Grand Rounds-Comprehensive Management of Pituitary Tumors

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- Hello, ladies and gentlemen, and thank you for joining us again for another session of the Delbonis Operative Grand Rounds. We're privileged again to have with us Dr. Gail Rosseau from Chicago from North Shore University Medical Center. She has extensive experience with treatment of Skull base tumors, including pituitary tumors. We're really excited to have her today to have her talk to us about comprehensive assessment and surgical treatment of pituitary tumors. I think this will be not only very useful for those who perform pituitary surgery, but also for those who will be preparing to take their boards. So Gail, onto behalf of our viewers, I wanna thank you, and we're very excited to listen to your thoughts, please go ahead.

- Yeah, nice to meet you again.

- Please go ahead.

- Okay. Well, we're all just dwarfs on the shoulders of giants, aren't we and I'd like to give a nod to Ed Laws, my mentor who, from the very beginning said, if you're going to be teaching and doing pituitary tumor work, you need to know about comprehensive management not only about how to do the surgery, although that's of critical importance, but really how to manage the problem for patients to be the quarterback of this problem. That's why we've structured today's talk on the comprehensive management of patients with pituitary tumors, but not to him and those who came before. What I'd like to talk about today are just a few general remark. Pituitary adenomas as you know, are the third most common of the primary brain tumors. They occur in about 20% of routine autopsies. Hence, the Pituitary Patient Association launching their one in five campaign to raise awareness about this condition. About 20% of primary brain tumors in US residency programs are performed via a transsphenoidal route and that number is increasing so we want to be sure that we are developing profound expertise in that surgical route of approach. Today, I'd like to talk about the diagnosis and medical management of pituitary tumors, as well as their microsurgical treatment, radiosurgical treatment. Say a few words about apoplexy and metastatic lesions, and just conclude, as we always do with patient advocacy and education. The Secretary tumor so of course need to be considered. First and foremost, the most common of these are prolactinoma, followed by acromegaly and Cushing's disease, and then the more rare tumors such as the TSH-producing tumors. Here's an example of a prolactinoma, which in my experience tends to be among the more invasive of the secretory lesions, in this case, invading the clivus. Now, when we're called to see patients who have an elevated prolactin, and a pituitary tumor, we want to be sure that we have evaluated all the many reasons why a patient might have a high prolactin because we know that one in five patients are going to have a pituitary tumors and we want to be sure that we are correctly establishing a relationship if there is one. Now here are several pharmacologic reasons why a patient might have an elevated prolactin, antihypertensives, ACE inhibitors, H2 blockers, psychotropics and opiates or cocaine abuse. When you're evaluating the patient with hyperprolactinemia, first and foremost, exclude pregnancy. We know that the normal pituitary gland can double in size during pregnancy and we never want to be making that mistake of associated hyperprolactinemia and pregnancy. We want to rule out thyroid, renal and hepatic disease which can also mimic a hyperprolactinemia state and pituitary tumor. Stop the causative medications which we just reviewed, then do an MRI and reevaluate this condition after menopause. Well, patients will often ask well what are the consequences of hyperprolactinemia and estrogen deficiency and otherwise? In other words, why should I care whether I have an elevated prolactin level and a small perhaps non-secreting tumor? Well, there are really two reasons why we should care. The first is osteopenia and the relative risk for osteoporosis in these patients is about four and a half times normal. Then there are the hypogonadal symptoms and these two things combined to make us want to treat hyperprolactinemia. The etiology of prolactinoma is generally monoclonal. There seems to be an alteration in the long arm of chromosome 11 and we know that in particular in the multiple endocrine neoplasia inherited condition type one, the locus is on chromosome 11, the Q13 Locus. If we go to medical therapy first and I would argue that as the quarterbacks of patients who have pituitary tumors, we should be familiar with medical management. Dopamine agonists are generally started initially, these include most cases bromocriptine, or Cabergoline, although others are known, and the dopamine agonist will generally produce a normalization of ovulation in 80 to 90% of patients and this is why they're so widely used. But we generally start out with Dostinex, the trade name for Cabergoline. The reason for this is that it's well tolerated, and it's easy to take with once to twice weekly dosing. The response rate seemed to be highest if it's used as the initial treatment that is in dopamine agonist naive patients. These should in most studies, normalize the prolactin in most patients and in the largest European study of normalized prolactin and 83% of patients in eight weeks and only about 3% stopped Dostinex or Cabergoline because of side effects. This is compared with 20 to 25% with bromocriptine. This is why we've gone to Cabergoline as our first drug. About 50% of patients will have up to a 50% reduction in tumor size. Now, the longer history, of course, is with the use of bromocriptine or Parlodel. This drug will normalize prolactin in 70 to 80% of patients. About 40% will have about a 50% reduction in tumor size over a variable time course. Even visual field defects will improve in 90% of patients who start with those visual field defects and are started on these medications. But we need to be aware that the decrease in tumor size may not correlate with a decrease or even normalization of prolactin. The side effects of GI complaints or orthostatic hypotension occur as they said in about 20% as opposed to 3% of those who use Cabergoline. There's the issue of whether this drug, or the other dopamine agonist caused bothersome, Perivascular fibrosis that may make subsequent surgery a little more difficult. But this drug has been studied most extensively for use in pregnancy and in childhood. What do we do if we have a patient who's presented with amenorrhea-galactorrhea syndrome and is started on a dopamine agonist. If they've been started on bromocriptine, it's generally felt that it's safe for the fetus of discontinued in four to six weeks gestation. If the patient harbors a micro prolactinoma, the risk of the tumor increasing in size off the drug is only one to 2% during gestation. With a macroadenoma, the risk of tumor increasing in size is higher, it's been estimated to be between 15 and 23% and in some occasions, the drug is continued during pregnancy. For Cabergoline, it seems to be more effective than bromocriptine, but there's less data on this drug which is newer in our armamentarium. But there does not appear to be an increase in adverse fetal outcome in it and so at this point in time, there does not appear to be any indication for therapeutic termination of pregnancy if a patient has been on Cabergoline and does become pregnant. What about the long term use of Cabergoline? In this cited article in the "New England Journal" published in 2003, patients have been kept on Cabergoline for seven years and it turned out that many of those patients were thought to be cured so a long term use of Cabergoline may actually be a cure for prolactinoma. We certainly recommend that patients who have been on this drug and then faced menopause, be reevaluated after menopause. In 2007, also in the "New England Journal," a new caution advisory for the use of high dose Cabergoline was reported. In patients who use high doses there's been an associated with valvular cardiac disease. This generally tends to be eight to 10 times the dose one would use for its prolactin suppressing effects in prolactinemia associated with pituitary tumors. It's more commonly used in this dose range in movement disorders, but the caution remains nevertheless. What are our indications currently for transsphenoidal surgery for patients who harbor microprolactinomas after failing a trial of medical therapy? Well, they fail to respond to medical therapy if they're intolerant to the side effects of the treatment. It may be a personal choice a chance for cure, the management costs of microsurgical removal of microprolactinoma versus drug treatment seem to be about the same at 10 years follow up. To take the case of macroprolactinoma following a trial of medical therapy, we usually recommend surgery in our shop if a patient has a visual field defect that is not improved on the medication or if there's a cystic, or hemorrhagic lesion, as you see in these slides, or you can predict that the volume of this mass is not going to substantially decrease even if the tumor has had a shrinkage effect using the dopamine agonist.

- Gail, I think those are great thoughts and one thing that has been my experiences occasionally, no matter how much you treat pituitary disease, you run into those patients do have a typical presentation of a sella tumor. Occasionally, the surgeon does not evaluate their level of prolactin, they go ahead and treat the patient off for surgery and they find interoperabilty that you're treating a tumor that is medically treatable. One approach specially for boards, and obviously, for practice and a good practice is that if any tumor has any connections to the pituitary gland, no matter how unusual the sort of pattern of growth is, evaluation of pituitary axis, or model access is important to make sure and exclude that this is not a prolactin-producing tumor, am I correct?

- You're absolutely right and this is why I think it's very important that we think of ourselves as providing care for the total patient with a lesion in and around the pituitary gland. We need to be as familiar with the medical treatment as we are with the surgical treatment, and as we'll see later, with the radio surgical treatment.

- Thank you.

- Just a few more words on prolactinoma and I included in the sagittal MRI images here, the largest macroprolactinemia for treated, this patient's initial prolactin level was measured in the low 90s and I thought, having learned from Bill Chandler about hook effect, we diluted it and in fact, this patient's prolactin level was 22,000. Just a word to the wise on how one can get fooled if you don't dilute it. Indirect signs on MRI can be very useful as well. I think sella excavation is more reliable than stalk deviation in this case. Finally, this is one of the happy corners of neurosurgery, isn't it because malignant adenomas in the pituitary gland are really unusual, I found less than 100 reported cases. We can generally let our patients know that this is something that can be managed and that really shouldn't, in most cases, shorten their life or affect their quality of life. Next, let's move on to another one of the secretary syndromes here be talking about acromegaly. I'd like to thank Ian McCutcheon for the bar graph here that shows what most neurosurgeons know about the somatic effects of acromegaly, have shown just some snapshots of what the broad paddle-like hand or the height that can be really large in those patients who develop this condition before the closure of the long bones at around age 18. This is an interesting article, one of our patients wrote about their own symptoms in the May 2010, "New York Times." This patient is a great example of how pituitary tumors can present with almost any symptom you can imagine. In this case, the chief complaint was sleeplessness, but the patient who was a very fit 40-something year old man had developed hypertension, diabetes, high cholesterol and found himself sitting in the orthodontist chair getting braces in his 40s and said, timeout there's something wrong with me. When things don't fit look further, very often we'll find that the master gland that little T-like pituitary gland is causing trouble.

- I think that's an excellent point. I have one patient who had interestingly, I'm sorry to interrupt you, had a pain in his joints and had a previous back surgery was taking methadone. Nobody really listened to him that all his joints are hurting so he went on internet and found out that's one of the symptoms of acromegaly and came to me and demanded evaluation for acromegaly. We did and believe it or not, he did have acromegaly. It's just a very peculiar disease. It's the master gland going wrong, that can manifest itself in many ways. Please go ahead.

- Well, you're absolutely right. I have a couple patients exactly like that, who started with spine surgery, didn't get better and ultimately, the diagnosis was made so point well taken. But to continue how we evaluate for acromegaly, of course, IGF-1 is the gold standard, it's always elevated. We used to call it Somatomedin C. The growth hormone level may be normal or even low. This is also something we wanna be sure every neurosurgeon knows, look for the IGF-1, the growth hormone level, because of the circadian distribution of its pulsatile effects. Its pulsatile secretion as you see here, you may or may not have an elevated growth hormone, the IGF-1 is the test to remember. Now on Cushing's disease which Harvey Cushing himself called a syndrome, whose presentation can be so many and so varied, as to baffle analysis. This is a real diagnostic dilemma probably the most difficult to diagnose of the secretary tumors. Of course, in Cushing's syndrome, you have ACTH-dependent versus independent Cushing's syndrome. A number of things other than Cushing's disease, can cause Cushing's syndrome, such as depression, anorexia, stress, alcohol, all of these things, increase cortisol levels. There are also drugs that can affect this. Similar to the analysis that we went through with hyperprolactinemia drugs, especially birth control pills can magnify cortisol levels. We want to be sure that we really nail down the diagnosis before operating. Again, there is a newly described entity called cyclic Cushing's and so we wonder about all of these things, we wanna be sure that we are working to correctly diagnose before we treat. Again all of this is in the setting of very frequent non-functional pituitary microadenoma, so we wanna be certain that the biochemical analysis is right. Urinary free cortisol over 24 hours has been the standard approach. But more recently, late night salivary cortisols have been found to be very highly sensitive, and specific, often over several nights in a row. Provocative testing is helpful, as is the CRH stimulation test, and petrosal sinus sampling as well. The IPSS Petrosal Sinus Sampling seems to be the most accurate test to do to distinguish the differential diagnosis in Cushing's disease. It's particularly helpful in the case of a negative Sella MRI. But despite initial reports, it seems to be unlimited utility for localizing the microadenomas in Cushing's disease. The venous drainage, it turns out of the pituitary gland is so varied that that may not be reliable. Well, once again Ed Oldfield and his group have been absolute leaders in this area and have been working toward non-invasive diagnosis and I would call the attention of all of our colleagues to the excellent work that they've been doing in the last decade on working toward non-invasive diagnosis of Cushing's disease. Well, moving on rapidly to thyroid disease, primary hypothyroidism is much more common, especially in the middle and elderly age group than a TSH-producing tumor so you always want to be checking for a free T4. This will be elevated in a TSH-producing tumor. If you get a referral to you of something that looks like a pituitary tumor was suprasellar extension on the left, let's be sure that we check that free T4. If the patient has primary hypothyroidism get them treated because you can see in the slide like, what that looks like and Aaron, I bet you've had cases like that as well. People get in the habit of referring to you for pituitary tumor and you just have to start at step one each time with your full endocrine analysis.

- I think that's very well said. If there is symmetric enhancements on the pituitary, you have to always question Gail, I think what the situation is, is this is a pituitary tumor? As you can see in this beautiful case, you just showed, it looks like a pituitary tumor, very symmetrical enhancement, but it's really not it's just overreaction of the tumor because of primary hypothyroidism. The moment you replace their thyroid hormone, the tumor, which really never was a tumor went away. This is so critical and I appreciate you mentioning that. I'm hoping to emphasize that, as you just mentioned. Thank you.

- Let's move on to microsurgical treatment and these are the areas that we will very rapidly go through. Well, first of all, the endonasal approaches have been around since the time of Hirsch, and the early 20th century and Halstead. There have been many recent advocates for primary endonasal approaches. Here's a slide of a Chilean four that makes me think about the endonasal approach and turbinates where we're just using the space given to us by nature. I put up this slide Aaron because that we were using it 15 years ago, when the first debates point/counterpoint talk started to be given about endoscopic approach versus the trans-labial excuse me, the sublabial transseptal approach and the arguments for using a purely endoscopy whereas you see it left patient comfort, the possibility we thought of more complete excision panoramic view of carotids. No need for packing, less impact on smell and taste. But those who said gee, we have a good operation and a safe operation, why do you wanna change it? Why do you wanna take three dimensional views in using the microscope and make it two dimensional with an endoscope? Why do you wanna need three hands to do this operation? The endoscopic approach was unfamiliar skills for many neurosurgeons. It was a paramedian approach and the concern was it would lead one cross the midline to the contralateral carotid that there'd be inadequate exposure or collision of instruments, that there might be turbinate injury or delayed hemorrhage from the coagulation, or resection of turbinate. These are all of the things that we've been talking about for the last decade and a half as we look at moving the technique forward, while at the same time keeping it safe and effective. Courtesy of William Chandler I love this slide the exposure, it should be the same no matter how you get there and that's probably the main point I would make when we talk about standard or more traditional transsphenoidal approaches versus purely endoscopic techniques. Make sure that the exposure is the same, no matter how you get there. What matters is what you do once you get into the sella. Would you agree?

- Absolutely, I think as Marty Weiss wrote in one of his editorials a couple years ago is there has been so much emphasis Gail on how to get there. But unfortunately, what's most important is what to do when we are there. Let's just say that, there's many ways to get there, but it's hard to get the job done right. That's what's most important and I think both of us agree that it's surgeon's preference. I think we talk about endoscopic endonasal versus microscopic versus endoscopic endonasal. I think either one is very good, they both do the job. It's certain whoever is comfortable with a technique, but as long as when you get there and you do the job right I think that's a critical point as you well mentioned it.

- If one is going to consider a transition from a microsurgical approach, which we all learn and which still serves our patients very well to an endoscopic approach, we have several options. There's endoscope assisted surgery, there's a surgical route that would be a purely endonasal approach, using a headlight and lubes. There's endoscopy with or without a transsphenoidal retractor. What I found is that if you go to pure endoscopic surgery without a retractor a surgeon's ease, at least in my case in making this transition. This was achieved after between about 30 and 50 cases. Either way upon is doing an endoscopic approach or a direct endonasal approach and then placing a speculum the identification and development of an enlarged sphenoid Ostia is step one. Then again courtesy of Phil Chandler, the surgical anatomy should look like this regardless of approach so that the sphenoid sinus Ostia are the upper outer apertures, if you will, to the window of bone in the anterior face of this sphenoid that you're going to remove. A sphenoid panorama should look like this where you can identify the inside of the sphere and see the carotid and so in about 4% of the time there'll be a dehiscence in the area of the carotid within this sphenoid sinus. That's one of the advantages of having an endoscope so you can see if you don't have that bony protection. Here's an endoscopic view of the sella. Now, many have said if you're going to move in the direction of a purely endoscopic approach, that image guidance should be used. I would saying that image guidance should be used or at least considered in these cases, for anatomical information, particularly on the beginning or if one is changing one's surgical practice. It's useful on microadenomas for the tumors will be very small. It's certainly helpful on a region transsphenoidal approach where the anatomy may be distorted by a prior surgery. If the carotid artery is medially deviated, it's very helpful to have image guidance. It's so widely available now in many ORS that getting used to using it in every case, is not a bad idea.

- I think as Ed Laws well mentioned is in every pituitary issue with surgery, you have to have some sort of guidance. It's lateral fluoroscopy. It's your tactic guidance, you need something and I believe that wholeheartedly. Lateral fluoroscopy does a great job. But I think in every one, you need something to guide you. Because if you get lost, the consequences are just too costly, in my opinion, and therefore, a lateral fluoroscopic guidance is so cheap, so available, as you mentioned, it should be used.

- I agree, I have a partner who calls this area at the high price real estate, because of the proximity of the carotids and both optic nerves and I think your point is well taken. There's multiple types of image guidance available we won't belabor that, but I think it's important. Looking at the last 12 years or so in our 900 cases, we found, as most do, our series broke down in a fairly characteristic pattern where non-functional macroadenomas were about 44%, prolactinomas were the most common of the secreting tumors, followed by acromegaly in our series, Cushing's disease, but notice that almost 20% were other conditions, the smattering of TSH-producing tumors, but you also have mucus seals, cranial for angiomas and other tumors that occur here. Knowing how to do transsphenoidal exposures, we said at the beginning becomes increasingly valuable. The good news again, it's a relatively happy corner of neurosurgery, isn't it where the complication rates are gratifyingly low. We tend to follow patients for hyponatremia. Every patient is asked to get thyroid studies and a BMP at seven to 10 days post-op. We learned from Dan Kelly that about 9% of patients will have a transient hyponatremia during this time course. Of course they're already at home. What about four patients have had to have treatment of their hyponatremia after discharge? We've needed new cortisone replacement in four, we've had a worsened visual field in three. One patient had a stroke. One lumbar re-exploration for fever because we're using lumber drains at that time, and we've had four CSF leaks interestingly, more recently with the endoscopic approaches. Now special considerations would include the surgical failures that we have in Cushing's disease. This history means a really difficult section of transsphenoidal surgery, because it's so difficult to make the correct diagnosis. The tumor can be missed at surgery even when we have the right diagnosis because the tumor can be multiple or there can be small areas of what you would square is tumor, these small areas of whitish discharge which look like they might be the rounded capsule of a tumor, which it turns out not to be, or the tumor can just be incompletely resected. So much of what I've learned about this, I've learned from Ed Oldfield and his group, these next slides are thanks to Ed Oldfield. He's written some beautiful papers about this, and all of our major journals. But these slides used with his permission show the idea of using a pseudocapsule. Here you can see the tumor within the normal anterior, adeno hypothesis, the neural hypothesis here. Here again, I'll refer you to Ed's beautiful paper on this in "Journal of Neurosurgery." But he describes stain outside of this pseudocapsule in order to be able to get a more effective, complete removal and well, he's really the master at that I've learned so much from him. There are other neoplastic lesions that can occur within the sella as well and certainly as more and more patients live longer with primary cancers, they will have more metastases. For example breast metastases which can occur to a highly vascular area like the sella, lung, GI and prostate. Adenomas can also occur in extrapituitary locations completely outside of the sella.

- Gail, I wanna say one more thing, if you don't mind. I think one important point about metastasis is that and you please correct me is that the patient's most often present with posterior pituitary failure initially, is that correct that's been your experience?

- It is. That is what is usually reported in the literature. What I have seen in the only two patients that I've seen who presented with pituitary metastases was Mass Effect.

- Oh, I see.

- It was Mass Effect, it was not affecting pituitary function, headache with cranial neuropathy.

- Thank you.

- Just a few words on pituitary apoplexy. Thanks to Warren Selman, who's done a lot of work in this area. We know that if you analyze as he did in this nice series from a journal of Intensive Care Medicine, headache and nerve palsies, decreased visual acuity are the most common presentations of this condition. If you look as Warren Selman and his group did at those 400 patients, we see that the gonadal and adrenal axes are the most commonly affected. W. Couldwell and his group looked at a grading scale in apoplexy to help us understand how far along or how seriously affected patients were, who had had apoplexy because we know that we get reports all the time, don't we? Radiology reports that describe apoplexy and very often it's subclinical can occur on radiology reports and have almost no clinical meaning. Recognizing this W. Couldwell and his colleagues graded patients based on their symptoms, and the MRI findings and divided them into three grades like this. What they found that may be very useful for us is that if and those patients who had a second sphenoid sinus mucosa, 57% were in this grade one, but 100% were grade two and three. The thinking was that this thickening of the sphenoid sinus mucosa might correlate with the acute stages of pituitary apoplexy, and possibly the higher clinical grades that might be more urgent attention. With any case of clinically suspected pituitary apoplexy treatment, the single most important thing to remember is prompt administration of steroids. I just can't emphasize this enough. Certainly if a patient has bad headache, visual symptoms, change in level of consciousness, we're calling the operating room, aren't we? But do not forget to give them that dose of steroids which may be life saving as you're getting them ready to get to surgery. Just a few words about the extended transsphenoidal approach. Those in favor of treating a large lesion like this or even a tuberculum sella meningioma with an extended transsphenoidal approach are the obvious advantage of no brain retraction. It's a minimally invasive technique. We all like that, patients and doctors alike. But there may be some cons, some disadvantages to this approach, traction on critical structures may be a problem. The risk of CSF leak remains one that can be developed as. Dan Kelly, Paolo Capobianco, and many others have published very thoughtful papers on how to repair the cranial base defects that come with this ambitious removal of tumors through this approach. I would refer you to this paper and others on this. But complication management, complication avoidance is always important and particularly important when we're causing large holes in the skull base. Let's move on now. Radiosurgical treatment of pituitary adenomas and just some summary slides here. Our goals of course, are always to prevent tumor growth, protect adjacent structures, and conserve endocrine function if we can. In 1978, the first papers documenting the use of Gamma Knife radiosurgery for the treatment of patients with pituitary adenomas republished. Now over 5000 patients are treated annually, and we're approaching nearly 40,000 patients now who've been treated for this diagnosis with Gamma Knife radiosurgery. But the patient pre-op testing is fairly well described. You need to have an MRI generally that's very thin, one millimeter slice thickness to determine the suitability of these patients for treatment. We'd like to see a two millimeter gap between the tumor capsule margin and the optic apparatus. You certainly wanna complete pre-radio surgical endocrine evaluation and visual field evaluation. Then finally, we wanna remember to discontinue the hormone suppressing medical therapies, probably two to four months prior to radiosurgery and that restart date remains controversial. You wanna use shielding as much as possible to spare the optic apparatus. We wanna keep the exposure of the optic nerves and chiasm to be no more than eight gray. If necessary, particularly in the case where radiosurgery is being used adjunctively one may need to target the entire cell if there's no discreet lesion noted. The desirable dose range for pituitary adenomas is higher with this secretary adenomas. Dose ranges that are recommended are between 18 and 25 gray for the secretory tumors, and generally between 12 and 20 gray for the non-secreting tumors. Well, what are the kind of control rates? Well, we have a number of series that we looked at here. Here's a very nice meta-analysis by Jason Sheehan's group, as well as Ed Laws' group looking at 48 patients treated with 12 gray, these are non-secretary tumors. They found the volume control was very high above 85%, but new hormonal deficits just under 40%. That would be an example fairly typical example of what we see. Visual complications are always discussed with optic neuropathy rates should be very low in the one to 2% range. You said earlier, we tried to make sure that the optic apparatus doesn't receive more than eight gray and I believe the lowest reported case of visual complications was 9.8 gray. But up to about half of those who have visual decline after radiosurgery well had a prior fractionated radiation and treatments and then had follow-up further adjunctive treatment with radiosurgery, so we wanna be careful about over treating patients. Vascular complications in this setting are very rare. I'm aware of only two symptomatic cases that have been reported. Patient advocacy is extremely important particularly in a condition that affects nearly one in five patients in the general population of refer neurosurgeons and neurosurgical patients to or the patient site. In conclusion, I'd say from microadenoma to macroadenoma regardless of what approach we use, our goals are always the same, to relieve symptoms and to preserve maximum symptom free survival. I'd like to thank you for listening to that PowerPoint presentation. Perhaps now we could look at a film of an endoscopic pituitary tumor. Here's an example of a purely endoscopic approach. The mucosa was elevated and now we're using a high speed one millimeter diamond burr. This is obviously elevated for a time but now we have identified the dura, we've opened it, in X-shaped fashion to maximize our dural opening. Now we're curetting with our sharp pituitary ring curette, always starting inferiorly a little bit of the known subclinical apoplexy, this patient has delivered itself spontaneously into the field. This is a three hand approach with an assistant holding the endoscope while the surgeon is using the suction in one hand, and the curettes and the business instruments in the other. Now we're using the zero degree scope to look at the sella. If one wishes with a larger tumor, we use the 30 degree scope and actually place it into the sella. Here we're reconstructing the sella floor, we generally harvest a little fat. In this case, the fat has already been placed and then a small pledget of gel foam. Then we're placing this piece of the patient's own cartilage intradurally and then using a synthetic fibrin sealant to seal everything in place. Then the closure is very simple. The septum is placed in the midline, and a nasal drip pad is applied. Thank you for your attention to what I had to present. Aaron, I think you had some things that you wanted to discuss as well.

- I appreciate it Gail. Thanks for very great points that really makes a difference in management of these challenging tumors. I wanna just very briefly go over through some details, I think the patient position is is something that's we should be aware of and I position patients just like Dr. Laws does, and I know you have trained with him, so you must agree with that, I hope. I wanted to show you an example of that, this has been obtained with the permission of the patient by the way. You can see we use fluoroscopy the patient's head is perpendicular to the long axis of the floor, but the body is turned away from you. That's get that shoulder away from you. As you can see, we use lateral fluoroscopy and that's for all the virgin cases. Some of the recurrent cases we may use, actually, stereotactic guidance. I think positioning the patient so that it's lateral shoulder is out of your way, can be very helpful. Some of the other ones, again, this is the position of the patient, you can see the long axis of the head is where you would expect to be perpendicular to the axis of the room, however, the patient's body is turned away from you, that sort of helps to get that shoulder a little bit out of the way and avoid some of the back pain. We put the surgical assistant against you across the table for easy transfer of the instruments. Some of the other details, we have reviewed previously, I think I'm gonna skip all of those and just go directly to our single case that I wanted to add some flavor in terms of technique. That's really Cushing's disease you very well mentioned, it's a very difficult disorder to treat. Often it's associated with hyperplasia of the gland and therefore no matter how much you take out, if you're leaving gland behind, unfortunately, you're not gonna cure the patient. This is a young patient, for example, again, a Cushing's disease and left sided tumor along the sella, we approach this from the right side, that cross-court approach that I think you also use as well. I would like just to show this surgical video and we're gonna start with the first part of this procedure. Again, I open through the transseptal approach, and as you can see, the dura has been opened. The tumors sort of come in at you relatively easy. Most of the Cushing tumors actually are not as easy as this one, they tend to be a lot more yellowish color. This one was an easy one after we sort of opened the dura, everything came out relatively easily. Then what we have learned works very, very well is trying to bring an endoscope, and using the endoscope sort of make sure the tumor has been removed completely. Again, people use it entirely endoscopic, but I had it's worked well for me to use endoscope to assure that tumor removal is complete, especially for microadenomas I think one would say the microscopic approach has pretty good, still usefulness in it. But for macroadenomas maybe endoscopes can provide extra advantages. Then I wrap the fat in a piece of gel foam and piece of I would say surgicel and this prevents the fat from fragmenting into pieces, put a piece of bone and this is interesting, I use Indermil. The same Indermil we use for closing the incisions and then put some of the blood of the patient that has been intravenously obtained by the anesthesiologist and the Indermil solidifies and creates a very beautiful reconstruction of the floor. I think we do a great job in packing but patients who have a CSF leak is because the packing is not held accurately, or well. If there's any way you can keep it there, the risk of CSF would decrease significantly and that's been our experience. I think our rate of CSF leak is almost less than two or 3% after using Indermil, with the blood of the patient to solidify that solid construct and reconstruct the floor. Any other last pearls and pitfalls in terms of management of pituitary tumors, Gail, if you please might add.

- Well, one thing I would say is that if you're going to be doing an endoscopic approach, it is just so helpful to find an ENT colleague who's a sinus surgeon, who is using an endoscope day in day out, at least as you're getting started to learn the anatomy from and learn the tricks of the trade. The endoscope is fairly new in our neurosurgical armamentarium and I'm so grateful to my colleagues in ENT in particular, who have taught me so much about how to use that instrument and about the details of the anatomy on the way to the sella that makes it safer when you get to the sella. I would certainly thank our ENT colleagues and recommend working with them, at least initially, if you're gonna be doing a purely endoscopic approach, which is what I'm doing these days.

- Gail, thanks again for your time. We appreciate all the discussion.

- My pleasure, really nice to be with you Aaron. Thanks.

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