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Thank you very much. Oh, notification. Got it. Um Yes, good evening everyone. And um thank you for joining and tuning in. I'm gonna try and take you through the, the pituitary gland and the disorders, um the control center of the body and my name is Anne, already known. I've got the privilege of being the um clinical pituitary fellow at Queen Square started in August last year and um will finish in August this year. So, um I've trying to figure out in terms of the cursor and using the cursor, I'm staying out of the um the full screen. So if it's too annoying, I'm going, in fact, you're going to see enough of me and hear enough of me. So I'm just going to take myself off the video a little bit. So that disappears. Now, I'm not going to linger on this slide at all. Um because I don't particularly like see pictures of myself, but I'm originally from Sweden with just a little bit of background. I've been in England for about 15 years. So I know now also a British citizen and um I did my neurosurgical training in the West Midlands and one part of it also down in Romford. So I sort of returned to London for a little bit naturally. I have an interest in, in pituitary and anterior sco base and I try to have a little bit of a life outside of neurosurgery. And as a former gymnast, I have the privilege of working for British gymnastics as their team doctor and I've seen a bit of the world with them so far. I took my partner his two boys and uh three dogs and found out that we can actually combine more sort of country side with London. Um Now this is why it's making a little bit tricky. There we go. So looking through this evening session, we are going to run through the learning objectives that I've been given. So I'm going to try and um give a relatively overview of the anatomy of the pituitary gland, obviously. And then understanding the relationship between the pituitary gland and the optic chiasm, which is extremely relevant in terms of tumor surgery and um, the vascular supply, obviously, and, and what can happen when we are there operating and also, um deciding whether a patient should be placed for surgery or medical management and finally looking at what can go wrong when we operate. So understanding the postoperative complications, I think we, we've agreed sort of if there's any questions, I'm more than happy to answer them, but might be easier towards the end. So if you want to put them in the chart. If it's something pressing, obviously, feel free to, to just er, shout out now, control center of the body. So I explain it to the patients mainly as a control tower at an airport. So the gland is the tower and the planes are the hormones that are sent in different directions to do different actions in the body. Looking at the anatomy, then we're gonna go through the embryology, we won't get, get past that. Um And then look at the structure of the gland, the vascular supply and the importance of the hypersal portal system. And um the hormones obviously and their feedback system starting with the embryology and just making sure we're happy with with the the view since I'm not in full mode, just a thumbs up would would be, would be great if I can see that. Yeah, perfect. Thank you. Um um So now I started pressing lots of things here, apologies, close that one out. So two things to start. We got the oral ectoderm that is merging with the neuro ectoderm. Now, this is probably a familiar slide to you, but it's always useful hearing it in different ways. So think about it, the rath pouch, the nice little pink structure here is the ectodermal lining of the developing oral cavity. It's epithelium in origin and it's what gives rise to the Aden hypophysis. OK. That in combination with the neuroectoderm, which then naturally is the reason for the neuro hypothesis. Now, this all begins sort of during week four of the fetal development. The pituitary organogenesis begins at that point and there's a thickening of the cells in the oral ectoderm that will form what's called a hypo placode. Um This is where I can actually use my mouse now because I'm out of it. Um So you have a, a growth of the MetaDerm here and um the hy plaque turns into the raths pouch and coming up to about week 6 to 8 is when it, it forms and disconnects and leave the oral oral um ectoderm um on its own. And at the same time as all of this is happening with the upward invagination of the raths pouch, we have a downward extension of the ventral cephalin. So the neural ectoderm which then folds in and then creates the posterior lobe. And the magic here happens when these two meet. And you can see that Pastor Vialli, which is one of the parts of the adenohypophysis loops around the infundibulum of the tract, um which is going to run all the, the neurohypophysis, neurohypophysis hormones along. And the connection when this is ready is obviously the adult pituitary that we have as an end result. Now, looking at the adenohypophysis, it's important to know it's it's an anterior part and a posterior part. Now the anterior part has an extensive proliferation and it happens relatively swiftly, cellular differentiation. It's during the 1st 12 weeks of gestation and it turns into the anterior lobe and it, it churns out the five principles, special specialized sort of endocrine cell types of the pituitary gland. Whereas the posterior part of the rass pouch um is much slower in proliferation and it results in the intermediate lobe. Um I'll talk a little bit more about them. But just in conclusion, is really overall is three steps of the embryo embryology, what you need to remember. So you have the initiation of the pituitary organogenesis. You have the formation of the raths pouch. Secondly, you have the evagination of the rath raths pouch and the cell proliferation and these meeting the ventral diencephalon. And then the third one is the liner determination and the cellular differentiation, which turns to the past totalis which is the the anterior lobe of the pituitary. So then looking, I'm struggling with the scrolling here. I apologies. So, looking at the structure of the gland, I've tried to keep it in the same sort of color coding. So overall, we have two lobes, the adenohypophysis and the neurohypophysis as we've seen. Now, the adenohypophysis is made up of three parts. So pass to stylus, which is where all the hormonal cells are sitting, pass intermedius, which is um a lineage pretty much in between the anterior and posterior lobe. And it's um it's more or less a remnant of the um the raths cleft. So it's rudimentary and adult pituitary and the raths cleft cyst remnants here is what can give course to the raths cleft that can be problematic of further down the line and require surgery as they can increase and have a cystic cystic component. The past tulis you saw was the was the bit that loops around the infundibulum. And the past tulis is containing the portal vessels which is obviously vital for the distribution of the endocrine so of the hormones later on. So it's arranged in cords and is in these cords where you've got the hypo portal vessels residing pa nervosa is the neurosis is we will talk more about it later on, but it's just the one pass infundibulum is part of the stalk. Obviously, it's mainly the connection between the hypothalamus and the pituitary gland for the posterior part of it because as you probably all well know, we haven't got a production, we have only got storage in the posterior pituitary. So that's the pathway where the hormones run down. And just to mention they are uh the, the pituitary in itself is functionally outside of the blood brain barrier. Now, back to the anterior lobe and looking at the principal endocrine cells, it's pretty self explanatory here. We've got the tyros, the lacto tropes, the cortico tropes, the somatotrope, the gonadotropin and you can read for yourself, the, the hormones that are produced from this. So these are the, the five principal endocrine cells. Um There's also 1/6 cell, which is the follicular Stella, they are not um endocrine producing, they're not hormone producing cells. They're potentially, it's a bit uncertain what they do, but it's part of intercellular communication or probably also aiding the structure of the pituitary. And they're mainly found in the past vais in terms of cells. But then more um in terms of the structure of these different endocrine cells and how they're set up as a um an impact on, on our operating. Obviously. So you can see that the growth hormone is quite lateral on the gland and the TSH is anteriorly and then centrally, we've got act. So when patients in particular, um Cushing's patients come in with microadenoma, which is a tumor which is less than a centimeter. Um We have to most of the time open the gland to get to these cells. Um and it's a slightly higher risk obviously of damaging the pituitary itself. So then moving on, on to the vascular supply to the pituitary. So um as you will probably know there's um uh they sa portal system. So I'm just gonna drink, I'm just recovering from two weeks of COVID. So, excuse my um throat and coughing from time to time, keep it to a minimum. Anyway, the vascular supply, we've got a superior epi facial artery which is branching off the intracranial IC A. And um this is what supplies the anterior lobe with the pituitary. There's an inferior hypo artery which branches off the cavernous IC. So it's part of the meningocele trunk together with marginal tentorial artery and lateral tentorial artery, very detailed in that sense. But the meningocele trunk you should know about. Um there's also an inferior hypo arterial circle that includes the capsular artery in the artery or inferior cavernous sinus as well as a backup supply. And in particular, in surgery, there is a risk of damaging the inferior hypo artery in normal adenoma surgery. So it's important to, to be aware of that because it can give rise to a POSTOP hematoma. But you can also just divide it because there's extra added supply. So that's the arteries. Then we have the long hypersal portal veins, um which runs into capillary beds and I will talk you through and we'll go to the next slide and this is a very busy slide. So we'll do it as structured as possible. And this is where I want my cursor in particular. So if we can then find focus on the anterior lobe to start with because that's where we've got the hypo portal system, right? We've got the um superior hypo artery running here. And this is the primary plexus up here in terms of capillary plexus. And then we have the long um portal vessels running down through the posture Vialli and down to the anterior pituitary lobe to a secondary capillary plexus. And what happens here is that there's marked out tuber scenario or median eminence here as well. Um This is the area where we have the hypothalamus, the part of the hypothalamus where the hypothalamic releasing or inhibiting hormones conversion and, and the system. So it's a pathway that the whole hyper portal system is the pathway connecting hypothalamus with the anterior pituitary. So that the uh hypothalamic hormones enter here and gets transferred down through here, activates the um pituitary cells who will then produce the hormones. So, um for example, the cortico trope releasing hormone comes from here runs through here and stimulates the ac th to then go out through to the end organ and, and produce the cortisol. Um And so, so this is, this is obviously something very vital. Um And in the function and the connection between the, the hormone hormonal secretion and the, the blood uh supply of the pituitary. Then uh we shouldn't forget the, the posterior um part of it as well. So you can see the supra optical hyper tract and the periventricular hyperthy tract. They originate from the supra optical and paraventricular nuclei in the hypothalamus. And there's lots of fancy words, but there, that's where you have the production of the vasopressin and the Oxytocin, which are the two hormones for the posterior lobe. And um they pass through and gets put in packaged up pretty much in vesicles that then are running through down. Um the hypothalamus hyper tract and into the posterior lobe and stored in the posterior lobe waiting for stimulation and send off through the, the capillary bed here um out through the bloodstream and then to target organs. Um So that's pretty much summing up the, it's like I said, it's a busy slide, but that's the, the gist, the general gist of it from, from that point. Um Looking at the right hand picture, this is actually looking into the third ventricle with um an endoscope and it's just to give you the anatomical location. Um And this is probably in anticipation of doing an endoscopic third ventriculostomy, right? So, you have the optic recess, you've got the optic um path and the pituitary stalk is running here, the tuber cerium, which is here, which is where the hormones enter the, the circulation and the portal system. And then you've got your mami bodies and the Basar artery here and you do your there. But it's just to give you a different view. It's obviously looking from up and, and down that way, then moving on to the Antero pituitary hormones. This is probably nothing new to, to either of you, but I I just always find it nice when it's a good sort of outline. Um There's five different cells but six different pitu hormones, obviously, um they all have their target organs and the effects. Um I'm not going to go through it in detail because I'm sure, you know, you're up to speed with these kind of things. Um And just to mention that we can't forget, is obviously the negative feedback axis and it's the body's own way of um controlling the secretion and, and um suppression of hormones. So, hypothalamus, which we've talked about creates the releasing hormone. Um and going back actually to one slide, it's um the only hormone that has an inhibition from the hypothalamus is um prolactin and the dopamine is the inhibiting hormone for prolactin and the tubule tract that you can see here is mainly, it's one for dopamine tracts really. But that's sort of mainly the part from that one. Um the growth hormone can, can have both an inhibitory and um a stimulating effect from the hypothalamic hormones. So, nonetheless, they have a function in terms of. So I've just written them here as a bit of a memory um map help but hypothalamus releasing hormone stimulating the anterior gland to release the pituitary hormone who then moves on to the target. And, and then we have an effector and, and um an end result, an end product and the end product can then loop back as you know, onto the anterior pituitary gland and inhibit the the secretion. And it can also loop back all the way to the hypothalamus and inhibit the releasing hormone itself. Posterior pituitary hormones. And we have mentioned them. So, antidiuretic hormone or vasopressin and the oxytocin, as you all know, the antidiuretic hormone um has an impact on the kidneys and the circulatory system and the, the fluid balance, water balance overall um really important in pituitary surgery. And it's something along with, with um obviously, the, the hormones itself, but, but the, the sodium level and the fluid balance is something that we monitor in post-operatively. And I will talk more about D I uh further down the line. And then the oxytocin is the hormone that triggers the uterine uh contractions during childbirth, which is also one of them stored posteriorly, really quick mentioning about the hypothalamic nuclei and just to show a little bit more in detail sort of where they sit because in relation to the posterior hormones. So you've got the paraventricular nucleus and the supraoptic nucleus sitting here. This is your optic nerve and coming into the chiasm which brings us on to the next chapter shortly. But that you can see the relation to the chiasm and the pituitary gland, how it sits there. Um But these are the two nuclei for the vasopressin and the Oxytocin. And the tuber scenario again is the median eminence where we send that where the hormone enter the, the uh portal system. So as I said, we'll, we'll move on then to the relationship between the pituitary gland and the optic chasm. And um we've got that picture which I'm sure you're very familiar with as well, but we'll talk through it. Um normal location of the chiasm sits superior to the pituitary gland. It's su it's, it's sitting in the suprasellar system. When there's pathology in the pituitary region, the uh field deficit that is sort of usually goes for the pituitary tumor is uh superior, potentially progressing to complete bitemporal hemianopia. And this is, this is a typical presentation. Now, then everything isn't as it as it should be. I was about to say, but there's always variations, right? So you can have um actually even just anatomically, you can have a prefix and a post chiasm in, in, in, in patients in, in general. But it comes into play when we've got tumors within the pituitary gland. So um looking at a junctional scotoma suggests that the chiasm is post fixed, which means that the chiasm sits behind the tumor and is being pushed backwards if that makes sense because it's either that or if you have the chiasm in a normal position just underneath, sorry, just above the gland and you have an anterior tumor spread, you get the same result in terms of the tumor is then looping from the front and pushing back again and same and rarely, it's the other way around with a macular bitemporal hemianopia or a homonymous visual field loss. So, suggesting that it's a prefix, so the call is sitting in front or you have a tumor that's sort of going behind the chasm and pushing it forward. Um And this and a prefixed chiasm makes it really difficult from a surgical point of view because when we open up, the chiasm will sit and stare us right in the face which makes it really difficult to get access. This is just a s schematic view and, and again, I'm sure this is something you're very familiar with. You've, we've obviously got the hypophysis or the pituitary gland right in the middle. Um We've got our cavernous sinuses here and the dural leafs around them and the chiasm is sitting here um, with the internal carotids running on each side. And I'm going to show you some pictures from an endoscopic view, which would make it a little bit more realistic because the sphenoid sinuses and the septum here is extremely thick. Um 3rd and 4th nerve and sixth nerve floating freely next to the carotid cavernous carotid and then V one and V two on the sides. So these are obviously in terms of if there's a large tumor or if there's a sudden hemorrhage or, or ischemia. So, such as an apoplexy, um these structures are all structures that can be affected and it's good to remember for, for clinical presentations. If you find symptoms relating to these uh structures, obviously think about an apoplexy, but we'll talk about that in a bit as well. So a little bit of surgery. So this is obviously a cadaver, but just to show this is our root um endoscopically into the pituitary gland. So we've got the turbinates here. I suspect that's probably the inferior, middle and superior there um going through into the sphenoid sinus. So we would normally open up a little bit of a window here. And then we've got a cellar here and this is obviously the Pituitary Gland or potential adenoma sitting there. And I think this is relating to the chiasm and this is just a more colorful picture of what it looks like. But you can see it's, it's pretty self explanatory but, but it gives you the idea, um which you probably you already know. But the location is, it's pretty much smack bang in the middle of everything. This is a surgical view with the endoscope and it's, it's located to where you come in. Um And you would always look so where this scope has gone through is the sphenoid ostium here. So we would identify this and there's mucosa around and open this ostium up which you can see on the bony window here and making sure we've got the quan in view and in between these two points, it's important to, to remember that we have a spen palatine artery that runs through here that supplies the nasal septum. And um you can sacrifice it on one side, preferably not on, on both sides for obvious reasons. Um But it's something that when we do a straightforward um endoscopic transferal that we try to avoid injuring it and peeling just the mucosa down before we go on, then we come into the, the um sphenoid fossa or sphenoid sinus rather. And you can see that these structures here are the carotids running. So this is quite a typical view. This is obviously your cadaver, but it gives you a good idea. Um You've got the pituitary stalk I think is what they wanted to indicate here. And um the optic nerves and the chiasm is expected just behind here. And these are the optic carotid recesses sitting here between the optic nerve and the cavernous carotids there. This is the cellar floor and the pituitary is coming through here and this is the clivus and the cli recess. So here they've done a clot toy and you can see the pituitary gland and the dural lining um sitting right in front. So normally for the adenomas, we would do a cruciate incision here and this is where the adenoma would be sitting. And we wouldn't be seeing this on a straightforward uh endoscopic procedure. But um more with an extended procedure um where we would, we would open up the anterior fossa floor to some extent. But in terms of what we're topic here is to find the chiasm and the relation to the pituitary gland. So you got the pituitary stalk here with the gland sitting there and obviously your chiasm here and the right optic nerve running off there and the left optic nerve running off there with the internal carotids on each side. Still looking a bit closer. You can see the ophthalmic artery coming off here with the IC and again, the chiasm uh and the optic nerves and moving on a little bit closer. Um They think, I think they've pushed down. So the pituitary stalk is here. So you would have the pituitary underneath. You've got the chiasm here. And this is looking into the third ventricle with the anterior communicating complex right in front and this is masa intermediate in the third ventricle. So it's amazing in terms of what you can see with an endoscope um through an extended procedure. And if say there was a big tumor sitting here, this is the anatomy that you would look at and it's genuinely beautiful um moving on slightly closer up. So this is back, well, actually, it's back up a little bit because this is the pituitary stoke here and the gland sitting down here, you've got the chiasm and the optic nerves, the a one in the background. Um So it's just PC is just a bit more towards the patient's right, looking at further deeper structures and coming up to the picture where they've lifted the gland up and you can see the stalk and you have the basilar artery, the third nerve um and the IC. So, and um I would say this is a les membrane. Um And then again, a detailed description of that, but it's, it's, it's really spectacular in terms of the anatomy sometimes, which is nice. Now, then, um when do we decide to, to operate and when is medical management the most appropriate. Um, it's obviously a very gray area. Um, nothing is, is clear cut. Even though there are certain sort of ground rules in terms of medical management, there's a fair bit of drugs out there. So the dopamine agonist, the cabergoline and the bromocriptine, as you know, it's treating the, um, prolactinoma. Um, and with a prolactinoma not requiring any, um, any surgical intervention, even a large tumor can shrink down. And um the endocrinologist love it because they feel like magicians when it's just gone. Um We've got to some statin analogs such as Pegvisomant um for the growth hormone. So, the acromegalic patients and when it comes to Cushing's patients, the metyraPONE and ketoconazole is a, is sort of the block preventing the um cortisol production. And uh they would then need to be on hydrocortisone uh in the same setting. So the metyraPONE is something that works directly on the adrenal cortex inhibiting the, the cortisol and the ketoconazole is, is a, is not, it's not first line, but it's something that works in a way to reduce the a secretion, but there's no sort of clear pathway there yet. Um in terms of surgical management and I've put it in this kind of way where I think it's easy to think about it from a surgical point of view. What do we want to achieve in an operation? So we want to preserve the vision. So if there's a large tumor, then that's obviously an indication. Um we want to obtain a tissue sample to be able to have a clear diagnosis of what we're talking about. And also if it's a, it's a microadenoma which is less than a centimeter. Um but a high hormone secretion, we obviously want to control the, the hormone secretion, apoplexy. I've put on here, it's um becoming less and less. It depends on what the symptoms are along with the apoplexy, but it's also sort of a surgical indication, but we'll come back to that, see if I can scroll this. Now. Um This is a, a description and I'm surprised actually that it's not our surgeons just saying no, it's rather someone else telling us not to. But um we like to operate but, but when it comes to mac macroadenoma. So, um diagnosing it and seeing patients with this do a prolactin as part of the pituitary profile because again, if it is a prolactinoma, it's something that we would in the first instance, send off to our endocrinology colleagues to treat medically. And we're talking prolactins, not just sort of to the thousands, but it's usually 10th to 100th of thousands in prolactin. Um So it's, it's quite high and uh I've put all of these things up here because these things with the headlines for pituitary disease, hypothalamic disease, other and neurogenic medications. These are all reasons for elevated prolactin. So it's important that um there's an endocrine team involved in terms of diagnosing in, in general, actually, with all the different types of, of um pituitary tumors, even if it's not adenomas. But um with the prolactin, they obviously play, play a significant role in terms of acromegaly. The uh primary pathway here is, is actually a surgical intervention. Now, um they can be controlled with um uh somatostatin, excuse me. Um But in the first instance, it's looking at surgical intervention and taking the, the obviously the cell producing hormone producing cells out. Um and regardless, it's something that would be be monitored. So the growth hormone, but the IGF one in particular, because um it's obviously an end result of the growth hormone stimulation. But the difference is that in terms of the growth hormone having a cyclic session, um throughout the day, the IGF is more steady and hence why we tend to measure it. What's worth mentioning in terms of the POSTOP monitoring um is a prolactinoma will give you pretty much an instant feedback if it's high and then it's dipped down straight after the day after surgery, then that's a good result. Um in terms of the growth hormone and the IGF one that is something that will take months sometimes to, to settle and it's difficult to know if we've ended up getting them into remission. Cushing's is also primary surgical intervention for the same reasons. Yet, on top of the, the hormone producing cells. And, um, I always talk through the patients when they come in that they might have a second surgery straight after in the same admission with a sort of a week or two in between because if we don't get them in remission, so what we're looking for here is a cortisol level dipping down below 50 that can sometimes take a few days. But if that doesn't happen, we might go in and instead of just taking part of the gland, we take all of the gland to make sure that we're treating the Cushing's. Um And what's mentioned here is also if there's significant comorbidities, it's probably applied for the acromegaly as well, treat the comorbidities and optimize these patients before they have an have an operation done for obvious reasons in terms of the systemic impact um from, from the disease onto these patients. Um with Cushing's. So I've written in Cushing's disease there. Um There's always this to remember, Cushing's syndrome is, is obviously um an elevated ACTH and deciding whether it's it's um so sorry, the ACTH dependent is the central part of it, right? So it's deciding whether it's centrally driven or not centrally driven because it's completely different management um ways here and the IPSS, the inferior petrosal sinus sampling, looking at the gradient between the periphery and the central will give us the indication. So all Cushing's patients would go through that before they're brought on to a surgical plan if, um, so remission is, is sort of up to 60 70 sometimes 80%. Um, but if that doesn't happen and they have a second surgery, um, then if, you know, there wasn't already, there would be adrenal imaging and potential unilateral or bilateral adrenalectomy. I'm not sure how useful this slide is, but i it's, it's sort of how the different tumors are, are divided. So they can either be a microadenoma or a macroadenoma, microadenoma less than one centimeter, macroadenoma, more than one centimeter giant adenoma, more than four centimeters. They exist and they're enormous and they're a pain to deal with. But um so looking at the micro adenomas, are they hormone producing? Yes. So then even if it's a prolactinoma, there's always, like I said, there's always um uh exceptions. So someone with a prolactinoma and having been on dopamine agonists and are either not tolerating them because it does have an effect of on people with um sort of underlying psychiatric um illness or depression or anxiety and these kind of things, they don't do well with these drugs. Um And some people have a resistance to the drugs. So then a prolactinoma can come in our hands anyway, even if it's a microadenoma or a macroadenoma, um micro adenomas and acromegaly, some of them, if the IDF and the growth hormone are controlled on medication, then it might take a little bit longer before they come around to a surgical intervention. And with the macroadenoma is really going down to the visual disturbance. Is there a compromise of the optic chiasm is the Chism pushed? Have they got visual field deficits? And if so then it's a relatively urgent surgery. Um So again, with a functional and nonfunctional, we've pretty much talked it through. So it was just trying to give a little bit on you apoplexy then um something worth remembering for, for clinical work in terms of the presentation tends to be a severe sort of frontal retro orbital headache. Most sort of 80 to 90% of cases present with this blurred vision is not that frequent. It's sort of around about 20% some around 7 10% present with with a facial weakness, um which is unusual obviously, but then cranial nerve courses resulting in diplopia most frequently for the chosen cranial nerves for obvious purposes in terms of the caviar sinus um is around 40 to 50%. And the by temporal hemianopia, it's anywhere between 30 to 70% in terms of the presentation. So the severe frontal smack bang, really bad headache and in some occa occasions, reduced consciousness should also obviously lead to other differential diagnoses. So subarach is probably the most important thing to to exclude hypo is rare in the context. But meningitis, migraine, carotid dissections, infarctions, carotid, you know, cavernous sinus, thrombosis, there are lots of areas reasons, but don't forget about the apoplexy. So what it looks like on AC T um if you can see. So this is actually a chap who was diagnosed in India last year in May with an apoplexy typical presentation as we just talked about. And he sent these across from, from um from India. So hence why it's not sort of one big screen or video, it's just on plain film um looking, I'm not sure if you can see. So it's obviously a CT and um non-contrasted axial imaging and you can see the hyperintensity here in, in the cell and there's a small little dot there as well. Um and distribution a little bit along here. So this was his apoplexy at the time, he had transient visual disturbance and um went on to have an MRI scan and when he came back to the UK last autumn, his MRI scan showed sort of a resolution of his adenoma and this is what can happen and that's why it's not always surgical. Um The important thing with these patients is to make sure there's no adrenal crisis present. All right. So look, make sure they are vas cardiovascularly stable. And um if, if you have time, you know, do a pro take some bloods off the patient, but straight off giving them a high dose of hydrocortisone, you can, it can be 100 mgs IV or 50 mgs QD S or TDS. So there's lots of variants, you can give them 20 mgs T DS orally again, involve endocrine but you're better off giving them hydrocortisone and then having a cortisol back that is normal than risking them going into adrenal crisis because that can be lethal. Get the endocrine team on board, assess the vision. And if there's a persistent visual disturbance, then that is the likelihood of us intervening. It's not a kind of emergency 24 hours. But if there's concern regarding the pituitary profile and the vision and it's persisting, then it's likely that this is a surgical management that's required. Um In quite a lot of cases, though they can be left and we can see them at a later stage and see if there's any requirement or if the, the gland or the tumor has shrunk down. Um as for all pituitary patients, making sure fluid balance and sodium uh is monitored as well. Moving on to understanding the postoperative pituitary complications as much as we would like things to go smoothly with. No problem at all. They obviously don't always do. Um what's been mentioned um in your objectives is the um diabetes insipidus, the CSF leak infection, meningitis and hematoma. So, um there's obviously more more to it. I would consent for injury to the pituitary gland and need for lifelong medication. The diabetes insipidus, the CSF leak, the infection and bleeding. Um but also looking at the nasal crusting and the sinusitis and and the altered smell in rare occasions. Less than 1% you have a stroke which results obviously in weakness or um paralysis or visual impairment. Um But let's go through the diabetes insipidus, then it's obviously a disturbance of the secretion of the vasopressin or the antidiuretic hormone, two main types. And naturally the central diabetes inhibitors is what we're interested in or what we would most likely cause in terms of a surgery or just a tumor on its own. It's a damage or dysfunction of the hypothalamus or the pituitary gland. So it's not just the pituitary gland and it's not just tumors or surgery. It's also a head injury or an infection. That can be the the the culprits, nephrogenic diabetes, insipidus is problems with the kidneys. They're not responding to the effects of the vasopressin. Um as they should, it's just worth remembering that it's not just a central d that can happen. Symptoms are polydipsia polyuria, dehydration, elevated sodium. And this is something that um we are very, very keen on keeping an eye on in our POSTOP patients, in particular, measuring in and output hourly is a must in pituitary patients. Um And there's a balance obviously when to intervene and when not to, but it's daily sodiums and watching them like a hawk from that point of view, anything that goes out or in is documented if there's a concern with was sodium, repaired osmolality, looking at the serum and the urine at the same time and doing a urine specific gravity and giving the desmopressin sometimes. So our endocrinologists are really good. So they have a good understanding. But elsewhere where I've worked where it's not as specialized, sometimes they have a slightly different view of the, the desmopressin administration. Um but and it varies also slightly in terms of guidance between hospitals. But a sodium that goes above 145 or 1 50. I probably have a higher threshold there for 1 50 with a serum osmon, you're more than 300 in combination with a negative fluid balance. So most likely urine output are more than two. So absolutely more than 2 50. But that can be up to 34, 500 mils per hour over three consecutive hours. And the specific gravity is usually more, not less than 1.15 with an hospitality. You need the urine less than 200 like this is D I. This is where you need to give this when pressing and we're talking micrograms 0.1 microgram if you're administering this IV um it's something if you're not happy and sure to manage, speak to either the pituitary team or the, or the endocrine team, obviously, or the medics to, to get some guidance. Um or sometimes I um and to say this is obviously, if there's a disruption to the, the posterior gland. Um and in most cases, what we would do in terms of tumor surgery would be affecting the anterior gland. And sometimes if we do see the posterior gland it's slightly more white and shiny than, than we are watching this more closely. A CSF leak in, um, endoscopic transsphenoidal surgery is sometimes intentional. I was about to say if there's a plain and sphenoidale meningioma, inevitably we have to open the dura and there will be a leak intraoperatively. Um Sometimes if we do a uh pituitary adenoma straightforward, um, we don't want to, we shouldn't cause a leak, but we can see the Arachnoid and the, the sort of um uh the dome settling down in where the tumor and filling up the space where the tumor was sitting. And if there's a tear in the Arachnoid, there, obviously, there can be a little bit of glistening. So intraoperatively, sometimes we don't see it and it happens after theater. But if we do do it intentionally, obviously, or if we note that we do it, we take a little bit of fat from the abdomen and we put it up the nose. Um and some, some units do a little bit of fascia and put it up and put some glue on top of it. But and the seal with that is, is quite good above certainly above more than above 90%. Um It can be delayed CSF leak with an infection causing problems or um not very often but sometimes a noncompliant patient. So we give them instructions to avoid blowing their nose, for example, um six weeks after theater and I can appreciate that's not an easy thing, but it's important trying to minimize the sort of raised intracranial pressure because we have gravity against us already for the repair. And if we then apply pressure from the inside, it's, it's just um reducing the, the healing diagnosing it. Every patient after theater would have to sit up and lean forward, lean over for about a minute to see if there's anything dripping. I've put the gin glass here, which have a nice little logo there. Um It looks like Gin. Um It's, it's obviously very clear and it's quite obvious most of the time, even if it's mixed a little bit with blood when it comes through the nose. Um But it, it's fairly easy to say whether it's CSF or not. Nonetheless, we can't just go and stick the finger up the wind and see where it blows. So we would collect it, send it off for beta transferal protein specific for CSF. And um if there is a concern that patients can have headaches with this, we would also do a CT scan, for example, to look and see if there's um pneumocephalus, for example, because that obviously suggests a direct communication to the outer world. An MRI scan can also be done if it's been an extended procedure. And we have, uh and or we, you know, we've done a significant repair to see where that, that its, if it's still in place or if there's a clear sort of tract um, into the nasal cavity. And there are different ways of managing the, the TSF leaks following an trans or lumbar drain is a classic. And sometimes if we know we're going to make a big hole, we put a lumbar drain in before the operation even stops and, um, keep it in for 3 to 5 days. So it's like an epidural. Yeah, it's just sitting and secured and with very close monitoring, that's just a normal collection system. We have aly that it's called that, that controls the output, which is excellent for LUM DRS because we have a um 10 to so 5 to 10 miles an hour and with the micro guard that gives us a more exact measures. So that's very good. Um If the lumbar drin doesn't work and there's still a leak and concerns we would do um a surgical repair. So we would go through, back through the nose, take things down and, and put a new new repair in and very likely keep the lari in for another few days after that until things are going dry. If that fails, potentially, the patient might need a, a ventricular peritoneal shunt as a final sort of move. But that's far down the line infection and meningitis is extremely, there's low. So in general, transsphenoidal surgical risks are low, there's a higher risk um in terms of for an infection or meningitis and it is directly related to intraoperative CSF leak. If the patient's diabetic. And if it's a radio surgery in the same area as before diagnosis is, is obviously obtained as with any infection or sepsis, a set of blood tests, clinical examination, is there an obvious neck stiffness? Is the patient drowsy? Um Is there a photophobia and uh a lumbar puncture sending off for a for um microscopy obviously to look at the white cells and the the poly count um and naturally for, for culture, discuss with your um micro allergy team in terms of managing with antibiotics. And if there is a noted CS freak that obviously needs to be addressed. And I'm just highlighting this here. So genital in the one neo surgery, they just did a study on 3000 patients um who had transoral surgery between 2012 and December 2016. And you can see that it's, it's very low. There's no point to 8% develop meningitis and same for bacteremia and looking at it gram positive organisms more for the for meningitis and the um um the Yeah, sorry, I'm seeing a hand there um get to so um gram negative in in the bacteremia. So what's important is that seven patients though out of all of these died. So it's still, even if it's a low um low incidence, then um it's still important to remember because it can be, can be um fatal. Um Arla, did you have a question? Yeah, I've got a hand here. No, I will carry on, uh, maybe at the end. Um ok. Yeah, I think just carry on, he'll ask, he'll uh you can type the question in the chat if you still have a question. Thank you. Um Then POSTOP hematoma after transoral surgery is, is quite unusual. Actually, the um presentation tends to be visual disturbance if there's a significant, you know, hemorrhage headache obviously comes with it and again, cranial nerve deficits. So seeing a patient postoperative complaining about these things, there's that's an urgent CT head to, to make sure there's nothing major there again, with a hematoma. Sure, there's no adrenal crisis. You might need to all patients after pituitary surgery go on to um an a sort of emergency cover dose. So we, we bring the, the hydrocortisone up to 20 mg tds, but make sure that that is in place and, and um that we're not risking an adrenal crisis. Again, it's rare to, to need to go back for a surgical intervention unless it's a really large hematoma. But again, that's really, really unusual. And sadly, if that happens and there's visual disturbance, the likelihood of that vision sort of recovering is, is, is not very large. Um It seemed to because it's a sudden sort of change, whereas when the adenomas have been in place, um they have longer time and there's quite a good um recovery from a visual point of view if there's a macroadenoma that's pushed on. So, um lots and lots of talking if you've fallen asleep or for any other reason, lost interest. So, just a quick whistle stop tour summary, what, what to remember in terms of your learning objectives. So the pituitary made up of the raths pouch from the Ectoderm and the neuroectoderm put together. So turning into two lobes and four parts. So the neurohypophysis is to pass nervosa and the adenohypophysis past the star lists to pass intermediate and the tubal list which keeps the portal system in its path six anterior pituitary hormones which you're familiar with. It's the prolactin, the growth hormone. Um ac th the LHFSH and TSH and the two posterior pituitary hormones, the oxytocin and the vasopressin. You have the superior hippo facial artery which supplies the anterior gland and the inferior hippo facial artery providing um blood supply to the posterior gland chiasm, it superiorly and slightly posteriorly to the pituitary gland. And this can obviously change with the pituitary pathology. And when uh doing a profile, please don't forget the prolactin because that will give us an awful lot of information. The patient would need an MRI scan, visual examination to determine whether this is something that would be uh surgically or medically managed and apoplexy can be an emergency surgical emergency. Um But, but most important for these patients don't forget to give them hydrocortisone after having done some bloods on them, remembering the CS F leak, the infection, diabetes, insipidus and hemorrhage are things that can go wrong after surgery, quick slide with just a few references on there. So that brings me to the end of the talk. So, thank you very much for listening. And are there any, any questions, shall I um have a look in chat and reply maybe? Yes. So there are a couple of questions. Um I think, would you like me to read them out for you? No, that's ok. I I've got the chat open here. So if we're sort of communicating through the, the, the talking. So, so communicating through the chat, that's absolutely fine. Um I think that's ok. Uh Is everything OK. Can you read the chat? I think you might be muted. Yes. Sorry. So do you want me to because I've started typing here so you can just um speak out. Yeah. No, thank you. They are good questions and, and really quite tricky in the sense. So with a bilateral IC, the plaque gradually blocked off. Is it possible to have pituitary Arop xy as well? So, thought process here would be something that is sort of gradual and chronic having collaterals. And, you know, in terms of the ICA occlusion, you would have, you would have a vascular supply to the pituitary with time. You, to be honest, it's something that I haven't quite come across. But I would want to say yes, there's a possibility for the pituitary apoplexy. There's, you know, what happens in an apoplexy is the sudden change in either a hemorrhage in a pituitary tumor or an ischemic event in, in the tumor. So you can still have the apoplexy, you can still have the sudden change um within the, the region of, of the, the cella if that makes sense. Um Then uh thank you. Yeah, thank you very much. So, 2.5 questions. Um Can you compare microsurgery to endoscopy? So we'll start with that one. First. I um have not been fortunate to, to experience microsurgery. Actually, MS Grieve was one of the consultants who retired in April last year and she was still using the microscope and that's obviously very for a long time. That's what we used. Whereas the endoscope has come along during the last couple of decades and become more and more common. I think the biggest difference in terms of what we see in patients that there is, there were certain blind spots using the microscope, which we now can get to in a better way because it gives you a much wider angle when you have the endoscope um up on onto the tumor and depending and how you angle it and you can use both nostrils to get to more towards the left or the right side. So I think that's probably for obvious reasons, the biggest change in that sense and the microsurgery would also have been sub labial, for example, in terms of the pathway. So it's slightly different in that sense. Um Do we use SRS S in our routine? What's the advantages and disadvantages? So this is quite a big, big sort of question from that point. So S RS can be used. So even if the majority, the pathology in the, in the cellar is 90% you know, very benign, um We're looking at the adenomas or the raths cleft or a craniopharyngioma or a meningioma. Um There are obviously other, other areas. So, um SS can be used. What's important to remember is that it's a very high dosage. And the important thing with this is the proximity to the chiasm and they are really reluctant to give any form of radiotherapy in particular SRS if we haven't made sure or, you know, if the tumor isn't far away from, from the chiasm in that sense, um, fractionated radiotherapy can also be given. So in, like I said, even if we deal with, with low, low grade grade one tumors, we would still um consider radiotherapy therapy, post surgery. Um if in, in older patients, if that makes sense. So some patients have an early presentation, they have three operations done and when they reach sort of an age of 60 70 then we're looking for the radiotherapy or SRS, then it obviously depends on where in the anterior skull base you have the SRS. Um But for the pituitary, the important thing with, with any radiotherapy is the proximity to the chiasm. So if it's something more suitable, even if we can go in and do an optic nerve decompression, for example, which means just removing the bone from the, from the optic canal immediately to give a little bit of extra space, that would be preferable if it's a very tight space. Um I've seen one patient today actually who's got a um sphenoid due meningioma and deteriorating vision and um talked to her through the um optic nerve decompression just to give, give way for a potential radiotherapy. Um How does a prefixed versus postfix optic chasm impact your surgical planning approach? Also a very good question. Um in terms of so a post fixed optic chasm in relation to a tumor is obviously the, the, the preference because then it's all behind and we can, we can work our way through and obviously the posterior edge, we need to be careful. But when it's prefixed and um there was a patient a couple of months ago actually, um what, what's vital is going through scans as for any operation, but in particular for pituitary surgery, you look at the nose and see the corridor. Um And uh how are the sphenoid sinuses? Are they, are they very small, is in Children, for example, sometimes they're no until they get to a certain age. Um because we don't, we're not born with them. And um, then you look at the C and where is it? And you try also to see on a T one non contrast of scan where you've got your neurohypophysis. So you work out where you have your, your pituitary gland. So if it's prefixed and this was, we looked at scans and when we opened up, the chiasm was sitting there right in front. Um And what it does is obviously it complicates the surgical root because now you have to find a path above and below to get to the tumor which you need to decompress. Um And it's really tricky and depending on the size of the tumor, um and the location of the tumor. And if it's a definite prefixed chiasm, if you can get to the tumor in a safe manner, supratemporally, that might be a better choice. So it's, it's finding the, the anatomical landmarks before you, you, you dive in and, and you can send the patient. Ok. Um Then uh feedback form, I'll skip that one. So what is the success rate of pituitary macroadenoma surgery? Uh Also good question. It's um it, it depends on the in terms of success rate. So, uh if you're looking at the, the actual tumor, tumor removal, um it's, it, it's all sort of up in, into 60 70 80%. So it depends on and then, then you can look into, is this in relation to a visual improvement or is it removing of the tumor tissue? Um Is it a a hormone production? Um Do we get them into remission. So, but, but everything is sort of sitting, nothing is up to 90 100% with, with relation to that. But, but the outcome in terms of the macroadenoma and improving vision, um, we always tell the patients that we want to prevent them from getting worse and if they have an improvement that that's a um that's a positive sort of outcome. Um But I think it's probably up to 40% of patients have an improvement in their vision. So I think that was, that was all the questions. Perfect. Thank you so much. No problem. I hope that it was sort of covering um a reasonable um uh amount of of in terms of the learning objectives that we we've got there. So no, no, 100%. It was very clear, very to the point, very informative. Thank you so much um for everyone else. Would you please fill out the post feedback form? Um and oh, sorry, I'm just trying to. Ok. And I think that's everything for today. That's great. Thank you very much everyone. Thank you. Ok, that's ok. You're the flight. No, I, yeah, you know ST ST yeah, you don't appreciate. Hi, just like my mother. I've been trying to take my mother but I should have been trying to take my dad.