracture. It's much easier sometimes to detect these. The septal hemorrhage, they happen under the menial hyaluronid matter, on top of the arachnid matter. And they are often venous, because they have this rupture of bridging veins. They tend to be concave, cross the sutures. So like here, frontal parietal extension, they tend to extend over the tentorium and along the phalx. So this is one big space, the septal space, and you can find all these hematomas here. Always check your midline. Now, if you have a trauma, or actually every brain case, you check your midline. Sometimes it's very difficult to find what's going on. If you draw the midline, you see here a slight deviation to the right, and you have the window level. And then you see this septal hematoma. So always check your midline, always window level. Sometimes it's very difficult to find these hematomas, but you often get a clue where's the impact on the patient. So we have here the impact on the patient, orbital left, then you know where's the contracrucite. The contracrucite is on the other side. And there's a density here, which in the actual plane is quite difficult to sometimes detect these hematomas. So always check your setitals. In the setital plane, you will see this thickening on top of the tentorium. Now, normally it's as slim as this. So this is a subdural hematoma. Also along the phalx, and also along the midline, you can see here a slight deviation to the left. Also along the phalx, here we see clearly that there's a subdural hematoma on top of the vertex, so it's an impact higher up. In the actual plane, there is a density here. If you're too quick, you might miss it, but always check your coronal. So please always check your coronal plane, setital planes, important. We move on to the subacnal hemorrhages. They happen under the arachnid matter, on top of the pia matter, which is actually the last layer above your brain tissue. You can find them in 40% of the moderate to traumatic brain injury, and it's the most common isolated finding in mild traumatic brain injury. They tend to be curvilinear hyperdensities. You find them in the cortical sulci, the sylvin fissures, the basal cisterns, and they are closely related to traumatic brain axonal injury, traumatic axonal injury. We'll come back to this later. Of course, this is a very clear case of a subacnal hemorrhage. You see blood everywhere, but you have to be careful if you have a case like this. Here you see the impact on the head, the subclinical hematoma, a small hemorrhage here in the pre-brontine cistern, a small hemorrhage here, powerful sign, and sometimes this is the only sign of hemorrhage here under the vertex in the sulci. You have to look for it. Interventricular hemorrhages, they have quite the same pathophysiology. It overlaps the subacnal hemorrhage because there's a continuum between the subacnal space and the ventricle system as the cerebrospinal fluid. You can actually find them, it depends on literature, between 3% to 35% of the traumatic brain injuries. It's due to tearing of the subacnal veins, and always look in the postural horns, there you'll find them. As also here, again, like the subacnal hemorrhages, they're closely related to traumatic axonal injuries. In this case, it's pretty clear at the left side, this is an interventricular hemorrhage after trauma, but in this case, it's sometimes the only sign you have of hemorrhage, so always in a trauma, check the postural horns of your lateral ventricles, there you'll find these small hemorrhages. So we covered the extra-axial spaces and hemorrhages, so we move on to intra-axial. We talk about pancremal contusion and pancremal hematoma, and the difference is, if you have a contusion, it's actually the brain impacts the skull face and you have brain metadamage, so the brain is really hitting the skull, you get cell destruction, you get microvascular hemorrhages. A hematoma is something in the pancrime of your brain, and it's bleeding, it's a mass-creating problem, and we'll come back to this later. Always check your cu- and contracrucite, and you'll find them in the temporal space, the frontal space, often, but there's a very rough surface on the skull base, so here you have the cribrate plate, there you can find them, or over the supraorbital regions. Anterior or posterior in the temporal fossa depends, of course, if you're hit on the back of your skull, you'll find them anteriorly, if you hit the floor on the front, you find them posteriorly, we have to check for it, and over the preterous bones. Again, this might be very difficult to find in the actual planes, here we have a patient, again, hit a subsequential hematoma on the left of the vertex, and in the actual plane, you see this. Sometimes really tiny to see, so always check your sagittal planes here, because you have a clear sight of your frontal, your cribrate plate, of your supraorbital regions, of your temporal regions, where you find these hemorrhages. Intercerebral hematoma, this is a wide matter problem. It happens due to arterial or venous hemorrhage in the prime time of the brain, so this is really a mass, so space-occupying lesion. Due to rotational strain or penetrating trauma, I don't, I'm living in Belgium, we don't have so much penetrating trauma as you have here, so I'm not going to show it, but you can imagine that all of you who are working in the emergency wards here, that you can have a brain intercerebral hematoma due to a penetrating trauma. Often in the frontal, temporal, and basal ganglia regions, so here we have a patient, again, fall on the head, here's the fracture, there's a big hematoma, with a, sorry, here is a subdural hematoma, always check your contracrucite, there's a small lesion this side, temporal left. If you find a large intercerebral hematoma, I advise always to do a CTA. Why? We are looking for the spot sign, so this is a big hematoma, and this is a CTA, you see this excavation, this is the spot sign, this is very important news for your neurosurgeons for their therapy planning. Some words on traumatic axonal injury, this is due to deceleration or rotational injury, former term was diffuse axonal injury, this term is abandoned actually, it's now traumatic axonal injury. It creates scattered small white metal lesions actually on the borders between the gray matter and the white matter where you have this shearing because of the difference in weight of your gray matter and your white matter, and you get actually shearing of the axons in this interface because of the deceleration or rotational energies. They can happen with or without hemorrhagic components, only 25% of these lesions will show hemorrhage, and often they are bilateral, and they can be a result of primary or secondary axotomy. The primary axotomy is, of course, the wheel shearing and your break of your axons. This creates, of course, also due to the trauma, a cascade of cytotoxins, and they can create apoptosis of your axons. So as said, they can be hemorrhagic, so we can see them at CT, but it's only the tip of the iceberg. It's an underestimation at CT, like in this case, you see here small dots, sorry, you see here the small dots, and two small dots here, so small hemorrhages. In these cases, you have to go to MRI. I always advise to go for a susceptibility-weighted imaging and a diffusion-weighted imaging. This is the same patient. We see these hemorrhages here, frontal right, so this is the susceptibility-weighted imaging on the left, showing hemocytogen deposits, and if you take a look at this diffusion-weighted imaging, P1000, you see these hyperintensities of ischemia. This is what we are looking for. This is actually the full exposure of the traumatic axonal injury. So what I'd like you to take to your work for primary brain injury is, if you see an epidural hematoma, check for the swirl sign. This is really important information for your neurosurgeon. For subdural hematomas, check the coronals and testicles, because this is a continuum, where you go over the tentorium and along the phalx. It's much easier to detect, so always check these reconstructions. For subdural hematomas, always check the midline, always mind the left of your images, so you can't miss, you won't be able to miss the hemorrhages. For subrectal hemorrhages, they are closely related to traumatic axonal injury, so think about it. If you have a story which fits in traumatic axonal injury, for example, a patient who had been conscious for a while after the trauma, do an MRI. For intrafascular hemorrhage, think of the postural horns. If you have a trauma, always check the postural horns. That's sometimes the only hemorrhage you will find. For pancreas contusion, check the saccitals, for your cribral plate, for your temporal fossa, for your superorbital regions. Intercerebral, do a CTA and find the spot sign. This is, again, really important information for neurosurgeons. And concerning traumatic axonal injury, I advise to go to an MRI and always do a diffusion-weighted imaging and susceptibility imaging. So I thank you very much for your attention. Our next speaker will be Dr. Divya Kumra. She's a tele-neuro-radiologist and assistant professor at the Cooper University Hospital in Camden, and she will tell us about skull-based trauma. Thank you for that wonderful talk, Hans. So I'll be diving a little bit deeper into this whole traumatic brain injury topic with a focus on skull-based trauma. So the objectives of my talk are to briefly review some relevant skull-based anatomy as it's relevant to trauma. We'll try to build a segmental approach to understanding skull-based fractures, and most importantly, we'll discuss complications based on location of the fractures. So unlike elsewhere in our body, the surgeons are trying to fix the fracture. And in the skull base, they're not trying to fix the fracture. They're trying to figure out what to do with the complications of the skull-based fractures. So the skull base, because it's in between the facial bones and the calvarium, it absorbs a lot of force from trauma, especially very high-energy blunt force trauma. And it's been reported in about 4 to 16 percent of all head injuries, and because it houses critical neurovascular structures, it has a significant morbidity associated with it. And like I said, high-energy blunt force trauma is the leading cause, with motor vehicle accidents being the leading cause of these injuries, but falls and assaults can also lead to these fractures. And because of that, it's often associated with significant traumatic brain injury, which we just heard about. So unlike a head CT or a cervical spine CT that we get for in the setting of trauma, we don't have a skull-based CT that we get. And so we're really relying on our head CT images for some clues to skull-based trauma, and that includes sinus opacification. When you see mastoid opacification, middle ear opacification, in the setting of trauma, especially if you know that it's high-energy blunt force trauma, and you see that this is high-density material with an air-fluid level, it's highly likely that this is hemorrhage. And so you want to look closely at your thin, sub-millimeter-cut axial CT images of your head CT to look for those skull-based fractures, because really, the volume-rendered images aren't very helpful in this situation. Some other clues to skull-based trauma include orbital emphysema, as you see in this case, with an associated superior orbital wall fracture and a contralateral orbital emphysema. And here we see very subtle pneumocephalus associated with a fracture going through the mastoid air cells. So some complications of skull-based trauma, obviously intracranial hemorrhage that has been extensively talked about, and vascular injury that will be talked about. And with skull-based trauma, it's important to note that once you see the skull-based fracture, it significantly increases the chance of vascular injury. So when you see these skull-based fractures, be sure to recommend a CT angiogram of the head and neck if the trauma surgeons don't already do it. At my institution, they just go ahead and do it themselves. And then we're also concerned about cranial nerve injuries and CSF leaks, which may or may not lead to intracranial infection. For the sake of time, I'll be focusing on the last two topics. So the skull base itself is going to, we essentially draw a line from just above the frontal sinus to the groove of the transverse sinus, and that encompasses the skull base that we will be talking about. And as you can see, it has a lot of foramina and neurovascular channels that, when injured, can lead to cranial nerve injuries and vascular injuries. The skull base itself is comprised of paired frontal bones, paired temporal bones, an unpaired ethmoid bone, an unpaired sphenoid bone, and an unpaired occipital bone. And together, this makes, this comprises the skull base. And classically, we talk about the skull base as the anterior, middle, and posterior skull base, but I really won't be talking about that in that manner, because I think talking about it in a segmental approach in this way, where we talk about frontal ethmoidal fractures, temporal bone fractures, transphenoidal fractures, occipital and clival fractures is helpful. Temporal bone fractures are going to be by far the most common, followed by orbital roof fractures, sphenoid bone fractures, occipital and ethmoid fractures. And that 1% of that chart makes up the clival fractures, which is important to note, because it can be associated with vertebrobasilar injuries and brainstem injuries. So the frontal ethmoidal fractures, again, the frontal bone that comprises the frontal sinus, the orbital roof, and the ethmoid bone, and the complications that come about it are associated with what part of that area is involved. So if you have orbital part of the frontal bone, you can often see orbital injuries along with intracranial hemorrhage. If you have ethmoid roof injuries, you can lead to CSF leaks. If you have posterior table of the frontal sinus involvement, you can, again, lead to CSF leaks, and then cerviform plate involvement can lead to injury to the olfactory system. So CSF leak and meningoencephaloceles. These are encountered in about a third of the patients with skull base fractures and 2% of all head injuries, but this is most common with frontal basal fractures, and that's why I'll be talking about it here. And that's due to the tight attachment of the dura with the frontal basal region. And this increases the risk of meningitis, and while 85% of them can heal nonoperatively, about 15% of them do need surgical management, and that's what I'll be focusing on. And we really can't rely on clinical science in the setting of trauma patients that have such significant blunt force trauma, because they're often uptunded. And they can't, just because you can't elicit a CSF otorhinorrhea does not exclude a CSF leak in these patients. So this is where we become important. This was a homeless man who had fallen off his bike and came in a week after the injury, had significant pneumocephalus on the right side, had a pneumocephalus on the left side. And when you see these skull base fractures that are over a centimeter, these are likely to be needing surgical management. And so you want to point those out. If you see a skull base fracture, yes, point it out. But when you see them where they have such a large defect, and when you see soft tissue going through the defect, that can indicate that it's a meningoencephalus seal that will need surgical management and repair. When you see these fracture fragments perpendicular to the dura, or if it's a comminuted skull base fracture, again, much higher risk of complications. So important to point that out. So what do you want to remember about frontal ethmoidal fractures? Is the posterior table of the frontal sinus involved? Is the ethmoid roof involved? Is the cribriform plate involved for its associated complications? So next we'll talk about temporal bone fractures. The temporal bone has these different segments. And so, again, when we want to point out which part of the temporal bone is involved, it's helpful to note that is it involving the petrous bone, the mastoid bone, or the squamosal segment, because really the squamosal temporal bone doesn't really have the same complications as a petrous temporal bone fracture. So, again, clues include pneumocephalus, error in the TMJ, EAC opacification. And so the complications are associated with what's injured. So you can have sensorineural hearing loss when there's cochlear involvement, conductive hearing loss with ossicular injuries, vestibular dysfunction with vestibular injuries, facial nerve paralysis, and CSF leaks. So the same principles of CSF leaks that I talked with frontal ethmoidal fractures apply here. I won't be talking too much more about that. Typically, when we talk about temporal bone fractures, we discuss them as if they're longitudinal, if they're parallel to the petrous temporal bone, or transverse if they're perpendicular. But you probably already know that we really don't talk about temporal bone fractures limited to just the direction of the fracture. Talking about them if and saying if they're petrous versus non-petrous, if they're otic capsule violating versus otic capsule sparing is a much better predictor of complications. And so the surgeons have moved on to talk about these fractures in this manner. So what is the otic capsule? It's the densest part of our body when we're born. And this is a newborn head CT. And you see that dense bone housing our inner ear structures, including the cochlea, the vestibule, and the semicircular canals. And these are only seen in about 2% to 6% of temporal bone fractures. So while we have this classification system, it's rare that you will actually see these. And these are a result of significant blunt force trauma. And they have a much higher risk of the complications that I just talked about. And so this is an example of an otic capsule violating fracture. It's going through the internal auditory canal and the cochlea and the facial nerve canal. And this patient had sensorineural hearing loss and a facial nerve paralysis. And this is in comparison to the contralateral side. So when we talk about a secular injury, we all know about the ice cream cone sign with the head of the malleus and the body of the incus. And this is an example. And this is what it should normally look like. And this is an example of a subtle incudomalleal subluxation, where there's joint space widening and there's air within the joint. I think we're all more aware of the incudomalleal dislocations and less so aware of the incudostapedial dislocations. You know, this is a MIP reconstruction of through our temporal bone. And it's showing that lenticular process in the stapes. And this is a pretty subtle subluxation of that incudostapedial joint, which is more posteriorly located relative to the stapes. And so this is an example of an incudostapedial joint dislocation, also important to look for. And this was a very severe trauma case where you have a temporal bone fracture, otic capsule sparing, and we completely lose that normal construct of our ossicular chain. When we talk about facial nerve anatomy, right, there's different segments of the facial nerve. But I really want you to focus on the segment that's important when it comes to trauma, which is the geniculate ganglia in here. Because a perigeniculate region of that facial nerve is the most common site of injury for these temporal bone trauma cases. And these are often going to be Oda capsule-sparing fractures and not violating fractures, even though there is a much higher risk of complication of facial nerve paralysis. So perigeniculate region. And when you see that these fracture fragments are this widely displaced, it's important to point that out, too, because it's a poor prognostic indicator of regrowth of that facial nerve and recovery of that facial nerve. So what to remember about temporal bone trauma. What is the general direction and segment of the temporal bone that's involved? What is the status of the Oda capsule? Are the ossicles and joints intact? Is there a defect involving the tegmen, which can lead to a CSF leak? And is the fracture traversing the facial nerve canal? So when we let's move on to transphenoidal fractures, when we talk about transphenoidal fractures, the lesser wing and the greater wing and the body of the sphenoid essentially make up that sphenoid bone. And this anterior clinoid process becomes important when we look at important anatomical structures. This is not a lecture on cranial nerve anatomy, but this is going to be helpful to know the location of the anterior clinoid process, medial to which is the optic canal, which can lead to traumatic optic neuropathy if injured, and lateral to which is a superior orbital fissure, which can lead to cranial nerves 3, 4, V1, V2, and 6 injuries. And then we obviously have the internal carotid artery near that sphenoid wing, which can lead to traumatic injuries of the ICA, which I won't be talking much more about. So this was a patient who had significant skull base fractures. He had a fracture going through the roof of that sphenoid, and you see that bony spicule protruding into that optic canal. Again, when you see these bony spicules protruding into these neurovascular channels, that is a much higher indicator of probably having a significant cranial nerve injury. This patient came back a year later. This is a coronal flare image with fat saturation that shows an abnormal increased signal in that left optic nerve with volume loss, and this patient ended up going blind in the left eye. So the thing I want you guys to remember about transphenoidal fractures, like Laforte had described a fracture pattern, facial trauma, some authors had described typical fracture patterns to expect with the sphenoid. And while it's not necessarily important to remember what these are called, it's helpful to know sort of the general direction of where these fractures go. And what's important to note is because the sphenoid bone is sort of at the epicenter of all these fracture lines, you often tend to see fractures going to the contralateral side. So don't have satisfaction of search when you see that skull base fracture. This is a left temporal bone fracture, and it's going all the way through that sphenoid bone to the contralateral greater wing of the sphenoid bone. So when you see a skull base fracture, especially with frontal ethmoidal and temporal bone fractures, follow that fracture to the end. So what to remember about transphenoidal trauma, the lateral sphenoid walls, sinus walls are relative weak points, and that's why fractures tend to traverse and go to the contralateral side. Assess the cavernous sinus and the cavernous ICAs for vascular injury in this setting, and assess the cranial nerve canals around that anterior clinoid process for cranial nerve injuries. So last but not least, we'll talk about occipital skull base fractures. Again, that occipital skull base makes up part of that clivus and the occipital skull base that goes to that transverse sinus groove. And because that transverse sinus groove sits there in that occipital bone, fractures often involve venous sinus injuries, and it can also involve epidural hematomas that Hans had just pointed out, and lower cranial nerve injuries as well as, because of the jugular foramen and hypoglossal canal involvement, and vertebrobasilar injuries. So the thing that comes up with posterior fossa injuries is epidural hematoma versus dural venous sinus thrombosis. So when you see these occipital skull base fractures, be sure to recommend a CT venogram if it's not already been done. And we want to look for that dural venous sinus thrombosis, of course. This is a very typical location for an arachnoid granulation and not a dural venous sinus thrombosis. And this is also not a dural venous sinus thrombosis. These often tend to, because these are venous injuries causing these epidural hematomas, these are small, and often only get picked up on these CT venograms. And the reason this is not a dural venous sinus thrombosis is that dural venous sinus getting uplifted, whereas this is a case of a dural venous sinus thrombosis where there is complete filling, central filling of that sigmoid sinus, and air within the sinus can indicate that there is an injury to the sinus. So what to remember about occipital skull base trauma. We should always recommend a CT venogram if it's not already been done to look for dural venous sinus thrombosis, and you'll often pick up small epidural hematomas in these settings. Look at the jugular foramen hypoglossal canal involvement, and look for a clival involvement because of its association with brain stem injury and maybe needing further evaluation with MRI. So in conclusion, let's scrutinize the skull base trauma in all high energy blunt force trauma cases, especially when you see calvarial fractures or facial fractures. Don't stop there. Look for the skull base fractures. If you see sinus or mastoid opacification or hemorrhage, look carefully at your thin cuts, millimeter cuts, and bone window of your head CT. Understand the anatomy of the neurovascular channels in order to report relevant information for surgical planning and your impression. And it's helpful to divide these fractures into temporal bone fractures, frontoethmoidal fractures, transfenoidal occipital and clival fractures, so that we know what complications to look for, and we know what to report as far as what complications to expect for the surgeons. And when you are at these very high volume level one trauma centers like I am, and you see these panfacial fractures, and you don't really know what to say in your impression, don't just say multiple facial fractures or multiple calvarial fractures. It really doesn't help anybody. I like to refer to the AO classification system for cranial maxillofacial fractures. It broadly divides these fractures into those fractures that involve the cranial vault here in green, those fractures that involve the skull base here in red, the midface in blue, and the mandible in orange. And the reason that's important is because if it's a midface and mandibular trauma, this becomes an oral maxillofacial surgeon problem or a plastic reconstructive surgeon problem. If it's a skull base fracture, this now becomes the territory of a neurosurgeon or an ENT surgeon with temporal bone trauma. And the OMFS and plastic reconstructive surgeons don't really want anything to do with this patient until that skull base and calvarial trauma has been dealt with and the head injuries have been dealt with, because this becomes more of a cosmetic issue and a functional issue. So I'd like to leave with that. And I thank you for your time. These are my references. And if you have any questions, feel free to email me. And that's my email address. Thank you for your time. We move on to the next talk. It's given by Karata Andreou Arasa. She's a neuroradiologist and assistant professor at the Boston University School of Medicine, actually working at the Boston Medical Center and Boston VA Health Care System. Karata will bring us a talk about traumatic emergencies of the soft tissues of the neck. Good morning. Thank you for the presentation. I'm going to be talking about traumatic emergencies of the soft tissues of the neck. Let's start with this obvious penetrating injury of a patient that was attacked with a broomstick in a jail fight on CT. The patient couldn't make use of the gantry, so the stick had to be chopped off. And as we see on coronal and axial images, the stick, made of wood, given the density, was traversing the neck from one side to the other. As CTA was done, there is a little bit of narrowing and anterior displacement of the right ICA. And in the other side, we see the stick and a flame-shaped morphology of the left ICA. Everyone would think this is a flow-limiting dissection. And there is an abrupt termination of the ECA in the left side as well. But the stick was carefully removed, and on DSA, there is normal opacification and preserved caliber of both ICAs. So this appearance was just due to mass effect and adjacent hematoma to the stick. And sometimes things look worse than they really are, only sometimes. Non-penetrating trauma or blunt trauma can be caused by a direct flow, blow to the face or neck, or indirect trauma, like in the setting of blast or sports. Penetrating trauma is less frequent and requires violation of the platysma muscle. We're going to see injury along the path of the instrument or the projectile, but also we may see lesions distant to it because there's a shortwave formation and cavitation that transmits kinetic energy to the adjacent soft tissues. There's been described bullet migration in the intravascular structures and in the intradural compartments. Let's start with vascular injury, and we're going to refer mainly to arterial vascular injury. Inflammation can be immediate with expanding hematoma or neuro deficits, or it can be delayed, and that's why we need to know when to screen these patients. The most frequent cause is motor vehicle collision, but minor trauma like chiropractic manipulation can also cause vascular injury. Anything that results in twisting or stretching of the vessels or indirect injury, a projectile or a little bone fragment from a fracture can cause also vascular injury. It's important to remember that vascular injury in the neck can have consequences in the brain with strokes, and when that happens, it occurs normally in the first 24 to 48 hours. The morbidity and mortality is greater when the carotid vessels are affected in comparison with the vertebral arteries. When to scan and what modality to use? The initial modality is going to be CTA, it's more available, it's less expensive and non-invasive, and it's been shown to have high sensitivity and specificity in comparison with DSA. In non-penetrating trauma, there are several groups that have published their screening recommendations. Probably the most frequently used and utilized is the Denver Group Screening Criteria that has been modified several times, and this is how they look now, and this is what we follow and the screening recommendations that we follow at our center. As you see, there are several signs and symptoms that require screening for vascular injury and risk factors like high-energy fractures to the maxillofacial bones, like LEFOR2 or LEFOR3, and maniobular fractures. Also cervical spine fractures, subluxation or ligamentous injury at any level are included in this screening criteria. Also upper rib fractures. This is a chart from a nice radiographics article where we can see the screening criteria from the Denver Group, but also from other groups. Now there have been discussions and talks about if we should have universal screening for vascular injury in all patients with Blount trauma. We can divide the vascular injury into five grades. Grade one includes vessel wall irregularity, dissection, or intramural hematoma with less than 25% of stenosis, and this is an example of a little patient with a little narrowing of the ICA. Grade two includes dissection or intramural hematoma with more than 25% of stenosis, like this case where there is narrowing of the left vertebral artery. Also includes distinct intramural thrombus and any raised intimal flap. Vascular aneurysm would be in grade three. This is an example of a patient with a widened left ICA, and we compare it with the other side, a set of aneurysm formation. Occlusion would be grade four. We have a lack of opacification of the left vertebral artery, and the right side is well opacified in a patient with a fracture of the vertebra. And grade five includes an arterial transsection and or fistula. Here we have a case of a patient with multiple maxillofacial bone fractures and opacification of the ICA on CTA and also of the cavernous sinus. And also there's active extravasation into what is left of the sphenous sinus. Let's review some examples. This is a 29-year-old male in a scooter being hit by a car. We see there is a dislocation, C4-5, with a jump facet, which required a CTA to evaluate for vascular injury, and there is a little hypodensity, an intimal flap in the right vertebral artery. The patient was treated. As you see, it's fixed here, and then with time, after three weeks of aspirin, the vessel looked normally opacified. Another patient that was hit by a car had fractures of both mandibles, and a CTA was done to evaluate for vascular injury. We see severe narrowing of the right ICA, and distally there is widening of the vessel with an intimal flap. And at the site of the stenosis, there is this classic T1 hypodensity in crescent-shaped morphology that corresponds to intramural hematoma. The patient was treated, but unfortunately, the stenosis persists with the intramural hematoma and distal widening of the vessel. An 8-year-old male that fell from his bike and hit the left side of his neck with the handle of the bike had a seroneurism formation with a large outpouching that is well opacified on DSA and was treated with coils. In penetrating trauma, we don't have screening criteria. Physical exam has been a good predictor for vascular injury. We have these hard signs that require surgery without prior imaging. Classically, it's been done this way because they are normally present in patients that are unstable. Soft signs are seen in patients that are stable and in which we're going to be able to do imaging before treatment. But it's been seen that negative surgical expiration in patients with hard signs is pretty high, up to 28% of the cases, and that's why some groups just try to do CTA in selective patients with hard signs and relatively stable to reduce negative surgical expirations and also in the case of injury to guide the surgeon. The findings we're going to see are indirect signs like pre-vascular hematoma or fat stranding, like we saw in the patient with a stick traversing his neck, and direct signs are pretty similar to those seen in non-penetrating trauma. We're going to see a transection, active extravasation, narrowing, certain aneurysms, or intimal flaps. A couple of examples. This is a 28, 25-year-old male with a gunshot injury, and we see a little bullet fragment located close to one of the vertebrae, and a couple of outpouchings, little set of aneurysms at the brachiocephalic artery. The patient was treated with a stent, unfortunately, incorrectly placed, a little bit too proximal, including the aortic arch, but not excluding the little outpouchings, and in a second procedure, a second stent was deployed a little bit distal, and this time, yes, the set of aneurysms were excluded. An unfortunate case of a iatrogenic penetrating injury in an attempt of placing a port-a-cat. We see this outpouching, erasing from the ICA, as we see on coronal images, and also there was a transection confirmed on surgery of the left IJV with active extravasation of contrast. The patient was treated surgically, and the vessels looked fine afterwards. Let's move to laryngeal tracheal injury. These are rare injuries, and frequently sometimes missed or underdiagnosed. It requires high-energy blunt trauma or penetrating trauma to the central neck. The most frequent cause is going to be motor vehicle collision. Either penetrating or non-penetrating trauma are going to have similar morbidity and mortality. We're going to scan these patients. There are multiple algorithms and protocols, depending on institutions, but in general, selective patients are going to be taken to the CT. The ones that have stable, the airways stable, when there is suspicion for laryngeal trauma. In some cases, there's going to be direct inspection before CT, and in other cases, we're going to do CT without direct inspection. It's rare to review these structures in general in all patients with trauma when we review CTs than requested for other reasons, to rule out vascular injury or to rule out spine fractures, because CTs that are requested just to rule out laryngeal injury are pretty rare. The modality of choice is going to be CT. MR is going to be left for cases with persistent clinical concern and negative CT. Search pattern should be scrolling slowly, even though if we are in a rush in cases with polytraumas, we have to scroll slowly from top to bottom, evaluating all the structures. Check the airway has to be patent. Make sure there's no asymmetries or extrinsic compression. We have to evaluate the soft tissues. Make sure there's no edema or hematoma. In the case of laceration, we may see little air densities deep to the airway, and we have to evaluate the laryngeal skeleton in both soft tissue and bone windows. We have to check in the laryngeal skeleton for linear discontinuities or committed fractures. Be careful in patients that are young. The cartilages are not ossified and makes it more difficult to see little fractures. In non-ossified cartilages, the cartilage may stream back after the initial blow, and in ossified cartilages, we're going to see a shatter, which is going to cause injury to the adjacent mucosa. When we miss these fractures, we're going to see deformities or subarthrosis. This is an example of a patient that had presented with hoarseness and old fractures. Here we see shortening of the left lamina of the thyroid, fracture of the right arytenoid cartilage, and subluxation of the left arytenoid cartilage. The patterns of fractures are variable in the laryngeal skeleton, depending on the mechanism of injury. The most frequently fracture or injury is going to be the thyroid cartilage. Classic fracture is this type of fracture, a vertical fracture to the lamina off to midline, like in this case. This patient that had a lacrosse ball hit her zone two of the neck. There is a little gap here in the lamina off to midline that we could easily miss if we don't scroll carefully. Also seen on coronal. In strangulation, we may see classic horizontal and bilateral fractures, and this can be a tricky type of fracture. This is a fracture of the superior horn of the thyroid. We see a little ossific density adjacent to the lamina with sharp margins, and we can't confuse it with this accessory cartilage that we may see sometimes in some patients. The accessory cartilage is going to have round margins in comparison with a fracture that we're going to have. We're going to see sharp margins. The cartilage is much stronger and less frequently injured. It requires high impact injury, and when it's injured, we're going to see associated soft tissue abnormalities with large hematomas, for instance, located posterior to the cracoid in a sandwich appearance between the cracoid and the C-spine. We have to remember that the normal shape of the cracoid should be ovoid, and when this ovoid shape is lost, we should suspect injury to the cracoid cartilage. The other components of the large L-skeleton are less frequently injured. There is a classification and a grading system also. Like in everything, this is the Schaeffer format classification, and it's for management purposes. We have type 1 fracture that is going to be treated just conservatively, and the other ones are going to be treated with endoscopy or surgery. Let's review how they look like. Type 1 injury is just going to be mild edema, and as we said, treated with observation, like this patient, where there is edema of the mucosa. Type 2 injury is going to include non-displaced fractures to the cartilages, like this one we see here. It's a vertical fracture, again, off to midline, with a little bit of associated edema. Type 3 injury will include displaced fracture of the cartilages, like in this case, where there is a displaced fracture of the left thoracic lamina. We're going to see, we can see exposed cartilages. We're going to see edema and hematoma of the adjacent soft tissues, and we may see also laceration of the mucosa. Like in this case, we have air densities deep to the airway, and also at the side of the thyroid haloid membrane that was suspected to be the cause of the edema. Suspected to be injured. Group 4 injury, or type 4 injury, includes displaced fractures at different sites, and massive edema and hematoma, and we're going to see endolaryngeal opacification and lacerations with air densities distant to the, deep to the airway. And the most severe type of injury is going to be the group 5 injury, or type 5, where we're going to see disconnection of the laryngeal structures. This is an example of a patient that had a blind ending of the laryngeal trauma, and then a tracheostomy tube entering distal, below to the larynx. The salivary glands are not frequently injured. The one that is more frequently injured is the parotid gland, and the superficial lobe more than deep lobe, because of the exposure. Normally it's going to be penetrated in trauma. There are several structures that we have to evaluate. The retromandibular vein, and running along to it, the facial nerve, and also the facial artery. This is an example of a patient with a laceration of the cheek after she fell on a rhododendron bash, which is this type of bash, pretty benign appearing, and very common in New England. The patient had a laceration of the skin and a laceration of the parotid gland with hypodensity and little air densities extending deep, adjacent to one of the vessels, and that's why we did a CTA and confirmed that the vessel was patent and well opacified. Late complications that we can see are fistulas during the first weeks. Here we have an example of a patient with a fistula of the main parotid duct with fluid density at the site of injury. And with time we can see xylosil formation. This is a patient with a scar from prior injury at the left cheek and a xylosil with a typical cystic appearance on CT and on MR. In muscular injury we're going to see edema, hematomas, lacerations, but also rhabdomyolysis. Trauma is the most frequent cause of rhabdomyolysis, and CK is going to be the most reliable diagnostic method. On CT we may have no findings, or we may see hypodensities in the affected muscles. On MR we're going to see still hyperintensity or T2 hyperintensity, and we could see enhancement in rim-like appearance or in little dots. This is an example of a patient that was found after a fall with a very high CK and still hyperintensity involving the left muscles of the neck. And another example of a patient that fell down the stairs with hypodensity and a little bit of enhancement in rim-like morphology involving the posterior paraspinal muscles, the left trapezius muscle, and the left sternocleidomastoid muscle. In summary, penetrating and blunt trauma to the neck can have potentially devastating consequences because there are vital structures at risk. It's important to report the critical findings for appropriate management. Remember when to screen for vascular injury and review carefully the airway and the longitudinal structures because little injuries can be easily missed. And these are my references. Thank you.

neurotrauma

RSNA conference

traumatic brain injury

imaging

skull-based trauma

vascular injuries

CT scans

MRI

surgical interventions