So we're going to start, the first session is going to be on pediatric head trauma. And hopefully I'm going to show you some interesting cases. Okay. So you might, I thought we would focus on pediatric skull fractures. And you might say, why are we going to look at skull fractures? That's so bread and butter for neuroradiology. And so if you read pediatric studies or you read out of the ED, you're going to read a lot of skull fractures in your career. And based on your report, they're going to, management decisions are going to be made. And if you read out a skull fracture and an injury pattern that does not match the cause of injury provided by the caretaker, that may lead to the child being admitted and an investigation initiated. And then CPT and the care team is going to come back to you. They're going to carefully scrutinize your study and you're going to have to articulate why you came to a certain conclusion and you're going to have to explain your interpretation of the findings. So it's a really important area to get your findings correct and accurate. So if you look here, here is a display of basically the gamut of skull fractures that we see in pediatric injury. And here you can see a right frontal non-displaced linear skull fracture. Here on the left, a diastatic fracture. This is a depression deformity fracture without a break in the bone. This is called a ping-pong fracture. And you can have ping-pong fractures because the infant's skull is so soft and plastic it can deform without actually fracturing. If the force of the impact is greater than the plasticity of bone, you will have a deformity fracture, a depression fracture like a ping-pong, but then at the base you can see the actual break in the bone. This is an infant that fell on a jagged rock. So you can see a depressed and displaced skull fracture. And here a comminuted fracture of the left frontal bone. So I thought we might start with a question that occasionally comes up in the reading room and which you will be asked to give an opinion on. And that is, in infants, so in the child with a soft, relatively soft and pliable skull, can a single blow to the head result in bilateral bone fractures? So a single blow to the head, can that give you contralateral fractures or bilateral parietal bone fractures? So I don't know what you think, yes or no. We're going to basically develop this question in the next 20 minutes. So we'll start with this two-year-old girl who fell off the couch onto a hardwood floor, so a hard surface, was brought to the ED by her mom. And these were the radiographs, and you can see that they're bilateral skull fractures from a single impact, fall off the couch. The radiology requisition said trauma, ruled out intracranial injury. Mom said that she did not witness the fall. She was in the other room, and the baby fell off the couch, and she heard the thump, but she didn't see it. She said the baby responded appropriately, cried immediately, there was no loss of consciousness, no vomiting, but then she became slightly lethargic. And so mom brought her to the ED. The GCS in the ED was eight, so that is not consistent with minor head injury, right? That's moderate to severe head injury. And she was intubated for airway protection. And she got the CT examination of the head, and you can see that there are bilateral skull fractures and there are bilateral scalp hematomas, so we know that both fractures are acute. If you look higher up, you can see that there was a hemorrhagic contusion of the frontal parietal brain. There was a large scalp hematoma, a diastatic fracture, and this was the contralateral fracture. On the coronal image, you could see that there was the hemorrhagic contusion, there was an epidural hematoma, probably a small cephalohematoma, and a larger subgaleal hematoma. You know it's subgaleal because it's crossing the midline. And a small volume of interhemispheric blood. The CT 3D showed that there were indeed bilateral parietal bone fractures and that they were contiguous across midline. And the intervening portion of the sagittal suture is widened, so it's diastatic. And so this is an injury pattern that you can see with a single impact, an impact to the vertex with fracture or diastasis of the injured suture and then extension of the fractures to both parietal bones. And so the question that we had in the reading room was, can a fall off of the couch result in this degree of injury? And there were some people that said, absolutely not, this is too much injury for a simple fall off the couch. And there were others that said, yes, you know, kids can be very active and they can huck themselves off of a couch and you can get this degree of injury. So there was a difference in opinion in the reading room. So this child went on to get an MRI examination because we wanted to assess the intracranial injury and also the superior sagittal sinus for injury or thrombosis. So this is the MRI examination and you can see there was a hemorrhagic contusion. There was the diastatic fracture. We know there's a dural injury because we have herniation of the left parietal cortex into the scalp soft tissues. There's a small epidural hematoma. There is a subperiosteal cephalohematoma or cephalocephaloma, and then the larger scalp swelling and injury. Because there was concern that this injury or degree of injury may not have been consistent with the history provided, we went on and we imaged the spine as well. And this was surprisingly what the spine images showed. So you could see in the upper thoracic spine that there were multilevel compression fractures. So then if you put the whole case together, we have a vertex injury, bilateral skull fractures, compression fractures of the spine. This together is consistent with a loading injury and you expect to see loading injuries when there's been a fall from a significant height, right, more than just the couch. So with this data in hand, we went back to the mom. The CPT group went back to the mom and they said, well, we don't believe your history. It's not credible based on the injury pattern we're seeing and the history you're providing. And so based on this, mom actually confessed to the true story, and that was that she was napping in one room and her two-year-old crawled out of the window of their second-story apartment, fell to the pavement, sustained this massive loading injury, was found by a neighbor. The neighbor run the baby back up to the apartment and mom brought the child to the emergency room. So it wasn't a case of abuse, it was a case of neglect and there were multiple other signs or indications of neglect in the household and this child was taken into custody. So that answers the question, I think, that yes, a single impact can result in bilateral skull fractures. And this comes up in time to time in the reading room. And when the ED physicians see these bilateral skull fractures, usually they'll consult CPT to make sure that they're understanding the story and the imaging findings correctly. And CPT will then often consult you back to you as the radiologist. So it's important for you as a radiologist to understand these different mechanisms of injury as well as the fracture mimics where you could have perhaps fracture on one side and a fracture mimic on the contralateral side. So the mechanisms for bilateral fractures are either double impact or single impact. If you have double impact, you have two separate blows to the head and that can be accidental or intentional. If it's accidental, the most common cause is a fall down multiple stairs where the head impacts multiple steps on the way down. But you can also see it from compression of the head between two surfaces like you might see with a motor vehicle accident or not uncommonly mom is walking trips and the head is crushed between mom's chest and the door frame and the wall or the floor. And then you can see it in non-accidental injury where the head is stomped or the head is compressed by the caretaker. So here was a rather dramatic example of a child that had double impact bilateral parietal skull fractures. Mom was coming down the stairs at the farmhouse. It was a witness event. She tripped and mom was actually an OB nurse and falling down the stairs tried to protect her baby and actually sustained cervical spine fractures and spinal cord injury herself. The baby hit more than one step and here on the 3D model, you can see bilateral parietal diastatic fractures. On the CT coronal, you can see extensive hemorrhagic contusions, epidural hematomas, and a large subgaleal hematoma. When you look at the 3D model from top down, you can see that there is diastasis of the sutures and that's not uncommon when there's increased intracranial pressure and you'll see a generalized uniform splitting of the sutures. But look at the configuration of the fracture. So while they do reach the midline, this does not look like a crossover injury as the fracture lines are petering out towards the vertex. So typically when there is a fracture, you're going to see most of the energy is delivered at the point of impact and then the energy dissipates as it extends up and you'll see a narrowing of the fracture line as it removes, as it moves away from the point of impact. You can see the narrowing here and the narrowing here. And then there is no asymmetric widening of the sagittal suture relative to the suture anterior or posterior to the intervening segment. You can also get bilateral skull fractures from a single impact, all right? So we looked at the mechanism where there is injury to the vertex and you get the bilateral parietal bone fractures. But we also know that you can get impact or injury to the occipital region and because of the plasticity or the pliable nature of the infant skull, you can actually sustain an impact posteriorly in the occipital region and the energy can propagate forward and you can end up with bilateral parietal bone fractures. So fractures that are distant from the area of injury. And we know this from a very interesting study that was done in the 80s by Weber in Germany where he took a large number of infant cadavers between zero and nine months and he dropped them from a three-foot height once, so a single impact, onto the floor. And the floor was, he did this on various surfaces. So a carpeted floor, a linoleum floor, tile, hardwood. And he then sectioned the cadavers and looked at the various fracture patterns. And what he found was that a single impact to the back of the head could result in multiple fractures, typically the parietal bones, and those fractures could be unilateral or bilateral. So from a single fall, this child had bilateral right parietal bone fractures, bilateral parietal bone fractures, and bilateral parietal bone fractures. He also found that if the single impact was onto a harder surface, like a hardwood floor or tile, those fractures would often cross sutures, okay? So here you can see a parietal fracture going into the occipital bone and a parietal fracture going into the frontal bone. He also found that most of these infant fractures begin and end at a suture, and he found that the fractures extend through the thinnest part of the skull, often the mid-portion of the parietal bone. So here's an example, this was a witness event of a infant that was in one of those vibrating seats put up on the counter by grandma, and then the vibrating seat just vibrated off the counter, and the infant fell back onto the posterior aspect of the occiput, and that resulted in bilateral parietal bone fractures, and you can see that the lamdoid suture in between is widened, so you could have propagation of energy through the suture and then into the parietal bones bilaterally. Note that this here is a accessory suture, this is called a median occipital fissure, and that's a right pari-sagittal fissure, and you don't want to mistake these for additional fractures. Bilateral linear skull lucencies do not equate, do not necessarily equate bilateral skull fractures, so if you see a fracture on one side, make sure that the other fractured linear lucency you see on the contralateral side is indeed a fracture and not a fracture mimic, and I'm just noting the timer is not going, so maybe Dr. Palacios can give me a hands-up when we're getting five minutes before. So it's important in infant skulls to differentiate fractures from sutures and synchondroses, and you're very familiar of the difference between a fracture and a suture, so fracture here in this example here, you can see the fracture, which is linear, it's sharp, it's lucent, it's usually unilateral, if it's bilateral, it's going to be asymmetric, and you're looking for secondary signs of injury to support the fact that that's an acute fracture. That looks very different than the lamdoid suture here, which is zigzag in appearance, it has sclerotic borders, typically they're confluent with other sutures, and if they're bilateral, they're symmetric, and you do not expect to see secondary injury signs adjacent to these, and they occur in predictable locations. So here you can see a fracture of the occipital bone, lamdoid suture, lamdoid suture, right? This is also an occipital bone fracture, you can see this jagged configuration, and that's not a predictable location for a suture, and then here, that's a predictable location for a suture, for a fissure, and that's called a midline occipital fissure, all right? And then the lamdoid suture, lamdoid suture. It can be somewhat of a nightmare interpreting fracture and distinguishing a fracture from a suture and a synchondrosis in a newborn infant with occipital region injury, and this is what your axials are going to look like, and if you are not reading infant skull brains a lot, this can be very challenging. So you can look these up, and you can also do a 3-D model, and the 3-D model is very helpful in distinguishing an occipital mastoid suture from the posterior intraoccipital suture from the occipital bone suture and the anterior intraoccipital synchondrosis, right? Midline occipital or median occipital fissure, skull fracture, right? But if you're not used to looking at these all the time, I would say just do your 3-D model, and even if you don't know the exact names of all these synchondrosis and sutures, you're going to be able to very expertly determine what is fracture and what is suture. So here you can see a diastatic fracture of the parietal bone. It goes from suture to suture, right? From coronal suture to lamdoid suture, and if you look posteriorly, their portion of the energy has gone into the lamdoid suture, which is diastatic, and then the suture continues into the occipital bone. If you look at it inferiorly, that occipital fracture component runs from the lamdoid suture to the innominate suture, also known as the posterior intraoccipital – sorry, posterior – I'm blanking on it – okay, between the two sutures. It's important to know the normal sutures and synchondrosis of the infants because then you can understand if there is a fissure in a predictable location that it is not a fracture. So in this case, you can see the squamosal portion of the occipital bone that's made up of the interparietal portion superiorly and the supraoccipital portion inferiorly. These two portions are separated by the mendosal suture. The mendosal suture also marks the location of the transfer sinus, and it also marks a demarcation of the skull cap that forms through membranous ossification and the skull base that forms through endochondral ossification. Inferior to that, we have the exooccipital segments of the occipital bone. They form the lateral margins of the foramen magnum. That's separated by the posterior intraoccipital synchondrosis. Anteriorly, we have the basioccipit. The basioccipit is separated by the exooccipital segments, by the anterior intraoccipital synchondrosis. And if you flip the skull inferiorly, you can see the same components of the skull bone. So the anterior aspect of the foramen magnum is formed by the basioccipit. The basioccipit is separated from the sphenoid bone by the sphenooccipital synchondrosis. Here we have the lateral segments, also known as the exooccipital segments. From here arise the occipital condyles and the jugular tubercles. We have the anterior intraoccipital synchondrosis, and posteriorly, the posterior intraoccipital synchondrosis. Anterior to that, we have a small ossicle that forms the posterior margin of the foramen magnum, known as Kirkring's ossicle. Posteriorly, the occipital mastoid suture, and then anteriorly, the petrioccipital sutures. When looking at the sutures, you can sometimes be confused by intrasutural bones, also known as wormian bones. The intrasutural bones have the same characteristics as sutures. So they're going to be, they have a zigzag configuration, they're sclerotic. Here you can see the sclerotic, and no signs of injury, and they can be increased in syndromes such as osteogenesis imperfecta. So here's a classic inca bone, and that's located between the lamdoid sutures and the sagittal suture, and note the zigzag configuration of the bone. On a cadaver specimen, note the zigzag configuration of the sagittal suture. The wormian bones also have that zigzag configuration, as does the inca bone. So look for that zigzag sclerotic configuration. You can have bipartite inca bones, but again, the dividing line is going to have the zigzag configuration and the sclerotic borders. Sometimes you can see multiple Wormian bones. You can look at it with different window settings, and I find this a very helpful window setting to look at. So, you widen your settings, and you get more of a transparent appearance, and that zigzag characteristic really comes through. And that can help in situations like this, where you have a large fracture here that can simulate an inca bone. Here is a large intra-sutural bone, like you see here on the right. Here you can see, with these 3D models, very distinctly the zigzag configuration of the lamdoid suture and the jagged, lucent configuration of the occipital bone fracture. Accessory sutures are common, so know where they're located. Typically, they're in the parietal bone or the occipital bone. They should be uniform in width throughout their course. So, what you don't want to see is widening of that accessory bone as it approaches the lamdoid suture, and you don't want to see focal widening of the suture where the accessory suture approaches. Okay. They're often bilateral. They're often symmetric, and you don't want to see secondary signs of injury there. So, these are bilateral accessory parietal sutures, and you can have parasagittal accessory fissures as well, and they typically cross the midline across the sagittal suture. Okay. So, here, a parasagittal suture, and here, another median occipital fissure in a child that fell backwards and had bilateral parietal bone fractures from a single impact, probably propagated, again, through that lamdoid suture. Look for secondary injury findings. So, here, you might wonder, is there asymmetric widening of that lamdoid suture? Look for your soft tissue emphysema and the soft tissue swelling that supports that there is a fracture here. Also, look for small avulsion fractures. So, tension is, if the suture is subjected to tension, the bone suture interface will fail before the suture itself. So, before the suture actually is disrupted, you'll see bony avulsion fractures. Here's a right occipital bone fracture, and there's right-sided asymmetric scalp swelling. If you are not sure, you can get a follow-up. That always helps. And here, three months later, that occipital bone fracture is gone. This is the last case. So, in looking at secondary injury findings, this was a boy that fell from dad's arms and struck his head. On the right side of his head, a single blow, wooden floor. There's a right-sided scalp hematoma. There's a skull fracture. Here's another skull fracture. Is that a fracture that was old, or is that a fracture from the same impact? This is what the CT looked like. So, could be a crossover fracture through the sagittal suture. This is what it looked like on CT, scalp hematoma, fracture, fracture, hemorrhagic contusion. We got an MRI examination on this child that showed the hemorrhagic contusion, the scalp hematoma. On ADC, you can see restricted diffusion of contusions. That's very classic. On ASL, typically, you do not expect to see increased flow within the contusion, but you will see increased flow around a contusion, right? And that's why we know that contusions grow with time on follow-up imaging. Because of secondary injury mechanisms, they call this a metabolic crisis around the contusion core. But look at the area deep to the other fracture. You can see that there was increased perfusion in that area and also restricted diffusion, so that's another secondary injury sign telling you that both fractures were related to the same injury. This child was intubated, and actually on the chest X-ray, we found these unexpected rib fractures. This ended up being a case of child abuse as well. Okay, so in summary, a blow to the back of the head can cause bilateral skull fractures. Okay, keep that in mind when you're consulted on these challenging cases. The skull fracture can occur at a site remote from the site of impact. So the scalp hematoma may be in the occipital region, but you may have bilateral skull fractures on your head CT. Fractures typically can cross or extend through the sutures if the energy of the impact is high enough. The fracture line will narrow as the energy dissipates away from the point of the initial injury, and then consider fracture mimics. And then I would emphasize the 3D model is your friend. Even if you don't read infant skull fractures much, make the 3D models. At our place, we don't automatically get 3D models because of a billing issue, so we have to ask for them. On our PACS, we can create our own, so it's very, very helpful in assessing these sometimes very tricky cases. And another consideration is sometimes you may have a fast brain MRI looking for injury. If there's any question about non-accidental trauma, you may want to go back and get a CT. Not so much because you don't know the fracture is there, but you want to be able to understand the fracture pattern and have more information about understanding whether the fracture pattern is consistent with the history provided. And with that, I thank you. I want to just bring to your attention this wonderful meeting that we're putting on in about a month in the warmest spot on Continental USA, Florida, Miami. It's two and a half days of just straight Pete's Neuro. It's jam-packed. We're very excited about it, so come join us, please. I think that now that for those of us who do a lot of, you know, question child abuse reads, it's really important to try and be as accurate as we can and try and figure out mechanisms and if the histories fit what we're seeing. I'm going to continue the theme of pediatric brain emergencies, but really focusing on non-traumatic causes. For the topic, I kind of broke it down into three big causes, and I put one under vascular, right? That's going to include hemorrhages, thrombus, stroke. I put moyamoya in there because this day and age, and I'm going to show you some cases, if you're not thinking about it and if you're not specifically looking for it, you will miss it. And these kids can sometimes be presenting with simple histories such as headaches. So we'll kind of take a look at those kind of sometimes subtle cases. The next overall topic I think I'm just going to kind of highlight is edema. So we certainly don't want to be missing signs of cerebral edema in the, you know, stack of kids that have headaches. So we're going to kind of look at a couple that have an underlying infectious cause or underlying metabolic cause. And I put subtle mass here, and I'm going to also show you a case of a very obvious mass, but I think I'm not worried about people in this room missing a big mass, but I'm going to show a couple cases of kind of subtle findings that I don't want you to miss. So we'll start with kind of vascular topics. And I think that everyone in the room can see the asymmetry on this head CT. This was a two-day-old that presented with seizures. And it's fairly easy to spot the area of loss of gray-white differentiation, this large hypodense area in an MCA territory. And so the thought really here is what is this due to, right? And so some of these patients are full-term, normal delivery, no significant distress. And so the thing to realize is that infants have higher hematocrit levels, and it's not uncommon for them to have a kind of a combination thromboembolic phenomenon from their high hematocrit levels. So certainly when we're looking for perinatal injuries, we're going to look for hypoxic ischemic injury, especially if there's a pertinent history of a difficult delivery or abnormal APGARs and abnormal gases and things like that. But when you're also dealing with perinatal issues, and particularly with a presentation of seizures, you should remember that they can actually present with embolic or thromboembolic phenomenon related to their high hematocrit levels. These patients will oftentimes, even if it's not necessarily recognized on a head CT, the babies that are presenting with seizures will get MRIs. And one of the things that is important to know, depending on the timing of when you're imaging, is you can actually see acute Willerian degeneration. So here you can see this MCA infarct on the left, but you can also see that there's restricted diffusion coursing through the corpus callosum, and actually you can see it kind of coming down the tracks as well. And this is really something that we're very familiar with seeing in follow-up examinations of strokes, but something to think about in pediatric stroke is that we'll see this not uncommonly, particularly in that two- to three-day window that we'll start to see acute Willerian degeneration in the babies. I think that there's kind of two ways of thinking about histories, and I do know that there are some radiologists that don't like to be biased by history, and so will try and read images before looking at the history. And I think that whether or not you read before or after looking at the history, really reading the history does give you some additional information. So this was a patient that came in, a neonate who arrested at home, and this is a neonatal head CT. This is what we get. And this is sometimes a challenge, right? You know, we just mentioned that infants can have a perinatal time, can have a very high hematocrit level, so you can kind of see that there's this area of increased density, but is that normal hematocrit level? We're looking at, you know, are there any areas of loss of gray-white differentiation? We need to look at the central gray-white differentiation as well. There are some machines these days that are super smart, and they try and actually do what we call an anti-cupping algorithm to actually subtract cupping artifact. The issue is that babies don't have very dense bones, so they don't actually have a lot of cupping artifact. So if your machine has an anti-cupping algorithm, it will actually subtract a little bit of signal from the cortex. So it can actually be very challenging to read neonatal head CT. Let's just take a look at what a normal neonatal head CT looks like. And here you can kind of see this is the same scanner. We're still looking at gray-white differentiation. I'm going to bring your attention to the deep gray structures. So here on this patient, we've kind of lost to that central deep gray differentiation with the white matter, and here you can see it. Now, we're always trying to keep the doses down. We have to have enough dose, though, to be able to make the diagnosis. So it is something that you have to kind of work with and get used to not only your dose, but what your images look like with the most optimized dose and where you feel comfortable reading. But here you can see that there's really loss of that central gray density here. This was the MRI for that patient. And you can see with this pattern, it's actually a fairly typical pattern for what we see with even full-term babies that have hypoxic ischemic injury. And it's basically all the areas where you know that there's high metabolic activity. Basal ganglia, you can see perirolandic regions. And these are all active areas of myelination and active areas of development. So it's no surprise that in a baby that has a hypoxic episode that you would get the central gray. So that's the tip, is just always make sure you're looking at the central gray, particularly in the neonates. This was a patient, and I actually always try and give you the real histories, the histories that we get. This was a patient that was scanned that had a history, like had just been diagnosed with endocarditis. And on head CT, you could see a few punctate densities. And we went on to do an MRI. And here you could see on the post-contrast T1, you can see these ring-enhancing areas. You can see areas of microhemorrhage and a little bit of restricted diffusion in them. So this one corresponded with this one, had probably had a little bit of central plus. But the teaching point here is that sometimes there is petechial disease. And you know, I think that one of the challenges that at least our residents have is detecting noise from petechial hemorrhages. And I think that that can be a challenge and a little bit of expertise. But particularly if you're given a history that might be leading, if you have fever or if there's something, an underlying congenital cardiac issue, something that you might know that might increase your concern for possible petechial hemorrhage. This is, of course, you know, the ones that you kind of get concerned about is a lot of us now to kind of help throughput and to decrease the amount of time it takes to scan patients are doing either fast MRIs with either limited sequences or MRIs that are a five-minute protocol where you're doing many of the same sequences. They're just decreased in resolution to decrease the amount of time that the kids are on the scanner. So a lot of our resolution is being lost to save in time. So if you are reading a T2-weighted image, it's extremely important to be looking for the flow voids. I think those of us who use macros or those of us who dictate free text, a lot of us put in our dictation the T2 flow voids at the skull base are intact or, you know, something of that sort. But it's really important to actually look in that area. And so here you can actually see that there's decreased conspicuity of flow voids. You have this abnormal flare hyperintensity in the leptomeninges. And you also have some deep white matter in kind of watershed areas that is abnormal. And so this patient actually has moyamoya vasculopathy. And this is the MRA for that corresponding patient. So I think it's really important, A, to look for the flow voids on the T2s, even if it's a limited-sequence protocol. But also the flares are extremely helpful. Here's another patient. This was literally a patient, 10-year-old girl normal, who was just complaining of headaches. And this actually was detected by our fellow. And you can actually see that there's decreased amount of normal flow void on your T2 through your circle of Willis. So when you see, sometimes you'll see that there's decreased caliber. Sometimes you'll actually see this patient kind of then came back for a full higher-resolution study. And you can see all the tiny little collaterals from all the moyamoya vessels. Here you can see, this is actually a post-contrast T2 flare, which definitely highlights leptomeningeal signal abnormality and is probably, is definitely on the short list of my favorite sequences. So here you can see kind of some of that IV sign that's described in the flare. And here you can actually see that on the post-contrast, it's actually very difficult to kind of see the same findings. But if you kind of compare this, the two sides, you can actually see that there's slightly less of kind of a normal flow signal in that region. So if you don't look for moyamoya, if you're not thinking about it, you could potentially miss it. And this is a patient who potentially could benefit from revascularization. And for us, you don't want to make the diagnosis once the child has had a stroke, right? So here, hopefully, when you make the diagnosis, then the patient could be worked up for potential treatment. Certainly if you're given a history for moyamoya-like vasculopathy, neurofibromatosis, Down syndrome, we have a large sickle cell population in Atlanta, so that's definitely something that we're always looking for. This is a patient that came in with papilledema and headache. And whether or not they actually come in with a history of papilledema, you may or may not get. This is a non-contrast head CT. And what you're noticing is that this is a 15-year-old. It's not an infant that has a high hematocrit level. You kind of have to look. All right. This density, is this density abnormal or normal? And so what I usually tell our trainees is you have to be looking at the other areas where you know there's going to be normal blood density. And so in the posterior fossa, I tell them to compare it to the basilar artery. And the basilar artery is nice because it's kind of on the same cuts that you would expect your transverse sinuses. So here you can see that this basilar artery is much lower in density than the transverse sinus here. If you actually look at your sagittal reconstruction, you get a sense that even the superior sagittal sinus has these patchy areas of increased density. This patient goes on and has their CT venogram. And you can see that there are areas of non-filling, both in the superior sagittal sinus and in the transverse sinuses. So it's very important not only to get the most appropriate study when you can. So, you know, in the middle of the night, if our residents are dealing with a question of possible venous sinus thrombosis, they absolutely can get a contrast CT scan to look to confirm that there is. Certainly we would tend to prefer MR, not only for the diagnosis, but to look for potential sequela of venous sinus thrombosis and any ischemia. Here's another patient with headache and vomiting. And here you can see, oh, well, that looks a little dense, but look at the basilar. So it's about actually similar density to the basilar artery. And but adjacent to that, there's actually this crescent of hypodensity. And on the coronary format, you can see that little area of hypodensity in that right transverse sinus. So we can see we've compared, but this time, instead of having hyperdensity, that's the concern, we have a little hypodensity. And so, we actually did an MRI to kind of further evaluate, given the symptomatology, and we confirmed that there was a filling defect in the right transverse sinus. And upon further history, this patient actually had had a severe ear infection and was treated with two weeks of antibiotics just recently. And so, the presumption is that the patient probably had a mastoiditis and had had an adjacent sinus thrombosis, and now was presenting with a chronic thrombus and headache related to that. This was a patient that had gastroenteritis, so was losing a lot of fluid, and then presented with mental status changes. And here, this one's a kind of fairly dense straight sinus here, so you can see that. You can also see that there's an area of abnormal density in the left thalamus, and so that's an area of infarction. So just remember, if you are considering venous sinus thrombosis, really look for areas that potentially could have venous infarction. This was a patient that actually did have an abnormal neuro exam, but basically, because of the febrile and the abnormal neuro exam, they did do a contrast-enhanced CT. And just to kind of remind us, and particularly if you're seeing sinus problems in the sphenoid sinus, always look at your cavernous sinuses. And so, this is a contrasted study. It wasn't a CT angiogram. You can see nice venous sinus opacification, but here, you are actually not seeing good opacification of the cavernous sinus. So in this timing, we should have nice filling of the cavernous sinus, and we really shouldn't really be able to delineate the cavernous portion of the carotid from the adjacent cavernous sinus. So this patient actually had cavernous sinus thrombosis. So it's just kind of a reminder that when you're looking at contrast studies, even if there's not proptosis or any signs of facial sequela, we always have to look at the cavernous sinus. These are just coronal reformats, also showing that there's no filling of those cavernous sinuses. I think cerebral edema is a challenge for our residents who are initially starting out, and it's absolutely reasonable because a lot of the trainees get used to seeing adult brains, and particularly even on the older side, and we are used to seeing a little bit of volume loss in the older population, but in the pediatric population, they still have nice full brains a lot of the time. So it can be very challenging for them to actually detect some subtle cases of cerebral edema. This was a teenager with altered mental status and was scanned, and here you can basically see that there's kind of just crowding throughout. You can see the ventricles, but where are the sylvian fissures? I always tell the residents that on the top four slices, whether you're getting three millimeter slices or five millimeter slices, on the top four slices, you should be able to see CSF in the sulci. And so this was a case that after calling and saying that the child had cerebral edema, we got the additional history that the patient had DKA, diabetic ketoacidosis, which is actually a fairly common presentation for the kids to have when they have an acute, severe DKA. A lot of them will actually have either some mild cerebral edema, and they'll have associated mental status changes. Here was an interesting case. This was a case that the child had a fever and a headache. They opted to get a CT as an initial study, and a lot of times we'll hear that meningitis, one of the early signs of meningitis, is temporal horn enlargement or mild ventriculomegaly. And here, it was hard to argue that the temporal horns were abnormal, but what was noticed was that there's a little bit of patchiness to the visualization of the sulci. So you could see the sulci in the CSF very nicely here, but not over here. And so there was concern that there might be some areas of cerebral edema, focal edema, or focal leptomeningeal abnormality. The patient went on to get a contrast-enhanced MR. And here, this is the post-contrast MR T1, and not amazing, nothing too impressive here. This is the pre-contrast flare, and then here is our post-contrast flare. And here, it's actually very easy to see all of this abnormal leptomeningeal signal. So the post-contrast T2 flare is my favorite for any leptomeningeal process. So anytime you're thinking about leptomeningeal metastatic disease, leptomeningeal process Sturge-Weber or anything like that, your post-contrast T2 flare is going to be super helpful. As I mentioned, we have a very large sickle cell population, and I just wanted to show this. We've had a few cases of kind of a similar story, where the sickle cell patient will complain of a severe headache. And so certainly, there's always a concern, are they having an infarct? And when they're presenting initially, they can either go through CT, and even potentially if there's a large enough concern, CTA, or they'll go through MR, MRA, non-contrast typically. That's the preferred method. Depending on what time they come, this patient was actually an inpatient and complained of severe headache. And what we noticed was that there was asymmetry in the frontal lobes. And on the reconstructions, we thought that the right side might be a little full, but then we were also, well, could there be volume loss on the left side? So to solve the question, we put the patient in the MRI scanner, and you can see all of this flare signal abnormality in the leptomeninges, particularly in the right frontal lobe. There is a little bit on the left. And you can see on the susceptibility-weighted images all of this abnormal hemocytin signal. On the non-contrast MRA, we actually saw what ended up being vasospasm. Initially, I had interpreted this as, you know, potentially a small aneurysm. The patient got a follow-up later, about two months later, and it was totally normal. So it's a little unclear, but we do know that some of these sickle cell patients can have these times of spontaneous intracranial hemorrhage. So it's something to be concerned about, also to know what their status is, because if they have vasospasm, it can worsen their sequela. This was a patient that had headaches and papilledema. And so I think one of the things to really remember is that we're seeing a lot more kids with idiocratic intracranial hypertension, so we really need to look at that. So we're looking for papilledema. We're looking for kind of a depressed anterior pituitary. You also look for any tonsils that might be low-lying. And then also look for areas of venous sinus stenosis. And kind of the last topic is mass. And this is the one I was like, all right, I'm not, I'm 100% sure none of you guys are going to miss this. You're not going to miss the cystic and solid mass causing obstructed hydrocephalus. The one that I wanted to mention that can be a little sneaky is one that's kind of relatively new in pathology grading from the WHO 2016 criteria. But basically, you can see that there's what looks like hydrocephalus here, but we're not seeing any obstructing mass. And this diffused leptomeningeal glial neuronal tumor can basically present with increased fluid, and it can look like hydrocephalus. But basically, you'll see some of these little nodules. They may not have a lot of enhancement, but you'll tend to see them on flares and post-contrast flares. They can have enhancement of some of the nodules, and you always do have to image the spine because they can have diffused disease, both brain and spine. The last couple of cases are just don't miss areas. Headache and vomiting. Don't forget the skull base. Remember that lymphoma and rhabdomyosarcoma, kind of love that nasopharynx. And you can always have abnormal lesions in that skull base. And it's not something that we kind of think about too much in kids, but it's a very important area to look at. So, in this patient, this patient had lymphoma. And basically, you can see this bony destruction here, and that had a soft tissue mass there. And then, this is my last case, and I think we can all see that there's a little focal density here in the third ventricle, or right at that kind of foraminal region of the third ventricle. It's increased density. This is a colloid cyst. This is kind of a classic imaging appearance for it. But what I am going to challenge you is that sometimes these patients are presenting through MRI because they're presenting with headaches. A lot of them are teenagers. So, to reduce the amount of radiation, they're getting MRIs first, and they can be very difficult to see. So, because we know where they love to be located, you have to be looking for it. So, always look in that same location for these colloid cysts. Here you can see it on the flare, which might be a little bit helpful. The high-resolution T1s are actually a good way of looking for it, too. This patient, because of the suspicion, high-resolution KISS sequence was performed, high-resolution T2 steady-state images. So, it was actually able to be seen on MRI as well, but be very careful because that's something that's fairly easy to miss on MRI. So, hopefully you've gotten a nice review of some of the things that I consider to be don't-miss areas and pearls and pitfalls in looking for vascular abnormalities, hemorrhage, thrombus, and ischemia. I think it's really important, if you're doing a head CT, you have all of this data at your fingertips. So, go ahead and get sagittal and coronal reconstructions. It's super important. And then, if you're doing an MRI and you're giving contrast, I think it's extremely helpful to do post-contrast T2 flare, and that's just like a personal love. And I think it's really important for us to try and remember that, despite the large number of studies we have to read, each study needs its own separate attention, and it's really hard to kind of stay focused towards the end of the day after reading your 48th study head CT, but it's something that's really important. So, thank you very much. Okay. Now, switching gears to imaging of pediatric head and neck emergencies. So, acute symptoms related to the head and neck region is a common reason for emergency room visits in children. The clinical diagnosis is often difficult because of overlapping or nonspecific symptoms, and also availability of limited history and physical examination in children. And as such, imaging plays a central role in diagnosis of these conditions. Let's start with infection of the sinuses and the temporal bones. So, acute sinusitis, as we all know, it's a clinical diagnosis and does not require any imaging. Although complications of sinusitis can have extremely fulminant cores and have a high morbidity and mortality, these would include osseous complications, such as osteomyelitis of the frontal or the sphenoid bone, depending on the sinus involved. Intracranial complications can vary from meningitis to epidural and subdural empyema, cerebritis, abscess, and sinus thrombosis. And also, paranasal sinus infections can spread to the orbits, leading to postseptal cellulitis, abscess, and cavernous sinus thrombosis. A quick word about the different routes of spread of sinus infection. So sinus infection can spread directly through the bone, and this could be through congenital or acquired defects in the bone. And congenital defects would also include the anatomical defects that is along the neurovascular structures. Another important pathway for spread is the presence of these valveless emissary veins that traverse the calvarium and allow bidirectional flow of blood. These veins are particularly numerous in kids and adolescents because of the rapidly growing calvarium and the developing paranasal sinuses. And also, sinus infections can cause osteomyelitis, and that would eventually provide a direct pathway for spread. So here are some examples. This is a 13-year-old who presented with clinical signs of sinusitis and headache. On this initial non-contrast low-dose sinus CT, we see opacification of multiple paranasal sinuses with an air fluid level in the frontal sinus. Also, there is a tiny speck of intracranial air in the frontal region, a small defect in the posterior wall of the frontal sinus, and on the soft tissue windows, we can see this subtle iso-intense extra-axial collection in the left frontal region. So this is suggestive of a complicated frontal sinusitis with intracranial extension. The patient had a MR subsequently, and we can see this diffusion restricting subdural and epidural collections in the left frontal region with associated meningeal enhancement. This child underwent drainage of the surgical drainage of the paranasal sinuses and broad spectrum antibiotics. However, transcranial drainage of the collections was not done. And when we did follow-up imaging three days later, there was significant worsening. Now we can see the subdural empyema extending over the bilateral frontal lobes, as well as an enlarging epidural abscess. Also now there is edema in the left frontal lobe, suggestive of cerebritis. So these infections, if not treated adequately, can progress very rapidly. This is another example of complicated frontal sinusitis. In the initial non-contrast HCT, we see opacification of the frontal sinus. On the bone window images, we see the permeative destruction of the bone, associated marrow enhancement on the subsequent MRI, and a large, overlying scalp swelling in the forehead. So this constellation of findings, which includes osteomyelitis of the frontal bone with associated forehead swelling, is described as the Potts-Buffett tumor. Also this patient has an intracranial epidural collection that demonstrates diffusion restriction and mass effect on the superior sagittal sinus compatible with an epidural abscess. The next case is an example of a sphenoid sinusitis, which is much less common than frontal sinusitis, sphenoid osteomyelitis. This is a 15-month-old who presented with fever and nasal discharge. On the initial CT, we see opacification of these partially pneumatized sphenoid sinuses with heterogeneous enhancement on the soft tissue images, with associated rim-enhancing fluid collections on either side of the sphenoid bone. On the subsequent MRI, we can see diffusion restriction within this collection in the floor of the anterior cranial fossa, as well as intermediate T2 signal and post-contrast enhancement along the margins of both collections. This is an example of sphenoid sinusitis with epidural abscess and a nasopharyngeal abscess. As I said earlier, complicated paranasal sinus infections require a prompt treatment. Typically the treatment includes aggressive antibiotics, sinus drainage by the way of functional endoscopic sinus surgery, and also there needs to be a low threshold for transcranial evacuation of any intracranial collections. In general, subdural empyema has a worse prognosis compared to epidural. The subdural empyema can spread rapidly over the surface of brain and cause increased intracranial pressure and herniation, while epidural empyema can sometimes progress gradually over a period of days before presenting clinically. Moving on to infections of the temporal bone, just like sinusitis, otomastoiditis is a clinical diagnosis and typically does not require imaging. Complications of otomastoiditis similar to sinusitis include involvement of the adjacent perioricular soft tissues or extension into the intracranial compartment. We'll also look at a specific type of temporal bone infection, which is pterosepisitis, which presents with characteristic imaging and clinical findings. So these are two different patients with complicated otomastoiditis. This is a much more flawed case than what Sarah showed us earlier. So the patient on the left side had a post-contrast CT where we see opacification of the middle ear and the mastoid, with associated erosion of the posterior wall of the mastoid. On the soft tissue images, we can see an epidural collection in the posterior fossa, as well as extensive retroauricular and occipital soft tissue swelling. The patient on the right side has similar findings on MRI. We see T2 hyperintensity in bilateral middle ear and mastoids. And on the left side, there is both extracranial and intracranial fluid collection, demonstrating diffusion restriction, suggestive of abscesses. Also on this sagittal post-contrast image, we see a large filling defect extending from the sigmoid sinus to the jugular vein, suggestive of associated sinus thrombosis. This is a five-year-old who presented with symptoms of otomastoiditis and facial pain, and this is an example of pitreous episitis. So on the T2-weighted MR, we see hyperintensity throughout the right temporal bone, including the pitreous apex. In the region of the cisternal segment of the fifth cranial now, we see the soft tissue thickening and enhancement. And also there is asymmetrically increased enhancement in the right cavernous sinus, as well as narrowing of the right ICA flow void, which was confirmed on the MRA. In addition, there is abnormal asymmetric enhancement in the inner ear structure. As we can see, this abnormal enhancement of the cochlea compared to the contralateral side and also abnormal enhancement within the IAC and the vestibule. So this is suggestive of pitreous episitis with labyrinthitis. So pitreous episitis typically presents with clinical syndrome of otomastoiditis with pain along the distribution of fifth cranial nerve and abducens palsy, which can be explained by the imaging findings here. Moving on to infections of the orbits. As we all know, the orbits are divided into pre- and post-septal compartment by the orbital septum, which is contiguous with the periosteum of the bone, and separates the orbital fat from the eyelids. The post-septal compartment is then divided into intra- and extraconal compartments by the cone of the extraocular muscles. So orbital infections have been divided into five categories by Chandler, and these are with worsening degree of severity. So the mildest form is the pre-septal cellulitis. The pre-septal cellulitis is typically secondary to spread of infection from the facial soft tissues and can also be secondary to spread from dental infection or from trauma or insect bites. On the other hand, orbital cellulitis or post-septal cellulitis is typically secondary to spread of infection from the ethmoid sinuses. You could also have subperiosteal abscess, which is also secondary to infection of the ethmoid sinuses. The next category is the orbital abscess, where we have a fluid collection within the intra-orbital fat. And the most severe is the cavernous sinus thrombosis, which can occur with or without the involvement of the orbit. So these are two different patients presenting with orbital swelling and inflammatory signs. Both patients have pre-septal cellulitis. The patient on the left has these diffused pre-septal soft tissue swelling bilaterally. Note the absence of any ethmoid disease and the absence of any post-septal involvement. The patient on the right has unilateral pre-septal cellulitis with an associated small fluid collection. Again, note the absence of post-septal inflammation. This is a 7-year-old with a florid case of post-septal cellulitis. We see this extensive inflammatory change in the left orbit with associated proptosis. In addition, there is this curvilinear hypodense fluid collection along the lamina paprecia, suggestive of a subperiosteal abscess. There is a pacification of the ethmoid and the maxillary sinuses, which is likely the source of infection. And also, when we look at the contour of the left globe, we see this posterior elongation in the region of the optic disc. So this kind of globe contour has been described as the guitar pick sign. And this can be a predictor of optic nerve injury or ischemia secondary to stretching of the optic nerve. There are a couple of mimics of orbital infections, which should always be considered, the most important one being serotumor or idiopathic orbital inflammation. And sometimes neoplasms, such as metastatic neuroblastoma, leukemia, lymphoma, can present with orbital involvement and symptoms which can simulate infection. So this is a 13-year-old who presented with bilateral eye pain. On the T2 and post-contrast MR, we see inflammatory changes in both in the intracranial orbits bilaterally, right more than left. Note the absence of any ethmoid sinus infection. So this turned out to be a case of serotumor or idiopathic orbital inflammation, and it responded well to steroids. Moving on to infections of the soft tissues. So infections of the superficial soft tissues, including cellulitis and abscess of the head and neck region and superior lymphadenitis are extremely common. Typically, they can be diagnosed by ultrasound, and CT can be reserved for cases where you suspect a deep extension or vascular involvement. I'm not going to show any examples of these. Also I'm going to show some examples of sialadenitis. So sialadenitis or salivary gland inflammation, they can be calculus or a-calculus. Calculus sialadenitis is more common with salivary glands, while the a-calculus is more common with the parotid glands. Also as far as the infectious agents are concerned, the sialadenitis can be viral or bacterial. Viral is more likely to be bilateral and typically involves the parotid gland. And in cases of bilateral parotid sialadenitis, also the autoimmune condition should be considered on the differential. So these are two different patients with salivary gland inflammation. The patient on the left side has an enlarged and hyper-enhancing submandibular gland suggestive of sialadenitis. And also we see this large calculus obstructing the distal aspect of the Vorton's duct. The patient on the right side presented with parotid swelling, and the ultrasound shows this enlarged and heterogeneous appearing left parotid gland. There are some small pockets of fluid within the left parotid and increased vascularity. This is the right parotid for comparison. And again, CT of the neck with contrast shows the corresponding findings, enlarged left parotid with small fluid collection. So this was a case of a bacterial parotitis with early abscess formation. Moving on to infections of deep soft tissues. So deep soft tissue infections in children are typically complications of pharyngitis, and they can present as peritonsillar or retropharyngeal collections. The main concerns are mass effect on the airway as well as vascular complications such as jugular thrombophlebitis or involvement of the carotid arteries. So this is a nine-year-old who presented with sore throat and odynophagia. On this post-contrast CT of the neck we see enlarged bilateral tonsils with an associated hypotenuating fluid collection in the left tonsillar fossa, which is causing a mass effect and anteromedial displacement of the tonsils. So this is compatible with a peritonsillar abscess, and this can be drained by a transoral approach. This is a younger child, a three-year-old, who presented with fever and throat pain. On this post-contrast CT of the neck we see a hypotenuating collection in the left lateral retropharyngeal region with an incomplete rim of enhancement. And if you look at the contralateral side, there is a prominent enhancing but non-necrotic lymph node in the same location. So the best description for this lesion is a superlative lateral retropharyngeal lymphadenitis. A true retropharyngeal abscess occurs when this lymph node, when the fluid ruptures through the capsule and it extends from side to side in the retropharyngeal region. The treatment for a superlative lateral retropharyngeal lymphadenitis is typically conservative, and drainage can be considered if they are large at the time of presentation or if they don't respond to initial antibiotic treatment. This is a 15-year-old who presented with fever and neck swelling. We started with an ultrasound. We did not see any fluid collection in the neck. However, we saw enlarged but morphologically normal lymph node. And when we looked at the vascular structures, we saw this echogenic material within the jugular vein with absence of flow, compatible with the left jugular vein thrombosis. The findings were confirmed on CT, where we see absent enhancement within the left jugular vein. So this constellation of findings of pharyngitis with jugular vein thrombosis has been described as Lemieux syndrome. And this is typically caused by infection by Fusobacterium species, which can be detected in the blood. And also, because this is a septic thrombophlebitis, these patients are prone to develop septic emboli, which we had in this case with multiple cavitatory lung lesions. Moving on to some of the primary infections of the airway, I'm going to talk about epiglottitis and croup. So this is a 4-year-old who presented with fever and change in voice. On this lateral radiograph of the airway, we see markedly thickened epiglottis and the area epiglottic fold, and mild distention of the pharynx and the hypopharyngeal airway. This is a normal for comparison. You can see the nice, thin epiglottis and the almost imperceptible area epiglottic folds. So epiglottitis is typically seen in children between 3 to 6 years of age, and it's caused by bacterial infection. Traditionally, H. influenzae has been the commonest organism. However, with vaccination, the incidence of epiglottitis is decreasing, and also now the most common organism is streptococcus rather than H. influenzae. This is a younger child, a 20-month-old, who presented with cough and inspiratory stridor. On the frontal airway radiographs, we see the smooth narrowing of the subglottic airway with loss of expected shouldering. This is called the steeple sign. And on the lateral radiograph, we see this distention of the pharynx and the hypopharyngeal airway. Again, this is a normal for comparison. We see the nice shouldering of the subglottic airway in a young child. So croup is typically seen in younger children than epiglottitis, the peak age is 6 months to 3 years. And it's viral in etiology. It's caused by either parainfluenza virus or RSV. And it has a favorable course and is managed conservatively. I'm going to show some examples of trauma. So these are two different patients with orbital trauma. The patient on the left side had a penetrating orbital trauma with a BB gun pellet. And we can see this right orbit has distorted contours with presence of a tiny airspeck dislocated lens. And we can see the metallic foreign body lodged in the orbital apex. So this is an example of open globe injury. The patient on the left side had a blunt trauma to the globe. The globe contours are maintained, no obvious hemorrhage. But when we look at the lens, there is loss of normal hyperattenuation of the lens. Again, you can see that on both axial and the coronal images. So this is compatible with the traumatic cataract after a blunt globe trauma. Foreign body ingestion is fairly common in children. And coins are by far the most common ingested foreign bodies. A swallowed coin in the esophagus has a coronal orientation. So you would see them on first on the frontal view and tangentially on the lateral view. While a coin in the trachea would be perpendicular to this, so it would be tangential on the frontal view. This is a pretty good rule, although it's not 100% specific. These foreign bodies are typically removed endoscopically. In this particular patient, we had a follow-up radiograph which shows the foreign body within the stomach. And the patient also presented three days later with progressive neck swelling. And repeat airway radiographs show mass effect on the trachea with a large prevertebral collection. So this is suggestive of a perforation secondary to foreign body. Again, this is very uncommon. This is another young child who presented with suspected foreign body ingestion. Again, we have a rounded metallic foreign body in the esophagus. However, when we look at it closely, we see these concentric rings on both frontal and lateral radiographs, which is not typical for coin ingestion and is suggestive of a button battery. So button batteries are very high risk for causing esophageal perforation or abscess and need to be removed emergently. A brief word about some of the congenital infections, congenital conditions that can present in the emergency setting. This is a two-year-old child who presented with neck swelling and fever. On this post-contrast CT, we see a large multiloculated peripherally enhancing fluid collection involving the left side of the neck and extending to the mediastinum. This is suggestive of an abscess, but the appearance is very atypical for a de novo abscess. So this turned out to be a super infected lymphatic malformation. Another case of extensive left-sided neck inflammation, this three-year-old child presented for the third time with extensive left-sided neck inflammation with some fluid collection and involvement of the left lobe of the thyroid. So whenever you have recurrent neck infections with involvement of the thyroid gland, you should think of an infected third or fourth brachial anomaly, which was confirmed in this case. The third and fourth brachial anomalies present with a fistula strapped to the larynx, which was diagnosed in this case on endoscopy. And the last couple cases are some of the neoplastic conditions, which can present in the emergency setting. So neoplasms involving the orbits of the globe, including leukemia, lymphoma, or neuroblastoma metastasis can present with acute symptoms. Also large masses in the neck, such as neuroblastoma or rhabdomyosarcoma, can present with mass effect on the airway. And finally, lesions like nasopharyngeal angiofibroma can present with hemorrhage and epistaxis. So these are two different patients with leukemia present with acute onset orbital symptoms. The patient on the left side has T2 hyperintensity and inflammation within bilateral orbits, but no fluid collection. So the differential for this would be orbital cellulitis or pseudo-tumor. However, with the history of leukemia, this was presumed to be leukemic involvement and responded to treatment. The patient on the right side presented with a large intraocular mass with mild diffusion restriction and enhancement. Again, on the differential would be a retinoblastoma, but this was a leukemia deposit. And this last case is a newborn who was diagnosed with a large neck mass at the time of delivery. Postnatal imaging shows these multiple, these large solid and cystic mass with some areas of mild diffusion restriction and post-contrast enhancement. So the mass is compatible with teratoma. Unfortunately, this was not known prenatally. That led to severe respiratory complications at the time of delivery. And the brain MRI showed this global hypoxic injury. If a large neck mass is known prenatally, then the delivery can be planned with what's known as the exit procedure, which involves delivering the baby's head and securing the airway before the umbilical cord is clamped. So in summary, for complications of head and neck infections, a knowledge of the routes of spread and high index of suspicion are essential for timely identification and treatment. CT is often the first modality in emergency setting, although MR can be used for more detailed assessment, particularly for intracranial and vascular structures. And whenever you encounter infection in an atypical location or a recurrent infection, an underlying congenital lesion should be suspected. Thank you. OK. OK. Welcome to the last session, the last talk in this session. So there are a couple of physiologic and mechanical differences to considering kids that really result in different patterns of injury and distributions of injury, as well as how easily detectable these injuries may be. And three things to really consider is that, compared with adults, children have a larger head size in comparison to the volume of the body. Their ligaments are not as strong and not as tight, and that they have incomplete ossification, so there are open physis and synchondroses. So these changes really affect the patterns of injury. And the larger head results in a higher fulcrum or maximal point of force for any flexion or rotational injury. It means high cervical injury is actually a lot more common in children, particularly the cranioservical junction through C3, most common in younger children. Around 8 to 10 years of age, there's a more adult pattern with a focus of injury generally centered around C5-6. The ligamentous differences really result in a greater preponderance of ligamentous injury, so ligamentous injury is more common than fractures for kids, as is cord injury without any plain film or CT abnormality. And then the incomplete ossification really leads to different areas of weakness within the spinal column, so the fracture patterns are a little bit different. It's important to remember these different patterns when we think about how we want to best image kids with trauma. And the approach to imaging spine trauma in kids is really not as robustly investigated as it is in adults, as with many things. There are a few clinical decision guidelines, and these have really been incorporated into the new pediatric-specific ACR appropriateness criteria. So I just want to highlight a few of the variants from a very recent publication on suspected spine trauma in children. So this is one of the variants considering children younger than three years of age with a relatively high suspicion for injury. And I'll just draw your attention first to the fact that CT is generally considered to not be appropriate in imaging these really young kids, so that's really a difference from adults and possibly older children, where CT is really the workhorse of your imaging. If we look at older children, the usefulness of CT really increases with age as the anatomic and physiologic profile really approach that of adults. So in children 3 to 16 years, if you look at CT or MR, there was a little disagreement in the expert panel, probably because this is really a very broad age range. So talking about a 3-year-old child and a 15-year-old child is really a different scenario. But CT generally has more of a role in imaging these patients as age increases. I'm just going to talk very briefly about imaging strategies. Oops, there we go. So plain films, two views, AP and lateral, tend to give a pretty good sensitivity. This 90% really is a lot lower in younger kids, studies that have looked at much younger kids. It's not quite that high. Lateral view alone, really not quite as sensitive as two views. And then the role of flexion and extension in odontoid views is really uncertain. There's a lot of conflicting evidence, I think, and opinions out there. Flexion and extension, certainly in the acute setting, can have some safety considerations as well as how accurate that is with acute soft tissue swelling. And odontoid views, particularly again in younger children, can be really difficult to obtain without a real increase in your sensitivity. For CT, obviously, pediatric dosing always applies. Reformations in bone and soft tissue algorithm, I think, is very important, and we'll see a couple of cases of that later on. In MR, this is our current protocol. Our protocols are a little bit in transition at the moment, but generally, fat-suppressed or STIR images, really useful, and I think the fat-suppressed or STIR technique, instead of some of the Dixon-type techniques, don't give quite as much soft tissue contrast. Gradient imaging can be helpful, particularly for cord hemorrhages and prognosis. I particularly like coronals to look at some of the ligaments and some of the relationships, but if you have a 3D and you reformat it, I think sometimes that's just as good. So let's talk about some of the normal developmental patterns. For C1, three major ossification centers. There's an anterior arch, bilateral neural arches. The anterior arch, about 20% are visible at birth, more than 80% by 12 months, so you don't generally see this immediately at birth, but you should see it by one year of age. The yellow arrows here point to the times of relative, relative times of closure of those synchondroses, and although a single anterior arch is the most commonly encountered developmental finding, there are a lot of variant ossification patterns, so be aware that this can have a bit of an unusual appearance and look for sclerotic margins and contours. For C2, there are five primary ossification centers. There's a DENS, vertebral body, and then bilateral neural arches, as well as an apical synchondroses, or an apical ossification that usually doesn't fuse. It's the last to appear and fuse around 10 to 12 years of age. The subdental synchondroses fuses around six or seven years of age, but actually is visible quite a bit longer. So there have been a variety of measurements that have been invoked to kind of tell if the craniovertebral junction is normal or whether it is injured, and I'll just go over a couple of the more commonly used measurements. So Bayesian DENS interval from the tip of the clivus to the top of the odontoid has been reported to really be less than 12 millimeters for plain films. Some people use less than 10 millimeters for CT. There's a little difference in magnification, angulation, visualization of the bony landmarks. Powers ratio, so a line from the anterior margin of the dorsal C1 arch, I'm sorry, from the Bayesian to the anterior margin of the dorsal C1 arch, and then divided from a line from the opisteon to the dorsal margin of the anterior C1 arch should be a ratio of less than one. If you draw a line tangential to the posterior aspect of the clivus, it should really intersect only the posterior most aspect of the DENS, and then some people use the Bayesian axial interval. So if you draw a line parallel to the posterior margin of the axis, extend it cranially, and then drop a line perpendicular to the tip of the clivus. That's been reported in plain films to be less than 12 millimeters. There's actually a fair amount of literature that says that that's not terribly reliable by CT, particularly in kids. I think how translatable, really, are all of these measurements to your practice, though, and I think there are a lot of difficulties in using these in children. One is even studies that look at children often have a relatively broad age range, and if you're gonna look at all patients under 18 years of age, well, clearly, there's a big difference in ossification. So how do you even measure some of these if you don't have a posterior arch? Obviously, there's a significant difference in the appearance of the odontoid over age. One measurement metric that I think has been a little bit more rigorously tested in pediatrics is the occipital condyle to lateral C1 mass. So in adults, this is reported to be less than two millimeters. In kids, there are some studies as well, and again, this is something that obviously varies with age-related ossification, as do most of these measurements. I will draw your attention to the fact that when we are measuring this, we're really talking about the lateral aspect of this interval. Don't measure it medially, you'll get artificially increased measurements. So whenever we're talking about this occiput to C1, we're really measuring it laterally. There have been some studies looking at this broken down by age. So if you can't see the fine print here, this is less than a year, this is one to two years, two to four years, and so on. You can see that in greater than 17 years, the average measurement is around a millimeter, but really it's quite a bit, more than two times that in younger children. So the authors of this paper had recommended that, again, for kids older than 12 years, 2.5 millimeters is still helpful, but if you're talking about younger than 12 years, probably less than four millimeters is a better measurement to use. If we move down just a little bit south to the atlantoaxial articulation, the atlanto-dens interval, the anterior atlanto-dens interval here, so from the posterior aspect of the C1 arch to the dens, should be less than 2.5 millimeters again in older patients and adults, and generally give it up to five millimeters or so in younger patients. Some people will also measure the interspinous distance from C1 to C2, that should be less than 12 millimeters. And there are new measurements coming out all the time, this is from a very recent article in neuroradiology looking at the atlas axis anterior-posterior distance. So drawing a line transversely through the widest part of C2 and then dropping a line perpendicular to the odontoid ossification should be really less than eight millimeters. Some other things to consider, spinal laminar line. So this is generally done on plain foams, but you can do it on CT as well. Along the posterior margin of the spinal canal, really shouldn't have more than two millimeters or so translation, and we can see a little bit of translation at C2, C3 because of normal pseudosubluxation in kids. Also remember that the vertebral bodies look different in younger kids than they do in adults, that there can be as much as three millimeter difference from the anterior height to the mid-vertebral body height, and the vertebrae basically get a more square or rectangular appearance as the patient ages. Also remember that the ring apophyses aren't completely ossified in younger children, and as they begin to ossify, they can look quite irregular. These really shouldn't be offset by more than about one or two millimeters in cranial caudal dimension and about three millimeters in AP dimension. So there are a lot of measurements out there, both for adults and for kids. For pediatrics, I personally, I do use the anterior lantodens interval, and I do use the occipital condyle to C1, but I think there's a lot of, there are a lot of measurements out there, and I'm not sure about the accuracy of many of them, and some of the points to consider when you're using these is, one, there's really limited validation for all age groups. There's very little information about how cervical collar affects these measurements. There are some studies, but not a whole lot, and I think that ligamentous laxity really leads to having a bigger difference in a collar and without a collar in kids than it does in adults. And also, there aren't really any studies that I know of that look specifically at male or female children, so the different ossification patterns, slightly different ossification patterns, can affect, might affect that, too. We don't know. Another thing to think about is that spinal cord injury without radiographic abnormality is unfortunately not uncommon, so it's estimated that maybe about a third of traumatic spine injuries don't have any findings on plain films or CT, so a normal CT doesn't really exclude trauma. And the cord really can't withstand the same degree of distraction that the spinal column can in young kids. One thing we can do to increase the sensitivity of CT, though, is look at the soft tissues, and not just the prevertebral soft tissues that everybody learns about early in residency, hopefully before you take call, but also suboccipital soft tissues. There should be a nice triangular fat pad posteriorly. And supraodontoid here, you can see, actually, part of the tectorial membrane, maybe a bit of the apical or alar ligaments here, so remember to look there. Also remember that the unossified odontoid tip is relatively hyperdense. This is not a hemorrhage. It has a nice, clean margin, nice, rounded margin, which you would expect where the odontoid is. But really, MR is the way to go for ligamentous injuries. So let's look at just a few of the normal ligaments. There's the anterior atlantal occipital membrane. Here in the orange, you can see it's the superior extension of the anterior longitudinal ligament, extends anterior to C1 and attaches on the ventral aspect of the clivus. Small apical ligament coming from the tip of the dens to the clivus. The tectorial membrane, which attaches posterior to the clivus, extends along the posterior margin of C2. There really should be no signal beneath this, between the tectorial membrane attachment and the dorsal aspect of the clivus. You don't wanna see any fluid there. You don't wanna see any edema there. And then the posterior atlantal occipital membrane, posteriorly here, extending from the C1 arch to the opistion. Also, transverse ligaments, or the transverse band of the cruciate ligament, extending posterior to the odontoid and inserting on the occipital condyles, and the aloar ligaments extending laterally from the odontoid. Okay, so let's look at a couple cases here. This is a 15-year-old who had a motor vehicle accident. And if we look at the occipital condyle to C1, lateral distance here, it's about four millimeters, so that's really too much for a patient of this age. The Basion-Dens interval is clearly elongated. And also, if you look at the soft tissue windows, again, I don't have reform as this was an outside CT, but even on axial soft tissue windows, you can see that there is hemorrhage in the spinal canal. On MR, we see many of the classic features of atlantal occipital dissociation. So the anterior atlantal occipital ligament here is completely ruptured. There is a lot of fluid around the clivus and odontoid. We don't see the apical ligaments. The tectorial ligament is evolved and ruptured. Again, you should not see any hemorrhage, any edema beneath that on the clivus. It's a very important thing to look for. The posterior atlantal occipital ligament here, as well, has been ruptured. This is on the STIR, really. We should see suppression of the normal FAPEC there, and there's a lot of edema. Obviously, a large prevertebral hematoma, and unfortunately, compression of the cranial cervical junction and abnormal signal in the spinal cord. This is a three-year-old with a history of a motor vehicle accident. This was a rapid brain that was done for injury. Maybe not the best way to look at the spine, but we did see, again, that there is abnormal fluid beneath the tectorial membrane. Again, there shouldn't be any fluid between that and the clivus. And on coronal imaging, we can see some fluid extending laterally through the cranial occipital junction. On MR, again, the general features that we will see of a cranial cervical dissociation here, there's rupture of the tectorial membrane, rupture of the anterior atlantal occipital membrane, rupture of the posterior atlantal occipital membrane. This is an 18-month-old younger child, MVA three weeks ago, no imaging at that time. This is from an outside hospital. She came to another hospital and had a CT when she was complaining of arm weakness. On CT, we can see that there's a cranial atlantal occipital dislocation and fracture through the odontoid. This is really through the odontoid synchondrosis, and this is the most common fracture pattern for younger patients. Most kids under seven years of age, if they have an odontoid fracture, it's really through the synchondrosis. On MR, again, we can see the tectorial membrane is a vulse. The anterior atlantal occipital membrane is ruptured. Posterior atlantal occipital membrane is ruptured. There's compression of the cranial cervical junction and T2 signal in the spinal cord. And also, this actually is a true history. So while these types of injuries are often fatal for adults and in children, they do tend to survive more commonly. This is a five-year-old with head trauma, pedestrian versus automobile. There's a significant amount of subarachnoid and subdural hemorrhage, as well as a retroclival hematoma, probably a tiny little avulsion fraction off the dorsal clivus. Also bring your attention to, you can see part of the top of the C1 arch only on really the margins of the field of view. But if you look at the scout, clearly there's been a massive and unfortunately fatal distraction injury here. So that, remember to look at the scout films. I think now with reformats, we tend to not look at the scout films as much for fractures and such, but the field of view is typically a little bit different. This is a one-month-old with subdural hemorrhage over the convexity and a history that was concerning for abusive head trauma. On spine imaging, there are additional findings of trauma and traumatic findings in the spine are actually fairly common in non-accidental trauma, predominantly ligamentous injury, particularly interspinous and nuchal, rarely unstable, but important nonetheless. Also soft tissue edema, hemorrhage, particularly subdural, which is thought to be settling from cranial hemorrhage, but still an important finding. And fractures are actually relatively rare. Just to give you a couple of images of what normal soft tissues look like on fat-suppressed ster imaging, you can see high attenuating vessels. They should be linear and branching. You don't wanna see anything that is obviously more significant as in this patient that had a car accident or in this patient that was a non-accidental trauma patient. Again, it's not really linear. It's too fuzzy along the margins. So that's really indicative of injury. Fractures obviously do happen in children as well. I won't spend too much time on this because we're running a little bit late. Hyperextension, injuries of the pars, Pangman's fracture. We can have chance fractures or seatbelt injuries, which are flexion-distraction type injuries. Generally unstable, have high association with abdominal injuries. Teardrop fracture, same as you would see in adults. And then to conclude, I just wanna cover a couple of non-traumatic issues in children. So this is a 17-month-old girl with a refusal to walk. On post-contrast imaging, we can see that there is smooth, diffuse, uniform enhancement of the nerve roots as well as associated thickening. This is a classic finding of Guillain-Barre syndrome. An acute progressive inflammatory demyelinating polyneuropathy typically presents with relatively symmetric findings. And this is usually clinically suspected with ascending weakness, CSF pleocytosis. But sometimes we are the ones to make that diagnosis. Transverse myelitis, another inflammatory disorder, often with a preceding history of earlier vaccination or infection. These patients present with motor, sensory, and autonomic symptoms. Generally central predominant, but involves a rather significant portion, cross-section of the cord. And then this is an eight-year-old girl with right upper extremity weakness. And in this instance, we see longitudinally extensive central T2 hyperintensity, non-enhancing at this point. She, in the emergency room, developed weakness on the other side, lower extremity weakness, quite rapidly progressive. Two weeks later, there's T2 hyperintensity in the anterior horns of the spinal cord. And some new enhancement in the cauda, guanda nerve roots. And these are very typical findings of acute flaccid myelitis, excuse me, which is a rapid-onset flaccid paralysis characterized by rapid-onset flaccid paralysis, typically asymmetric, but rapidly progressive. Has an association with viral infections, particularly enterovirus D8. And generally there's thought to be both an inflammatory component and a direct infectious injury to the anterior horn cells. I wanna bring this up now, particularly because this has a biennial distribution or outbreak distribution. So if we look at the CDC numbers for the last few years, there was an outbreak in 2014, one in 2016. Last year, this gained a lot of press in the US as a polio-like viral outbreak. Didn't hear about it too much this year. Probably next year, this will come to attention again. Infections in children as happened in adults. More often, these are posterior if you have an abscess in the spine, more longitudinally extensive than in adults. And with kids, you always wanna be aware of any underlying developmental abnormality. Is there a sinus tract that wasn't diagnosed? This is another patient actually from last week where there was a small deep paraspinal abscess and an epidural abscess within the spine with some diffusion restriction. Diffusion imaging I think is helpful but not necessary to really make these diagnoses. Cord infarcts do happen in children as well. Rare, can be associated with trauma, although the trauma is not always significant. As an adult, a central T2 hyper-intense pattern is typical, maybe some cord expansion or diffusion restriction. Often the etiology is unknown. This is a patient from recently where they had a proximal vertebral arterial dissection but the nature of the dissection or the etiology wasn't really diagnosed. Tumors, as we talked about, I think in the head and neck section, these are generally not emergencies. They present more typically with insidious weakness but they can still present occasionally with acute neurologic changes, particularly if there's hemorrhage or you reach a critical point. Intramedullary and extramedullary lesions, there are a variety in children, both aggressive and more benign or developmental lesions. And then in summary, I just want you to remember that children have characteristic patterns of traumatic spine injury. Younger children in particular are more susceptible to high cervical injury and to ligamentous injury and cord injury without fracture. So really remember to look at that area and also have a healthy suspicion for CT in this population. And then inflammatory infectious causes are also a common concern for acute spinal cord changes in children.

pediatric head trauma

neuroradiology

skull fractures

linear fractures

diastatic fractures

ping-pong fractures

brain emergencies

vascular emergencies

venous sinus thrombosis

head and neck emergencies

sinusitis complications

spine injuries

transverse myelitis