So, it's nice to have a chest radiologist at this awesome chest meeting. Really excited to be here. And we're gonna, you guys are all here really, really early. I don't know who thought about the 7 a.m., but I've been up since four, so. We're gonna talk about an update on radiographic classification in mediastinal compartments using CT. Disclosures for this talk, and they're not relevant for this. Outline for this talk, you know, the whole point of this talk, for me, is to talk about how we've evolved from plain film. So we've used plain film to look at mediastinal masses, and we've given differentials on that. But I think we can be much better with CT, and I think I'll convince you of that by the end of this. I'll also show you the role of MRI for evaluation of mediastinal lesions, particularly within the anterior mediastinum. We'll define the mediastinal compartments by CT, and this will be a case-based approach. This is a fantastic reference for this talk. I used a couple images from this talk in from this reference, and it's in Radiographics from 2017. Feel free to take a look at this. They really have reclassified how we evaluate the mediastinum using CT by this paper here. So the importance of mediastinal compartments. I think we all know, if you see a mediastinal lesion on CT or on plain film, a focus differential for these lesions is super important, because we wanna be able to communicate with our surgical teams or our interventional teams about how to obtain tissue and what that lesion could actually be. Most systems, be aware, historically use landmarks on the lateral radiograph. And so these landmarks on plain film typically divide the mediastinum into the anterior, the middle, and the posterior compartments. And this is really done arbitrarily, done by non-anatomic divisions of the chest. We'll show you that on a plain film. CT, as I hope I'll convince you, can really divide anatomically these spaces. This division uses a prevascular. You can think about it as an anterior mediastinal compartment. It also uses a visceral compartment. Think of that as the middle mediastinal compartment and a perivertebral compartment. Think of that as a posterior mediastinal compartment. Again, ultimately, we wanna provide algorithms to potentially evaluate these mediastinal lesions with either surgery or intervention. So mediastinal compartments by radiograph. Let's take a look at this. We all know the lateral radiograph. We love it. I tell my residents and fellows, you gotta embrace the lateral radiograph because we gotta be good at being able to evaluate things on the lateral radiograph. So the first thing I'm gonna point out to you, and you can't see my marker, but take a look at the anterior aspect of the trachea, and we're gonna draw a line right there all the way down to the IBC. Everything anterior to that line is going to be, historically, what's called the anterior mediastinum. The second line that's of importance to us is this line that we're gonna draw, and it's gonna be posterior to the cortex of the thoracic spine, about one to two centimeters. Everything anterior to that is gonna be the middle mediastinum, and everything posterior to that blue line is gonna be the posterior mediastinal compartment. And so be aware, this is what everything was sort of based on when we came up with our many differentials, and I think we can be a lot better than that. And when we look at mediastinal compartments by CT, let's compare that lateral radiograph to now this sagittal CT, and if you look at that, we can really define mediastinal compartments. If you look to the retrosternal area, anterior to the heart and the thoracic aorta, this pinkish area we're gonna define as the prevascular space, also the anterior mediastinum, a really nicely defined anatomic space. This area here in the blue is gonna wrap around the heart, the thoracic aorta, and the grade vessels of the mediastinum, the airways as well. This is gonna be the visceral compartment or the middle mediastinum. And then also, we're gonna continue with that same line, which is posterior to the thorax of the spine. That's gonna be your perivertebral area or your posterior mediastinal compartments. We all like to look at images in axial, and if you look at these images in axial, again, you nicely define the area of the prevascular space or the anterior mediastinum. That's gonna be anterior to the aortic arch and also the SVC. The middle mediastinum, you see how it's wrapping the aorta, the SVC, the central airways. That's your middle mediastinal compartment. We draw our line on the thoracic spine, and everything posterior to that is gonna be your posterior mediastinal compartment. As we continue more inferiorly at the carina, same distinctions also along the heart as well. Everything anterior to the heart's gonna be that anterior mediastinum. We're essentially wrapping the heart in the middle mediastinum, and everything posterior to that spine is gonna be the posterior compartment. Now let's apply what we've just learned and use a case-based approach to evaluate the mediastinum. Case number one is a 43-year-old male with a history of RCC. This is a presentation radiograph. I'm gonna give you literally two seconds to look at this radiograph, and then we're gonna mag up on the abnormality here. The abnormality is this tiny line here, and so that is, this tiny line here is displacement of the AP line. This is suggestive of an anterior mediastinal process. So let's take a look at this patient's follow-up CT, and the follow-up CT confirms the finding in the plain film that we have a soft tissue lesion there in the anterior mediastinum displacing that AP line. Where is this lesion? It's in the anterior mediastinum, right? We're gonna wrap this with our purple color there, and you can see that we're anterior to the thoracic gate order and SVC. This lesion ended up getting worked up, and this ended up being a thymic cyst. We'll talk about that workup here in a second. So as we continue to look at this anterior mediastinal mass, just be aware, plain film subtleties can be really difficult. I didn't train primarily with plain films. I make fun of the people, we call them the purists, but I say it secretly because then they'll get mad at me. So the purists love to talk about lines and displacements and this and that. I would tell you if you see an abnormality on a plain film, just pull the trigger and get that CT. I would get a CT with contrast. You're gonna know what compartment that lesion is. CT division is less arbitrary than the kind of non-anatomic divisions I've shown you on plain film, so be aware of that. The whole point here is we wanna improve differential diagnosis of mediastinal masses. Where I think it's really helpful is a large mass. So imagine you've got a six centimeter mass that shows up on a lateral radiograph. That's gonna spill over into the anterior, middle, and potentially the posterior mediastinal compartment. You're not really gonna know where that lesion is. I think with CT you can really help figure that out. Certainly think about evaluating lesions with mediastinal protocol MRI, but I would tell you, make sure you have a person who knows what they're doing, who's gonna read that study and make sure that protocol is appropriate. I have seen this mediastinal protocol MRI muddy the waters in many mediastinal lesions that have come from outside centers. Here's a companion case of a similar lesion in the anterior mediastinum, and this is a follow-up mediastinal mass MRI. If you look here, where's the mass, right? So this is the MRI scout image, and of course it's in the anterior mediastinum. We see this high signal lesion there within the anterior mediastinum. It's anterior to the pulmonary artery, to the heart, and the thoracic aorta. We're gonna continue to evaluate this with a cardiac MRI. Here's an SSFP image. That name is not important to you, but we see this bright structure that's sitting on top of the heart. We've already defined it within the anterior mediastinum. What can we continue to do with this lesion? So with this, we can essentially, all we know is we've got a bright lesion, and so I need to do things to this lesion to determine if it's actually fluid or if it's fat or if it's soft tissue. So our first thought was, this looks like it could be fully fluid, and so we provided an inversion sequence, which basically gives a negative pulse to anything that's fluid. Fluid will drop out if it actually is, in fact, fluid. And if you take a look at that lesion, oh, it didn't work. Okay, you're gonna have to trust me. I don't know why my animation's not working. That lesion actually drops out. It's homogeneous black. So those are the kind of things we can do. We can do these aversion sequences to drop out signal of fluid and fat. Here's a companion case. So this was the companion case, which ended up being a thymic cyst, just like that lesion, which is how that lesion was worked up as well. Here's another companion case of an anterior mediastinal lesion. It's a 27-year-old female undergoing chemotherapy. Here's the presentation CT. And the concern was here within the anterior mediastinum, where we had this soft tissue, triangular-shaped mass. There was concern that we're actually dealing with an anterior mediastinal lesion. And so a follow-up thoracic MRI protocol was ordered. I am not gonna teach you the MRI physics of in-phase and out-of-phase imaging here at our chest meeting, but I'll tell you, if you've got a lesion that's thymic tissue or you're worried about thymic hyperplasia, it should be homogeneously bright on the in-phase image. And if you perform an out-of-phase image to that lesion, it should homogeneously darken, which is what this lesion did here. Again, make sure your protocols are really good before you start making these calls. This lesion ended up being thymic hyperplasia, and we recommended no further follow-up, especially in this patient undergoing chemotherapy. Case number two is a 73-year-old female with new onset shortness of breath and mental status changes. Here's a presentation radiograph. We're not gonna get into being a purist, but I'll tell you, there's a large right-sided mass, right? It looks like it's in the mediastinum, a large right-sided mass. We are gonna get excited about this video that I created. Oh my God, I'm not gonna be able to show it. Oh, yes I am. Okay, awesome. So I was able to do this anterior recon, so I got really excited. I was trying to show you the appreciation about where this lesion is from the start. I'm going anteriorly now here, and you can feel like it's an anterior lesion. We're gonna flip to axial imaging, and we've got an anterior mediastinal mass there. And so I would be remiss if I didn't talk about a follow-up CT-guided lung biopsy, because I do a lot of lung biopsies at Duke. We've got a lot of interventionists here. We have great discussions about who should be doing biopsies. But in this situation, I got right by the internal mammary and performed this biopsy. We got a bunch of tissue, and this lesion ended up being a thymoma. So your differential for anterior mediastinal mass is really important for me that you walk away with a great way to handle these lesions. I would tell you, I tell my residents and fellow, let's just keep this easy. Make your patient 40 years old. If you've got an anterior mediastinal mass in a patient that's younger than 40, we're gonna be thinking about germ cell tumor. If you've got an anterior mediastinal mass in a patient older than 40, we're gonna be thinking about thymoma. And remember, what's gonna cross talk between both of those groups? Lymphoma. That's just an easy, clean way to evaluate, hey, this is my differential for anterior mediastinal lesions. We're gonna jump to case three, which is a 67-year-old male with a history of melanoma. Here's a presentation radiograph. I promise I'm not trying to be a purist, but there's the anterior, there's the AP window. And if you look, there's a little bit of lateralization in the AP window. I don't, I would never call that, okay? So this is lateralization of the AP window. This indicates a middle mediastinal process here. And again, we're gonna look at the follow-up CT for this lesion, and it confirms the finding on the plain foam, which is pretty remarkable. We've got a middle mediastinal mass, necrotic center there. And again, where is that? Of course, that's in the middle mediastinum, right? We're wrapping the descending thoracic order around this. This lesion ended up being a paraganglioma. Moving on to case number four, a 38-year-old male with new onset chest pain. Here's a presentation radiograph. I think we all can see in this patient who's got a prior sternotomy that there is a large right-sided mass. And if you look at the right-sided mass, it's actually silhouetting the right heart border. And so when we silhouette the right heart border, we think of a middle mediastinal process. Here's the follow-up CT, which is really pretty dramatic. It looks like a vascular structure that's connected directly to the ascending thoracic gate order. We always talk about not biasing lesions in the mediastinum. Certainly, you wouldn't wanna be sticking your needle into this thing. And where is this? This is a middle mediastinal lesion. And this ended up being an ascending aortic pseudoaneurysm status post-repair. So be aware, vascular lesions as well. Your differential, really briefly, for middle mediastinal lesions, vascular, be thinking about it. Aneurysm, pseudoaneurysm, most of the vascular structures are centered in the middle mediastinum. Also, dissection in an acute patient. Cardiac patients, right? We're gonna be seeing pericardial cysts often. And so that's gonna show up as a middle mediastinal mass. Have a good MRI protocol for that at your center. Also, cardiac aneurysms, pseudoaneurysms, in those patients that may have had prior MI. We didn't have a chance to talk about airway tumors at all. But squamous cell carcinoma, adenoid cystic, foregut duplication cysts, those will show up as well in your middle mediastinal compartments. Case number five is a 72-year-old female with new onset chest pain. Here's a presentation radiograph here. And so the first thing I'd draw your eye to is just take a look at those hyaluron contours, right? They're standing out, they're staring at you in the face. Also take a look here at this lateral radiograph and look at that spine fracture. So first we're gonna draw our eyes to the hyaluron contours. And I would tell you, purists would call this a hyaluron overlay sign. So that means that I can see the pulmonary arteries through something that looks like it's over those pulmonary arteries. That's a hyaluron overlay sign. You only know that you're dealing with either an anterior or a posterior mediastinal process. The lateral radiograph is gonna help you there because you see that it's centered on the spine. There's soft tissue there. And so again, hyaluron overlay sign, the lateral radiograph helps us here. This patient had a follow-up CT. Big destructive process centered on the thoracic spine confirmed in coronal imaging here. You can nicely see this big angry process going on there. Where is this centered? Of course it's in the posterior mediastinum. We're centered on the thoracic spine. The lateral radiograph again shows us the finding that we saw on plain film confirmed on sagittal CT as well. A really pretty impressive case of a posterior mediastinal lesion that ended up being osteomyelitis, disguidance with paraspinal abscess. Our last case is a 26-year-old male with chest pain. Here's a presentation radiograph. And I'll give you two more seconds to look at this. We're gonna mag in here and you're gonna notice that you see the right heart border, but inside of that right heart border there's another line. And so what is this? This is a displaced paraspinal line. This is indicative of a posterior mediastinal process. Follow-up CT for this patient pretty strikingly shows the soft tissue lesion there adjacent to the thoracic spine. In addition to that, we see enlargement of the thoracic posterior ribs as well. And that's confirmed on plain film as well. So enlargement of the ribs, the soft tissue lesion centered on the posterior mediastinum. This last case ends up being extramedullary hematopoiesis in a patient with sickle cell anemia. A nice look for a posterior mediastinal mass. Have a good differential. Be aware of the descending thoracic aorta lives there. So any kind of vascular abnormality could certainly be in that differential. Bony findings such as discitis and osteomyelitis or hematoma, I do a lot of biopsies for posterior mediastinal masses that end up being neurogenic tumors. So schwannoma and neurofibroma as well. So mediastinal compartments by CT, I hope I've convinced you they are so much better at defining what a lesion could be over plain film. We've shown you the role of MRI. I would tell you I'd reserve it for anterior mediastinal lesions. That's all gonna help with your differential diagnosis. Thank you all for your time. Appreciate it. All right, next I'd like to introduce Labib Dabian. He is an interventional pulmonologist at Henry Ford where he also serves as director of pleural diseases. Good morning, everyone. Thank you for participating in this session. My name is Labib Dabian and I'm gonna be presenting to you today on infection in the mediastinum. I have no disclosures. So what I hope to achieve today is to be able to provide an overview of infection in the mediastinum but also maybe highlight some key elements related to the diagnosis and the management of this condition. We're gonna start with a quick poll question. If you wanna pull up your phones and scan that QR code, I'll give you a few seconds here. So the first question is, which of the following is the most common cause of infection in the mediastinum? Self-visual perforation, trauma of the chest, chronic fibrosing mediastinitis, mediastinal extension of lung infection, head and neck surgery, descending infection, or cardiovascular surgery? The poll should be active in a second. Okay, I think we've got about 24 votes. So, oh, I see a mixed response here. With the vast majority choosing actually mediastinal extension of lung infection, it's actually the second most common. Cardiovascular surgery, post-operative mediastinitis is the most common cause of infectious mediastinitis. So, we talked about anatomy through chest X-rays, plain films, and CT scan, but I wanna remind everyone, if you go back and review anatomy from Moore's Clinical Anatomy or Netter's, all the stuff that we studied in medical school, they actually define the mediastinum as two compartments, superior and inferior, and then the inferior compartment is actually subdivided into anterior, middle, and posterior. And this has been separated by the sternal angle line. Now, this definition is the classic definition, but what we've noticed with time is that organs do cross from a compartment to another. So, when it comes to the infection in the mediastinum, we need to locate the source and where the injury happened, and it could be affecting more than one compartments at once, and so, hence, in more modern days right now, with the CT scan and the high quality of CT scans, we're kinda drifting away a little bit from this and just trying to divide it into three compartments, as we just heard earlier, anterior, middle, and posterior, and we think of them as cylindrical spaces, vertical spaces. So, when you review the literature, you may see the word superior mediastinum used quite often because it's well-published in the literature. So, what we need to be aware of is what organs run where when we're worried about infection in the mediastinum. The anterior mediastinum, the most important thing is gonna be subcutaneous tissue, in fact, connective tissue, maybe some remnants of the thymus, some lymph nodes. The middle compartment is predominantly the heart and the roots of the blood vessels, and then the posterior compartment's gonna have most of the important intrathoracic organs, with the exceptions of the lungs and the pleura. So, that's the esophagus, aorta, SVC, azagus vein, trachea, et cetera. The superior mediastinum, the one that we're not necessarily using as a terminology a lot these days, do contain a lot of important structures, too, and could play an important role with descending necrotizing infection. And to mention a few, that would be the trachea, the esophagus, the aortic arch, the branches of the aortic arch, as well as the SVC and brachycephalic vein. An important understanding of the anatomy is key here, because when we're facing a patient with a potential infection in the mediastinum, we wanna know and understand very well what the anatomy looks like. So, mediastinitis, in general, is a life-threatening condition. If someone has a diagnosis or you're suspicious of mediastinitis, it's an urgent thing to address and treat as soon as possible. If you wanna define it, it's inflammation of the mediastinal tissue, and it can be divided into acute or chronic. Acute typically tends to be the infectious type, and the most common organism is a bacterial infection. Chronic mediastinitis is predominantly inflammatory, although it could start by an infection that could be the inciting event, and then it turns into more of a chronic inflammation, such as chronic fibrosic mediastinitis that we're gonna hear about a little later today. So, causes, direct invasion from surgery. We said that's the most common, it's post-operative, but also extension from any surrounding tissues. It could be the head and neck above the mediastinum, could be the lung, the chest wall, esophagus, retroperitoneum. Very rarely, it could be a hematogenous spread or lymphatic spread. Incidents, in essence, not quite common, 0.5 to 2.2%, but if you practice in an area where there's a large cardiac surgery population or heart transplant population, that incidence is much higher and can reach 7.5%. It's usually within the first 30 days and typically within actually the first seven days that you should encounter it. Symptoms like any infection, fever, tachycardia, cellulitis, but on top of this, we're gonna look at sternal instability, crepitus, subcutaneous emphysema, wound dehiscence as a hallmark of that disease. Now, when you think of what's gonna predispose my post-operative patient for mediastinitis, we have to think of risk factors. Some of them are preoperative, some are intraoperative, and some are post-operative. The most important three preoperative risk factors are nasal colonization with Staph aureus, that's collected on the nasal swab, diabetes, and obesity. If you're gonna remember any of those, those are gonna be the top three. Obviously, tobacco smoking and stage three disease, COPD, all that will predispose you as well. The intraoperative risk factor is the duration of the case and how long are they on bypass and how long is that aortic clamp for. And obviously, emergent-urgent surgery. So the longer the duration of the procedure, you suspect the higher the chances this patient may have an infectious mediastinitis. And post-operatively is gonna be how long are they spending in the ICU, how long are they on the ventilator, do they need to go back to the OR for a redo surgery, all this will predispose them to that condition. So there has been some risk indices that were designed so that clinicians could use them and try to predict the chances of this happening. I think the one that I liked the most was by Friedman and colleagues because it simplified it into a three-point scale. Do they have diabetes, yes or no? Is their BMI between 30 and 35 or above 35? And you can see for each one of them, you get a point and if you're more than 35, two points. every point will double the risk of infectious mediastinitis. So you could do the math depending on what your patient has. Infectious mediastinitis postoperatively tends to be monomicrobial as opposed to descending necrotizing mediastinitis which tends to be polymicrobial because it affects the skin, the oral flora. And the most common organisms by far are actually staph organisms between MSSA and MRSA. You're about 61%, so it makes sense to cover for that first or at least definitely ensure that we cover for that organism. But it can happen with gram negatives, can happen with streptococci as well. There has been numerous case reports of all sorts of mediastinitis, Legionella, mycobacteria abscesses, outbreaks. All of these are possible, not quite common though. So on imaging, imaging by the way is the diagnostic methodology of choice for that condition. And we're looking at multiple different things. We're looking at sternal disruption. Sometimes in the mediastinum there'll be some swelling. We could see air in the mediastinum. I do wanna caution you that postoperatively air is not uncommon after CABG or cardiac surgery. But when it lasts more than three weeks and with presenting symptoms, you should suspect potential mediastinitis. And obviously fluid collections are not expected for a long duration of time postoperatively. So how do we diagnose postoperative infectious mediastinitis? We need to have one of those three per CDC guidelines. Number one, either a positive culture, that is you aspirate the mediastinal fluid or you get some tissue that you culture. Or you can have evidence of mediastinitis on pathology. Those are patients who go for debridement and they collect tissue collected and you can see it on pathology. If you don't have the first or the second, you should have at least one clinical sign of either chest pain, fever, sternal instability. And another accompanying sign of either purulent discharge or mediastinal widening to make that diagnosis. And the management is gonna be a combination of both medical and surgical. Medical usually with antimicrobial therapy. You wanna cover for MRSA for sure and some grand negative bacilli until you have a culture. The optimal duration is not known yet. But for the most part, if the infection is close to the sternum and you have concern for osteomyelitis, most likely it's gonna be prolonged four to six weeks. The surgeons have different strategies of addressing postoperative mediastinitis. But for the most part, it's either gonna be a debridement with initial closure or debridement with placement of a flap or debridement with placement of a wound vac. And the wound vac in a meta-analysis was shown to actually help with the drainage, promote granulation tissue. It even decreases the length of hospital stay and reinfection. But in all reality, none of them have been compared to each other to know which one is superior. So it's actually left to the clinician's decision to choose whatever is fit for that patient. The second condition we're gonna talk about today is descending necrotizing mediastinitis, second most common. It is still a rare condition, more common among men and typically in their 80s. And diabetes, once again, is a predisposing factor. But here we have smoking, heavy alcohol use, IV drug abuse, all of that, and poor dentition obviously can predispose you to this condition. So this is another slide summarizing anatomy. So the anatomy of the head and neck is quite complex. But what you wanna think of is there are multiple fascial layers that kind of overlap and sometimes even it invests the different organs. And by coming close to each other and away from each other, they create potential spaces. And the three most important spaces we need to remember are the retrophangial space, which is just behind the pharynx or posterior to the pharynx, and then the prevertebral space. And in between, there's a space called the danger space or danger zone. And the reason we call it the danger zone is because that space that's here in green, it's the one that actually extends way down and communicates with the mediastinum. So an infection that spreads from facial layer to another facial layer and hits into the danger zone could potentially lead into a descending necrotizing mediastinitis. And I've included this post-mortem dissection just to kind of like remind myself and make myself truly believe in facial layers because they actually do exist. You can see them, you can dissect them. But for the most part, that space is collapsed and it's a potential space. So what can cause, what are the most common causes of descending necrotizing mediastinitis? Either it's coming from the oral cavity tooth or dontogenic or it's pharyngeal abscesses, infections, et cetera. Now a lot of other infections within the oral pharynx and nasopharynx could lead to that condition as I've listed here, including traumatic intubation that can cause laceration, introduction of a microorganism and eventually an infection. And we've all heard of Ludwig's angina, which basically is an infection of the submandibular space and the floor of the mouth. Diagnosis, once again, CT scan is the modality of choice where you're gonna use it with contrast for that purpose. We're looking at increased density in the adipose tissue. Sometimes those mediastinal planes become a little bit obliterated. We can see air fluid collections and obviously lymphadenopathy in the head and neck as well. As for the treatment, we have to think of the source since this is coming from the oral pharynx or nasopharynx. This is polymicrobial, so we need to have broad spectrum antibiotics covering for gram-negatives, gram-positives and anaerobes. But also assess first if the patient is safe in terms of airway patency because many times those abscesses or swelling in the oral pharynx may require protection of the airway before proceeding with surgery or any other treatment. And as to what thoracic surgeons would wanna approach this, it depends on where the infection is. Is it in the anterior mediastinum or posterior mediastinum? In the anterior mediastinum, it makes sense to have a medium sternotomy with quick access to it. With posterior mediastinum, sometimes they do the clamshell incision that they do with lung transplants. Sometimes they need to do unilateral or bilateral thoracotomies to be able to do the tissue debridement that's necessary. So the last condition I'm gonna talk about out of the many is actually mediastinitis from esophageal perforation because it's something that we all encounter in day-to-day practice. And it's rare, but it's catastrophic. As you probably know, those patients can go from being just clinically stable to septic shock in the ICU with high mortality rate, up to 40%. And where is the weakest point in the esophagus? It's usually at the physiologic narrowing. So that's up at the cricopharyngeus muscle or down at the GE junction. And obviously, risk factors predisposing to this would be prior alcohol use, malignancy, anything that can weaken the esophagus. If you look at the vast majority of causes of mediastinitis from esophageal perforation, it's usually atrogenic. So if you get sent a patient who just recently had an EGD, we have to just, and they're developing chest pain, a new left pleural effusion, fever, et cetera, we should be highly suspicious of this condition. Overall, the incidence from irregular standard diagnostic EGD is not high. It's 0.5%, that's why we don't see it a lot. But if you proceed with doing dilation of strictures or akalasia, the process of dilation could increase that incidence up to 6%. Obviously, during surgery, if you're doing anatomical lung resections or cardiac surgery, the esophagus, if it's in the way, you could potentially injure that. So that's your 50%. But obviously, heavy retching like Burhaff syndrome can cause a spontaneous perforation, trauma, malignancy, with necrotizing masses can lead to that, and foreign body ingestion as well. And what you're looking at are symptoms of mediastinitis. Infectious mediastinitis would be classic fever, tachycardia, hypertension, but we add here chest pain, vomiting, and subcutaneous emphysema as well. Your microorganisms are pretty similar, for the most part, to descending necrotizing mediastinitis. You're gonna have a combination of anaerobes, aerobes, and sometimes even fungal infections such as candida. So again, when you're doing your antimicrobial therapy, you wanna make sure you cover for all that. CT scan, again, is the diagnostic modality of choice. We can give it with oral contrast. You wanna make sure you choose a water-soluble one, such as gastrographin. And it will show you if there is esophageal thickening, if there is air fluid collections. Sometimes you have an associated pleural effusion, which typically is on the left side, or a pneumothorax. Studies have looked at analysis of pleural effusion post rupture, and it tends to be an exudative with a low pH and low glucose, and a high ratio of pleural to serum for amylase. So amylase is one of those, I guess, tests that you wanna check on your pleural effusion. Obviously, the LDH is quite high. It's an exudative effusion. And here, the last slide about management. The management of esophageal perforation depends on the presentation. That could be a medical, surgical, or interventional. Medical treatment, antibiotics, with attention for antifungal coverage. But also, you wanna make them NPO, put a feeding tube, and decrease the acidity in the stomach by doing acid suppression treatments. Surgical repair, it depends on how stable they are. If they stay able to undergo a surgical repair, this is probably the mainstay, and this is everyone's goal, is to try to get them there so they can get a buttressed flap and debridement of the necrotic tissue. You leave a chest tube for the infected pleural space in mediastinum, and sometimes, you even have to do a lung decontamination. But occasionally, patients are sick enough that they cannot undergo that, and this is where we go to minimally invasive approaches, such as placement of endoscopic stents. So take-home points from today. Infection in the mediastinum, just think it's life-threatening, high mortality, 40%. Most of the time, it's gonna be bacterial infection, so this is what we're gonna cover for. And the most common cause of it is postoperative mediastinitis, if any one of you is rotating in the SICU or surgical ICUs, just remember this. And chest CT scan is your diagnostic choice of modality. If you're ever suspicious of it, try to get that done as soon as possible. And it's very important that we have a high degree of suspicion of infection mediastinitis, because the sooner we know of it, the sooner we can treat it, the better the outcomes are. Thank you. So, what is inflammatory and congenital disease in the mediastinum? I have nothing to disclose related to this topic, and I'm just gonna touch on the big highlights of these benign etiologies of mediastinal disease. So, mediastinal granuloma, chronic fibrosing mediastinitis, and then I'll hit the most common congenital abnormalities, which are cysts in the mediastinum. So, first, mediastinal granuloma. So, I'm not just talking about the little calcified granulomas that you get from histoplasmosis, right? I'm talking about a granulomatous mass that occurs in the hilum or mediastinum, and that can be an uncommon immune response to prior insult or infection, and it might account for up to 10% of mediastinal masses. Generally, we think about it being related to the fungus where the patient has lived or where they're currently living, but truly, less than 1% of the patients, for example, that live in histoprone areas actually go on to develop either mediastinal granuloma or fibrosing mediastinitis. Other infections to think about, of course, are TB, aspergillus, and there's several others, but those are the big ones, and then it's important to think that most of the time we don't know the exact organism that caused this immune response that led to the granuloma or actually, alternatively, the fibrosing mediastinitis. Certainly, the granulomas are more common, and then what happens is generally the involved mediastinal nodes will enlarge and often they'll coalesce, and they can become, if it's caseating, a big necrotic mass, so here's a nice picture of a subcarinal. Generally, it can actually be self-limiting, and they can get spontaneous resolution unless there's notable compression causing symptoms or if it develops into a fistula. Often, they're found incidentally, again, in younger patients, so 20s to 40s. It's generally heterogeneous density, you get rim-enhancing and scattered calcifications, and often you'll see other things that lead you to believe it might be due to an endemic fungus, whether it's other areas of calcification in the spleen or within the lung. You can biopsy if your radiologist says it's atypical or you can't quite figure out because it just doesn't hit a traditional picture. You certainly can biopsy, and at that time, you'll see significant inflammation with either caseating or non-caseating granulomas, but again, generally negative organism staining. You'll find occasionally an organism, if you get it right after an acute infection, if the patient's immunocompromised or alternatively, if there's significant necrosis. And how do you manage these? Generally, most patients are asymptomatic, so you're just gonna follow them radiographically over time. And again, if it's an atypical presentation and you're not quite sure what's going on, do an EBIS or a mediastinoscopy. And then if they're quite symptomatic, of course, you can send them for an excisional biopsy. Here's a nice picture of a granuloma from histo. And then there's the chronic fibrosing, otherwise known as sclerosing mediastinitis. It's quite rare, and it certainly can mimic malignancy. It's quite aggressive fibroproliferative process that can encase things in the mediastinum, whether it's airways or vessels or the esophagus. And it's really just a super dense fibrotic mass. Generally, though, it's in younger people. And symptoms vary depending on what's being constricted. So whether it's short-windedness, hemoptysis, dysphagia, hoarseness, pleuritic pain. We think that it's mostly related to infectious etiologies. And again, it's an aggressive sort of immune response secondary to a prior infectious insult. So generally from histoplasmosis, but certainly other areas of the US with endemic fungi, we see it as well. TB, parasites we've seen. And then there's other potential etiologies like IgG4-related disease, autoimmune disease like lupus, some of the ankylovasculitis diseases. And then sarcoid, of course, and prior radiation to the mediastinum. And there's the idiopathic multifocal fibrosclerosis, which is super rare. And then medication that used to be used for migraines that's no longer on the market because it had so many side effects. So what does this look like? On chest X-ray, there's, of course, diffuse widening of the mediastinum. And then on CT, you get this dense infiltrating fibroinflammatory tissue. And I think the key here is that it disrupts the mediastinal fat planes. And often, they'll end up in our clinic because everybody's worried that this is a potential malignancy. And it can encase or invade adjacent structures. And again, often you'll see sequelae of granuloma disinfection, whether it's calcified granulomas in the lung, the spleen, other calcified lymph nodes. And if, again, it's not a typical presentation, or if you can't rule out that malignancy is involved, or that this could be malignant, then you definitely wanna biopsy it. Whether it's EBIS, mediastinoscopy, VATS, just remember that it can potentially lead to increased rates of bleeding. And if there is concern for potential underlying autoimmune disease, or IgG4, you can certainly get labs as well. And this is a nice picture of on biopsy. Yeah? You know, you certainly can, but the challenge is, if it's an aggressive inflammatory process, it's certainly not gonna, you're still gonna be left with what caused it, right? Here's a nice picture of kind of acute and chronic dense fibrosis on pathology. So what do you do about this? Well, the challenge is, there is no curative therapy, right, for this fibrosimediastinitis. Certainly antifungals have been tried, but actually with minimal success. If it's related to an immune process, an autoimmune process, certainly immunosuppression may be helpful, and is worth a try. But generally we focus on treating the symptoms associated with it, stenting of the compressed airway, the compressed vessel, esophageal stenting, certainly all is possible. And if they're having hemoptysis, you can certainly have IR do an embolization, or alternatively, if you're bleeding from the airway, endobronchial ablation. I put together a little chart that anybody can come back and reference that I felt like helped me better differentiate between granuloma and fibrosimediastinitis that kind of helps better understand how, where they come from, how they present, what they look like radiographically, and then how to treat them. Next I'll move on to the congenital lesions of the mediastinum, which generally I'm gonna hit the big things, which is really just cysts. 20 to 32% of the lesions within the mediastinum are congenital, and gosh, almost up to 20% of those mediastinal lesions are cysts. Bronchogenic cysts are the most common. Here you can see the other types there. And excluding those that generally only occur in women, the malarian differentiation cysts, generally they occur in males and females equally. And just like everything else I've talked about, it's commonly detected in patients in their 30s and 40s. Most of them are not found incidentally when you're getting a CT scan for some other reason, and most of them are asymptomatic. Most of the congenital cysts that I'll talk about today are actually in the middle mediastinum, and that's where they're found most frequently. And this is just, again, one that you can go back to for reference that kind of goes through all of the big cystic lesions, features, and their pathologic features. But bronchogenic cysts being the most common, I'll spend kind of the most amount of time on. It's the result of, again, an abnormality during embryonic development in the tracheobronchial system, and it's essentially a foregut duplication cyst that happens between 24 and 40 days of gestation. You can see here what the pathology looks like with its pseudostratified ciliated columnar cells. Most of these patients are asymptomatic, but many of them, up to half, can go on to have symptoms. And just like everything else I've talked about today, their symptoms are related to what is being compressed. So whether they get a cough, dyspnea, dysphagia, infection, arrhythmias, it just depends what they're pressing on. And radiographically, here, of course, there's the chest X-ray that shows something rounded and well demarcated, and with a fluid density, but obviously it's a lot easier to see on CT. Occasionally they can be parenchymal, but generally they're mediastinal, round-shaped, thin wall, homogenous, and generally not a lot of enhancement. Next, the pleural pericardial cyst. Unilocular, and it's a nice single layer of mesothelial cells, if you go ahead and biopsy it or resect it. And it is derived from the mesothelial lining of the thoracic cavity, which is why most of them are located in the right cardiophrenic angle, and they're rarely connected to the pericardium. Again, symptoms are related to whatever it's compressing. Generally you can get shortness of breath, cough, arrhythmia, and if it's real big, you can get some right heart failure. Thymic cysts, a small percentage of mediastinal cysts are thymic cysts, and they arise from a remnant of the thymopharyngeal duct. Here you can see the pathology there. The key is finding thymic tissue in the biopsy, and it's generally a nice, clear fluid in there. And of course, generally it's found when you get a CT for another reason, but you can be symptomatic if it's compressing anything. And then I'll briefly touch on the enteric cysts. So again, all of this has to do with abnormal development from the foregut, and they grow as blind sacs containing whatever type of enteric epithelium. So whether it's esophageal, which I'll talk about first, or gastric, which I'll talk about in a second. Here, potentially it's more common in men, but generally we see these in kids more so than adults. And for the esophageal cysts, they're generally adjacent to or within the esophageal wall in the lower posterior mediastinum, and they can certainly cause dysphagia, cough, shortness of breath. And they're more likely to be associated with esophageal atresia, TE fistula, or a pulmonary adenomatoid malformation. And here you can see the pathology and the radiology there. Again, most of the time they don't make it to our clinics because they've been caught before. And lastly, gastric cysts, kind of equivalent in male versus female. And they're often symptomatic because of the acid secretions of the gastric cells that are there, and certainly can lead to perforation, erosion, cough, vomiting, infectious symptoms, and it may be associated with other abnormalities like a vertebral malformation. And here you can see it there on pathology with gastric epithelium and a thick fibromuscular wall like the stomach. And then, so what do you do about these once you find them? Again, most of them are asymptomatic, at least initially, so often you just follow them radiographically or, you know, with observation. And then if they're symptomatic, surgery remains the gold standard of treatment. Generally it's via vats. They often, if they're quite big though, they can get a thoracotomy. And certainly if it's ruptured or there's severe adhesion to the nearby structures, then of course you'll have to do it open. And the complication rate can be quite high. And theoretically, although not statistical, you can get an increased amount of complications if the patient is very symptomatic. And these include bleeding, mediastinal structure injury, infection, and persistent air leak amongst, we're kind of the top four there. And then of course you can go to your interventional pulmonary colleagues and ask for therapeutic drainage of the cyst. And generally we think about doing this in patients who are not surgical candidates or if you need to urgently decompress to minimize the surgical risk. And if you're very worried about infection, you could certainly do that. And the theory with EBIS drainage is, of course it would immediately help the symptoms, but it also allows the cystic walls to collapse. And the injury induced by the needle penetration and the walls coming together could theoretically cause adhesion and reduce recurrence. It does actually have the same complication rate as surgery and includes infection, recurrence, rupture, and arrhythmia. And there's several articles out there that just suggest for all of these patients you do it on using antibiotics afterwards. And here's a nice ultrasound EBIS picture of the cyst, stabbing the needle in it, and then sucking out the fluid. And it gets smaller as you do it. I'd like to introduce your own guest author. He is an associate professor and associate director of interventional pulmonary at UCSF. Thank you, everyone. So we're going to talk about the malignancy aspects of mediastinal disease. These are my disclosures, not relevant to here. And basically, the aim of today is just to give you enough nomenclature and enough sort of insight into what the discussion should be in handling these malignancies in an interdisciplinary fashion. I'm really just going to cherry pick a few sort of top malignancies to talk about and then give some cases. And I'm extremely grateful that Joe went over this article. I think it's a great article, whoever has a chance to read it. So I'm not going to go over sort of that in detail. That again, the only thing I do really want to touch on and spoke about sort of the tissues in each mediastinal compartment and the rationale behind each organ that exists in each sub-compartment would give rise to a specific tumor. That's important to know also. But just the mass effect and the infiltrative effect of a tumor. The chest is a fixed box. There's not a lot of room for places to grow. If one organ grows, it displaces another. And that's usually where we get involved as pulmonologists, the displacement of airways, the invasion of airways, and the vascular piece. We're going to go pretty quickly through the posterior and the middle aspect, middle compartments, and then we'll spend a little bit more time on the anterior compartment, which I think is more relevant to us. So posterior mediastinum tends to be neurogenic masses, tends to be schwannomas, nerve sheath tumors, tends to be less invasive with age. Younger kids tend to have more metastatic disease. Less common, you can have sort of extensions of thyroid goiters, esophageal masses. Diagnostics tend to rely heavily on imaging, and oftentimes you can even just proceed to surgical resection, not so much for sort of prevention of metastatic disease, but even just for local control. A lot of times these patients have pain, sort of neurological complications, and the decision can be made to proceed to surgical resection even without biopsy based on imaging alone. Two main modalities, as we were talking about before, CT scan is good to identify the site of origin, identify sort of any local invasiveness, but also to look for metastatic involvement elsewhere. MRI is very helpful to sort of subclassify, and again, if you guys have questions, Joe is on the second row. Please feel free to talk to him after. Middle and medistinum, this is actually a frequent place where we as pulmonologists visit. This is where we're working when we're doing bronchoscopy. This is sort of our wheelhouse. Most commonly we're going to be evaluating for metastatic involvement, either from a primary lung cancer or metastatic disease from somewhere else, or lymphomas, either primary or secondary. Esophageal thing, we spoke about the cysts. Most commonly we're going to be talking about lung cancer staging. Probably talk all in and of itself, so I'm just going to sort of ignore it right now. The most common cancers, carcinomas that we're talking about are going to be the lung, head and neck, breast cancer, and melanomas. I just brought here an image of Castleman disease, which is something we don't see common, so I thought it was kind of cool. Very hard to biopsy in terms of getting a pathological confirmation of, yes, this is Castleman. I usually start to think about Castleman's when I'm biopsying it. I know I'm in the lesion, and Pat keeps saying, no cancer, nothing, nothing, nothing. That's when I start to think about Castleman, so I just thought it was a cool image to talk about. And this is a complex way of talking about what Joe has so eloquently and simplified. Less than 40 germ cell tumor, above 40, you have to start thinking about stuff like that. What was it, a thymic disease, and in between, lymphoma. This is basically saying that. That there's a lot of age impact and gender impact on what the disease that you're thinking about in the anterior amyotostoma is. So, just like we said, with age, the proportion of lymphoma decreases. Thyroid cancer increases a little bit with age, and thyroid cancer and thymic cancer. Excuse me. So, let's talk about thymic cancers. Not gonna go into this too much in depth, but it's important to realize that there's also a bit of a spectrum to thymic cancers, right? So, the way the WHO classifies this is from A to C, with different mixed morphologies, where A is essentially benign disease, B where you start to see malignancy, and basically C defines straight out carcinoma. Then there's all sorts of mixtures of A and B. And a lot of the staging, the T component of the staging, has to do with capsular integrity. And I'm glad that we have a thoracic surgeon in the audience who can keep me sort of straight about this. But one of the main considerations, and I'll talk about this a little bit later, is when to biopsy these versus going straight to surgery. And a lot of that, again, has to rely on sort of what's the concern of this being a true carcinoma, and versus breaching that capsule. Because breaching the capsule can have its own set of issues, which I'll go through in a bit. You know, how do you start to think about thymic cancers? Typically, incidentally found on imaging, but oftentimes you can evaluate it for other associated diseases, such as myasthenia is a common autoimmune disease that's associated with it. The main differential you're gonna think about are NUT, which is basically midline cancers, squamous, and various thymic hyperplases or cysts. Another thing to think about in the anterior mediastinum is gonna be lymphomas. Most common mediastinal malignancies can be lymphoma. There are two, there are a few ways to sort of classify mediastinal lymphomas. There's gonna be primary versus metastatic from elsewhere. We'll talk right now just more about the primary mediastinal lymphomas, where T-lymphoblastic lymphomas are gonna be the most common. PMBCL is a type of diffuse B-cell lymphoma, felt to be potentially originating from B-cells in the thymus, tends to be very aggressive. These are the ones that we're gonna hear about. These are the ones that are infiltrating the airways, causing various SVC syndromes, things like that. Mediastinal gray zone lymphomas, when it's sort of non-classifiable, felt to be similar, also can behave in a very aggressive fashion. And then there's Hodgkin's lymphomas. I give you guys an example of Reed-Sternberg cell. One of the issues with lymphomas is that it's very important to be able to give the pathologist enough tissue so that they can define the structural architecture of lymphomas. It's key for treatment, it's key for prognosis. One of the issues that we struggle with in small samples is providing that level of detail to the pathologist. Crushed artifact, all sorts of things that just basically ruin the sample. Which is why, though FNA is very safe and very easy to go, sometimes it's not enough. And we'll talk about that also in a little bit. I'm also, sorry, I should mention, IHC. They go through a lot of stains with these. Tissue volume is also very important. So here I'm just going to give a quick example of a patient, 30 years old, who, never smoker, and very healthy, presents with weeks of dyspnea. This is his initial imaging. And on core needle biopsy gets a diagnosis of PMBCL. I get involved as the interventional pulmonologist saying, hey, should we stent that lesion? This is a great case of when not to do something. Admitted him, he was able to get therapy pretty quickly, and his disease melted pretty quickly. And he has sustained benefit from therapy going three years later. Next tumor that I want to talk about is, okay, I'm going to run, sorry. Next tumor I'm going to talk about is thyroid disease. Increasing in incidence, very common. A little bit more predominant amongst women. Very few different types. Most commonly we're going to classify these according to well differentiated versus poorly differentiated. Well being papillary and follicular, poorly differentiated. I'm going to shelf medullary carcinoma for a bit. All you need to know is that it's an aggressive tumor, typically sporadic, but can also be familial. But really just the spectrum of disease between poorly differentiated and anaplastic, which can be very aggressive, and can often be concomitant with well differentiated carcinomas. Ultrasound and FNA are essential diagnostic tools. Typically you can even make the diagnosis on FNA alone, and I'll talk a little bit about that. But one thing that we have to think about as providers is what's the genetic profiling? BRAF mutation is one example. RET is another example, which have been really paradigm changing for these aggressive tumors. I'm talking mainly about the poorly differentiated and the anaplastics. This is a case that I'll just skip through really quickly, but a patient with anaplastic tumor who presented, had airway involvement, got involved, stented the airway as a bridge to therapy, got a RET-targeted agent, and was able to sort of get the stent out after regression of her tumor. Here I'm just going to say diagnostics, really imaging. The issue with labs and clinical evaluation is very vague and very nonspecific, but I think it's just good to know about these biopsies, biopsy routes, right? So really three main ways to think about biopsy routes. One is needle, which we all know about, bronchoscopy, endoscopy, and surgical. Some consideration for what biopsy approach to think about. And this is where the imaging will really inform you. With thymic malignancies, for instance, if you breach that capsule, you can either track seeding or drop meds, which can be seen up to a decade later in their case reports, where basically you sort of cause pleural seeding later on. And this is one example that we had where just years later after surgical resection, a little thymic implant at the base sort of leaves you wondering, which is why it's very important to get surgical input up front to see if you need to get just resected without even doing a biopsy. Lymphoma we spoke about. There's a wide range in terms of what's reported in the literature as diagnostic yield. I typically cite 80% for E-Bus and small needles. I try to really identify different sites for excisional biopsies. Thyroid, FNA is great for the well-differentiated. The problem is that there's a lot of times concomitant, well-differentiated anaplastic tumors, which you might miss. Very important to sort of think about that. And sometimes you need to do excisional. Start with surgical approaches for biopsying the anterior mediastinum. You guys all know mediastinoscopy. Historically, this was the main workhorse for evaluating the mediastinum. Do an incision in the neck, and you sort of blunt, dissect through sort of fascial planes. That's them telling us to stop? Okay. You guys feel free to leave, I'm sorry. Anyway, overall very safe. Some events that can happen, recurrent laryngeal nerve disruption, which can get better. Life-threatening bleeding, which can be a problem. And tracheal tear and pneumothorax, which are less common, but can also be an issue. One of the issues with mediastinoscopy is that once you've done a mediastinoscopy, it's hard to go back. You scar up the area, it becomes very difficult. Another thing that I like to sort of compare between mediastinoscopy and E-Bus, which has sort of become really the workhorse and has really replaced mediastinoscopy for the routine evaluation of the mediastinum, is that the access to different sites is much better with E-Bus. We don't have access to periaortic, like five and six. There are some case reports, but it's not something that I recommend routinely. Where you can do with a lateral Chamberlain procedure, or left anterior mediastinoscopy. And there are all sorts of ways to do additional, sort of enhanced surgical accessing of the lymph nodes, which we won't go into. But this is just a comparison between mediastinoscopy, which is really bound by the central airway and restricted to some of the main vessels. So, for instance, going to the subcranial area for mediastinoscopy can be very difficult because of vessels, whereas E-Bus, you can go all the way to secondary and sometimes even third carinas. So, you know, there's a lot of overlap between what E-Bus and C-MED can do, where the reach of E-Bus can go a little bit farther out. Last two cases, I'll try to run through these. This is a guy, 56 years old, never smoker, prior resected, well-differentiated carcinoma, now presents with a bout of hemoptysis. And this airway, this is where IP gets involved. Initially, you know, sort of getting the, letting the dust settle on what's going on with the airway. But then when he codes on the floor when he's getting a CT scan, really the description of the code is not so much an airway thing, but they describe that his eyes are bulging out, his face becomes purple, he becomes really, like, engorged, making you think more about a vascular process, right? So we do, we send him to IR for an angio. This is the, the image on the left is before, the image on the right is after revascularization, but not before he codes peri-intubation for the procedure. They did everything right. Patient was seated upright, awake, fiber-optic, but just coded, lost his airway, resuscitated him for three minutes. We were able to revive him. We decided to proceed with the procedure, and he wakes up with now neurological issues. We cool him, and then we take him for airway stenting, and then, you know, get him home, okay? Where, I'd love to say that he's in remission right now, but unfortunately he did pass, but he passed outside of the hospital, which, for me, was a win. Anesthetic considerations, you have to think about the blood vessels, you have to think about the airway. Try to avoid use of muscle relaxants, try to do fiber-awake, try to get all the troops in the same room when you can. Anesthesia, IP, people who are comfortable with airways, spontaneous ventilation as much as possible, try to intubate distal to the airway compression, and rigid as backup. Sometimes even that vascular, that compression on the airway that you can get from the weight of the mass, you can stent it open with a rigid. And, you know, I hate to say it, but you have to evoke ECMO. Last case, this is a patient who presented with an esophageal mass, gets biopsied squamous, gets airway stenosis, gets stented for the airway stenosis, starts chemo and radiation, does really well. Two weeks later, coughs out the stent. Great, I don't need to get it out. After two months, comes back much worse, shortness of breath. You can see the large TEF. You can see it sort of pooling pus on that bottom-left image. Taken for an airway stent with external fixation, and, you know, we watch him. He's still getting therapy. I think about two months later or so, gets more dyspneic vocal cord compression, vocal cord dysfunction is getting worse. This is when we decide that we're also gonna have to trach him. But we can't trach him and take out the stent because we wanna cover that airway defect, right? Because if we just leave the trach, it's not gonna be protective of the TEF. So we decide to do a joint procedure where ENT does an open trach. We make a window through the stent, place the trach. Now we've gotten the vocal cord taken care of. Now we've gotten the TEF. Passes away nine months after initial presentation. The reason I bring this case is really to highlight the importance of interdisciplinary work. Airway is a major issue. It's what the patients die of a lot of times. We can push the envelope, but it really has to be in a team fashion. We have to think about vocal cord paralysis, which can commonly occur, concomitantly with esophageal masses, or with any of these, right? Tight space, tumor is gonna have mass effect. This is gonna be my summary slide. I'm gonna hang back. Sorry that was a marathon run, but I wanna get you guys to where you need to be. Thank you.

radiographic classification

mediastinal compartments

CT scans

anatomical divisions

mediastinal lesions

CT and MRI scans

postoperative infectious mediastinitis

descending necrotizing mediastinitis

mediastinal diseases

interdisciplinary collaboration