Chapters Transcript Video Optimizing Perioperative Outcomes in Pituitary Tumor Surgery: An Endocrine Approach Dr. Radwa Osman describes the importance of the preoperative endocrine evaluation in pituitary tumor surgery. And good morning thanks for everyone who's here and who's everyone who's on the virtual um and um I did wanna take that opportunity first of all to uh say that uh I'm very grateful for it. I think this is a great opportunity. A great chance to kind of, you know, cross that bridge between the medical and the surgical worlds and come together and discuss some of our common and maybe even the uncommon grounds um I mean there's a lot of patient complexity when it comes to this specific situation and I think uh it's very important for us to collaborate in a multidisciplinary team to for patients' best um outcomes so I didn't find a better topic than this to discuss today because this is a situation when. We kind of all come together in the hospital to help those manage those patients together so today I'll talk about optimizing perio-operative outcomes and pituitary tumor surgery from an endocrine approach. I'll walk you through through the outline of my talk today, so I'll start off with epidemiology of pituitary tumors and talk about preoperative perio-operative, as well as postoperative endocrine management to include monitoring for acute post-op complications and hormonal evaluation. Um, we'll, uh, wrap up by talking about the importance of a structured multidisciplinary approach and some key points for optimizing patient outcomes. I do wanna say that those listed down here are not gonna be the focus of my talk today for the sake of time I'm not gonna be talking about functional pituitary tumors. The focus is going to be on the non-functioning tumors. Um, of course I'm not gonna delve into surgical approaches, so I'll leave that up to you all, and, uh, there's not gonna be much about imaging studies and, uh, non FDA approved medications will also not be discussed today. Nothing to disclose. All right, so when it comes to, uh, pituitary tumors, we really don't know why they happen and, uh, the, the prevalence varies according to what series you wanna look at. So when we looked at autopsy series, it could be as common as 25% of cases. And we know that uh from the early 1930s when uh there was a pathology resident who um worked in Rochester, Minnesota in Saint Mary Hospital who dissected 1000 pituitary glands um and those people that actually died from unrelated causes and what he found is that 1 in every 4 had a pituitary lesion. Um, of course they were not, uh, uh, you know, big enough to cause any significant clinical impact because the prevalence of those that are really, uh, you know, of clinical significance is much lower, but he found that 1 in every 4 glands did have some sort of an identified pituitary lesion. And so what we did is we replicated uh that prevalence uh many years later with the improvement of scans like CTs and MRIs. Now we see if you look at a CT series, uh, you can see up for up to 20% of patients will have a pituitary lesion, even higher, 38% of patients who get MRIs for unrelated reasons may have a pituitary lesion. We don't know much about the natural history of asymptomatic patients though. Here's uh uh some data, uh, from the central registry of brain and CNS tumors from 2016 to 2020. They identified 455,000 patients and they looked at the, the, uh, uh, prevalence of, um, of pituitary tumors and you can see here that it's second common to meningiomas when it comes to brain tumors in general, about 17.2% and if you look on the right side this is the age specific incidence rates, so in the pediatric population. Uh, the incidence really seems to, uh, uh, take a steep curve around age 10 to 14. Um, while in the adult years fairly common across the board with a little steeper curve closer to age 60 to 64. Out of all pituitary tumors we see prolactinomas more often um than others, about 53% of them, 30% are non-functioning pituitary tumors, and that's followed by growth hormonal secreting tumors which is about 12% and then less likely, uh, uh, uh, less commonly seen as the Cushing's or ACTH secreting tumor is about 4%. Over the years we have learned that uh between functioning and non-functioning tumors it's really not black and white it's more of a spectrum or a continuum between the two so on the left hand side here you see the non-functioning pituitary adenomas which could be anywhere from null cell to silent cell, uh, where you see patients mostly with biochemical and clinically silent disease and when we stain their tumors they're both hormone and, uh, uh transcription factor negative. On the right hand side here you have the functioning pituitary tumors where you have both clinical evidence of of hypersecion, biochemical. Evidence and then when you stay in their uh uh tumors they're positive for both hormone and transcription factor and then in the middle you have uh you know that that spectrum there where you have some people have clinically silent tumors where they could be just very mildly uh clinically um abnormal and with very mild uh biochemical evidence and then you stain their tumors and it's positive for both so just to say that that it's more of a spectrum it's not black and white. So let's delve into the preoperative evaluation for pituitary tumors from an endocrine standpoint. Um, really a lot of times that preoperative evaluation occurs in the, uh, initial neurosurgery office visit. A lot of physicians, once they see a pituitary tumors, they just, you know, route patients to neurosurgeons. So often times this happens in in the neurosurgery office. So of course it's very important, uh, to get a complete medical history, physical exam. Send patients for formal neuro ophthalmological assessment with formal visual field testing if the MRI shows evidence that it's uh the the tumors abutting or compressing the optic uh chiasm, although I have to say this is where the strongest uh data is we, we still tend to send patients a lot to, uh, get the formal neuro ophthalmological assessment even if it's not really touching or abutting. A lot of it is also for medical legal reasons. Uh, also it's very important to evaluate for potential medical comorbidities, diabetes, cardiopulmonary disease. Uh, those all need to be optimized before patients go to surgery, and at the end we need to assess for either hyperfunctionality or hypofunctionality of the pituitary gland. So what is really the prevalence of hypopituitarism in general? This is data from the new guidelines from neurosurgery that was published in 2016. They analyzed over 300 studies and they looked at the prevalence of overall hypopituitarism, uh, and it ranged anywhere between 37% to 85%, and this is more so for non-functioning pituitary tumors. That is, uh, followed by uh growth hormone deficiency. So first thing that usually goes down is growth hormone deficiency, and that's because if you see the distribution of growth hormone secreting cells in your pituitary gland that's more so on the periphery, so it's susceptible to compression from the outside by pressure of the tumor. About 61 to 100% of patients may have some degree of growth hormone deficiency, um, when they have an identified pituitary tumor. And that's usually followed by hypogonadism. Uh, gonadotropes are usually, uh, dispersed all over the gland, but they tend to be very concentrated around the pars intermedia here between the anterior lobe and the posterior lobe. So again, any compression from the outside is very likely to cause hypogonadism. About 36 to 96% of patients will have uh some evidence of hypogonadism. And then the less likely is hypothyroidism and adrenal insufficiency, the more you go into the pituitary gland, the more cells that are tucked in in the middle, the more resilient they are for pressure for compression from the outside. So less often we see low uh uh TSH or central hypothyroidism and again it's very wide range here anywhere from 8 to 81% and then last of course is the adrenal insufficiency uh where you um. Have a range between 17 to 62% prevalence for patients that come in with pituitary tumors. So this is really the the last thing to go down most of the time. It's very unlikely to have a low ACTH and everything else intact. So every patient who um get yes, Doctor Sarraj, is that you? yes yes yes yeah they differentiate whether these are I'm assuming size yeah I yeah, they didn't. Yeah, great question. Uh, I knew someone was gonna ask that question. They did not, no. So this they just grouped all the tumors, but they did not yet classify them based on the size. Great question, yeah. Because we know, you know, the bigger tumors, macro macro uh adenomas tend to cause more hypopituitarism than micro but they that I, I'm assuming that's why the range is very, very, uh, wide. So any patient who gets sent to surgery should get preoperative endocrine evaluation. Um, in the form of morning fasting, uh, uh, serum, uh, uh, level of prolactin IGF one. Um, cortisol with an ACTH, uh, a free thyroxine level, a TSH, um, LH and FSH, along with, uh, either estradiol in females or testosterone in males, and then, um, urine ozonality and serum sodium is, is more so on a case to case basis for, uh, ruling out DI, although it's far less likely to have uh to occur with uh pituitary tumors as an initial presentation, but again it needs to be identified and taken care of before surgery. I do wanna spend some time talking about hyperprolactinemia, uh, you know, prolactinomas for surgeons is, is usually a a stop sign, you know, once you, you get a prolactinoma, uh, you say, hey, this is not, you know, that's not mine, just send it to endocrinology. Most of the time those patients' standard of care is to get medical therapy before we even consider surgery. Um, prolactinomas really the general rule of thumb is the bigger the tumor, the higher your prolactin levels are going to be, so the size really correlates with the degree of elevation of prolactin. So, um, we typically expect prolactin levels to be higher than 250 if you have a prolactinoma. Uh, there are situations when you have discordance between your biochemical evaluation and your clinical presentation, for example, when we encounter stock effects or some situations when your assay will fail, for example, the hook effect or even macro prolactinemia. So I think we all agree on, you know, stalk effect if you have a big tumor, uh, that you would expect higher levels of prolactin if it is in fact the prolactinoma, uh, but the levels are really modestly elevated. That's when you should think about stalk effect. There's really no magical number that delineates between whether this is clearly a stalk effect or this is clearly a pluralinoma, but. Yeah, it all, you know, depends on where you wanna draw your line when it comes to your sensitivity and specificity. There's a lot of retrospective studies that looked at this, and they saw that levels that were lower than 100, 150 were exclusively associated with stock effect. Anything that was higher than 250 was exclusively associated with prolactin illness, so that's where this number came from. And we thought this represents a acceptable false um uh negative uh uh result. So usually stock effect is anywhere, uh, lower than 100, 150. There are some studies that showed that growth hormone deficiency in addition to the uh prolactin levels being a little elevated, was more common in patients that had non-functioning pituitary tumors than with prolactinoma. Of course, if you take it into the context, the picture that can add to it. Now macrop prolactin is actually fairly common and in a meta analysis it was up to 19 to 20% of patients have macroprolactinemia, and that's something you should suspect if you have a patient coming in with modestly elevated prolactin levels, but they're completely asymptomatic, um, so what happens is macroprolactin is a large molecule which happens when. Uh, uh, your small prolactin molecule gets aggregated, binds an antibody, and then forms this much bigger molecule. The issue with macroplacin is it's inert, so it's, it's biologically, um, inactive. And it gets picked up by the assay. When we check prolactin levels, it gets picked up so it can give you a falsely elevated prolactin levels well it's not even biologically active, uh, prolactin. So what we do is we ask the lab to precipitate uh the the uh uh glycosylated macroprolactin we precipitate it by polyethylene glycol and that leaves the small prolactin, um, molecule behind and then now we can measure it and identify whether it actually is a true hyperprolactinemia or macropinnemia. Hook effect is not so much of an issue nowadays, um, I think it was back in the days before the advancement of the assays. Uh, but you should really suspect hook effect when you have a large tumor and you have a patient who's severely symptomatic for hyperplaplaxinemia, and then you check their prolactin levels and it's just mildly elevated. Then you may think maybe there is some interference with your assay and you wanna ask the lab to do serial dilutions. So the, the issue is the assay we use to check prolactin is um a non-competitive immuno acid and it's the same with assay. So when you have a lot of prolactin in your serum, which is the analyte, it binds to the, uh, between the labeled antibody and the captured antibody previ prevents the complex formation and then you don't end up detecting the real amount of prolactin because of how, how high it is in the serum. So what we do is we call the lab, we ask the lab to do serial dilutions, and then they call you back and say, oh, the prolactin levels is not 70, it's 7000 for example. But again, our assay here, especially in Centera is the Roche Alexis Prolactin 2 assay incredibly resistant to analy excess. So this hasn't really been an issue for a while, but it's just also something to keep in mind. So really, um The big question is who gets surgery when it comes to pituitary tumors and I kind of wanted to plug in both our, you know, guidelines here to show you that I mean a lot of times in the medical world, you know, those guidelines don't agree with those guidelines, but this is really a situation when we do agree so this is uh very similar indications here for surgery between both our guidelines, uh, uh, the endocrine Society just grouped it into a high quality evidence which are the top ones, uh, where they recommended. Surgery for pituitary incidentallomas and those who have a visual field defect due to the lesion or ophthalmoplasia, neurological compromise due to compression of by the lesion. Which again crosses over to the neurosurgery guidelines here and they agree. Pituitary apoplexy, um, with visual uh disturbance, lesions abutting or compressing the optic chiasm on MRI, uh, hyper secreting tumors, of course, other than prolactinoma, but that's also another indication for surgery. So again they both align. Uh, down at the bottom here is the lower quality evidence. So, uh, the endocrine Society will suggest surgery for those, um, that, uh, have loss of endocrine, uh, function, which is also something that neurosurgery, um, uh, recommends and unremitting headaches which of course are felt to be attributable to the pituitary tumor, and again, uh, that's similar to neurosurgery. Maybe the minor differences between the two is um the endocrine surgery suggests surgery for um clinically significant growth of the pituitary incidentloma and then a lesion that's close to the optic chiasm and if a woman is planning to become pregnant. So really the decision to proceed with neurosurgical tumor resection can be quite complex and it's best considered in a multidisciplinary clinical setting. Uh, those are things that we need to identify and treat before we send patients to surgery. So adrenal insufficiency, we need to initiate appropriate hormonal replacement pre and perioperatively if in fact a deficiency has been identified and then ensure glucocorticoid coverage during the surgery. Hypothyroidism needs to be identified, patients need to be replaced, which could prevent potential surgical complications like cardiac dysfunction, um, hyponatremia and ileus, and then AVP deficiency, of course, more likely to occur with the supercellular masses, um. But we need to identify it with certain electrolytes and you're in specific gravity. And then initiation of sex steroids and growth hormone replacement therapy is typically deferred until a later point in the post-operative management. So let's delve into the perioperative management. I did want to spend some time talking about uh perioperative glucocorticoids, um, of course in patients who do not have, uh, a pre-existing diagnosis of adrenal insufficiency. There's always been two schools. It's either impaired glucocorticoid coverage or the steroid sparing protocol. And there's data to support either so you know there's no one best approach maybe steroid sparing protocol, uh, can minimize unnecessary glucocorticoid exposure and may mean um shorter length of stay. So let's look at some data. First question that comes to mind is, uh, patients who do not have preoperative adrenal insufficiency, what are the chances that I'm going to induce iatrogenic adrenal insufficiency while the patients, uh, get their pituitary resected? So here's a prospective trial that looked at about 72 patients with preoperative uh 72 patients who who are undergoing pituitary surgery. And they found that about 14 of those 72 patients had in fact preoperative hypocorticoemia. Of those, um, all the 14 also had hypothyroidism and hypogonadism again as expected by the distribution of the cells. Only one patient who had preoperative adrenal insufficiency improved after surgery, so just to show you that patients who start off with adrenal insufficiency are very, very unlikely to improve after surgery. Now out of the 58 patients that were susceptible for postoperative adrenal insufficiency because they didn't have it to start with only 6 patients developed postoperative hypercortisonemia, and none of those, uh, patients actually had any symptoms of acute adrenal failure. It was solely based on their AM cortisol which they defined here as less than 8, to define adrenal insufficiency postoperative. It's important because. We tend to not expect patients to have significant hemodynamic compromise even in the setting of iatrogenic adrenal insufficiency, and that's important because um your mineral corticoid access and your adrenal gland is completely normal so chances are they're not going to go into hemodynamic compromise and they're being watched in the hospital very closely, but yeah, it's, it was really important to see that none of those patients really developed it. It was solely just based on the fact that cortisol was low. And they also mentioned that out of those 62 of them, this was actually their 2nd surgery for recurrence. And then 4, they mentioned that normal pituitary tissue wasn't seen um during the surgery. So let's talk about some randomized control trials here, so. This was a study done in China uh back in 2022 big trial, 436 patients I believe. Uh, where they randomized patients to either receive hydrocortisone pretty high doses perio-operatively versus non zero of course patients that did not have preoperative adrenal insufficiency, and then they looked at, uh, uh, how they did after surgery. This is the first randomized control trial that actually sets postoperative adrenal insufficiency as their primary outcome, which was great. And their second outcome was new onset adrenal insufficiency by post-op month 3, so they even followed those patients for 3 months after to see if they developed adrenal insufficiency. And again you can see here there was really no difference between the two groups, yeah, maybe some superiority, uh, towards group two, which is the hydrocortisone dose when it comes to new onset AI, but it really didn't reach the significance. And then when they followed them by post-op month 3, it, it even became less and less, uh, different or significantly different between the two. And then they had some pre-specified outcomes, for example, new onset diabetes, of course, patients received high doses of glucocorticoids, so there was superiority to group one which did not receive any hydrocortisone. And of course there was superiority to group one as well with uh when it comes to new onset hypernatremia, hypokalemia, hypocalcemia, things that you usually expect with um with iatrogenic Cushing's. Um, new onset DI also did not really differ much between the two groups, so there was a signal towards maybe group two, which is the patients that took hydrocortisone, which was a little more superior to group one, but again did not reach statistical significance, and the authors at the end, uh, concluded that the preoperative cortisol levels less than 9.3 was associated with a high risk of primary event, um, and the odds ratio is about 3. And then they followed the cortisol levels after surgery. And they showed How it actually almost doubled on post-op day one then post-op day 2 here, the, the, the green, I think it's a green line, uh, you see how it was, um, closer to 10 post-op day one it jumped up to over 20 and so it's post-op day 2. So just to show you that uh stress response that can happen and if you follow those patients post-op they want to usually see uh a robust, um, intrinsic uh uh stress response from your pituitary gland. Here's another prospectus study which looked at something that's very important, which is the length of stay. So when they looked at the length of stay and compared the group that did not uh uh get any steroids to those who did get steroids, there was a significant difference, so it was about 3.6 mean for those who did not receive in about 5.04 with a highly significant p value. And then here's the meta analysis of 4 different randomized control trials again looking at pretty much the same thing which showed that when it comes to transient adrenal insufficiency incidences after surgery between steroids versus non-steroids, again, no significant difference between the two groups, same with permanent adrenal insufficiency. And then, um, when they looked at DI also permanent DI uh was similar between the two groups and uh transient DI uh barely made it to statistical significance and was, uh, favorable with the steroid group and the non-steroid. So, uh, really the question is what are the disadvantages? Are we harming patients by giving them impaired glucocorticoids? There are several disadvantages. One is you can unmask underlying DI. High doses of glucocorticoids can down regulate your your V2 vasopressin receptors on the kidney, increase free water clearance. There's also data to support that it suppresses AVP production, so you can't go ahead and unmask DI when you give patients too much glucocorticoids unnecessarily. It also alters the postoperative assessment of the HPA axis, which can result in patients being unnecessarily discharged on steroid replacement and of course the hyperglycemia that ensues uh could impair wound healing and increase the risk of infection. Here's the protocol that we use here, um, so in patients who do have preoperative adrenal insufficiency, of course, and post-op day zero, we give them hydrocortisone 100 mg before the OR and then we taper it down to 150 mg Q8. Post-op day one, if a patient is able to tolerate PO, we can go ahead and switch them to pills. Um, if they go home we send them home on 25 3 times a day. Post-op day two we instruct them to go to their, um, home dose which is usually around 15 mg in the morning and 5 in the afternoon. Uh, when it comes to folks who do not have preoperative adrenal insufficiency, uh, on post-op day zero, and that's been the case for, for many years here in our institution, we, we give them a dose of hydrocortisone 100 mg before or for one single dose and then we hold and then depending on um the cortisol levels on post-op day one. Which should be drawn at 8 a.m. and should be at least 24 hours from your last hydrocortisone dose. If levels are lower than 5, we treat patients for adrenaline sufficiency. We send them home on 15 in the morning and 5 in the afternoon. If levels are higher than 10, we usually say you're good, no hydrocortisone is needed, and if levels are between 5 to 10, that's based on your clinical judgment. Dexamethasone is used by some anesthesiologists during induction of anesthesia, and that's usually to decrease the risk of postoperative nausea and vomiting. It's not recommended. It causes a lot of suppression of the HP axis and then usually subsequent unnecessary glucocorticcord replacement. Let's talk a little about um alterations in sodium and fluid balance which is relatively common in the early post-operative phase. It could be either insufficiency which will cause AVP deficiency, or it could be excess leading to syndrome of inappropriate ADH release. As I'm sure all of you know, the, uh, or diabetes incis name has changed in 2023, was published in seven international journals, and it was done out of concern for patients' safety and preference. So ADP deficiency may occur in up to 25% of patients after pituitary adenoma surgery. It's most frequently observed within the 1st 48 hours of surgery. So after that 48 hour window, if patients do not develop it, chances are they're not. Um, it's usually transient. Uh, it could be permanent, uh, but very rare if there's a stock transaction up to 2% of the cases can have, um, permanent DI. Here are some risk factors for developing AVP deficiency. So tumor size more than 1 centimeter, uh, craniopharyngioma, uh, rathous left cyst, intraoperative CSF leak, Cushing's disease, visual abnormalities on presentation, uh, if there's supercellular tumor extension, patients who had previous stunt endoscopic lesion resection. Uh, gross stool resection of the pituitary, uh, craniotomies are more associated with the development of, of AVP deficiency and again routine perio-operative use of high doses of glucocorticoids, and I can show you here on the right hand side this was a study that looked at those patients who received conventional very high doses of hydrocortisone around surgery and they had a 52% chance of developing DI. As opposed to the low dose hydrocortisone which um only um uh the incidence went down to 24% of patients developed DI. Here's the criteria we use for uh diagnosing AVP deficiency after this type of surgery, so patients should have uh polyuria, usually more than 300 mLs an hour for at least 2 to 3 consecutive hours. Fluid balance should be negative, urine specific gravity less than 1,0005. Their plasma sodium is usually high, but it could still be normal if if free access to fluids, um, and if they have an intact thirst mechanism, and so does serumozality, um. Urine osmality is low, less than 300, and we of course have to exclude other causes of uh polyurea such as the intraoperative or postoperative fluid, use hyperglycemia, and so on. How do we treat? Of course, number one, we encourage patients to drink to thirst. If your output is still excessive with hypernatremia and patients are sedated or they're unable to maintain adequate oral intake, that's when we give a dose of DDAVP, about 1 mcg in an as needed fashion in the beginning because again postoperative AVP deficiency will be transient most of the time and all you need in general is between 1 to 2 doses most of the time. But if it persists beyond 48 hours, most of the time you will schedule uh Decimalpressin. So you give him 1 mcg of IV or subcutaneous desmopressin and that is sufficient to increase your urine osmolarity to 700, 800 and it really suppresses diuresis to a very minimal amount within the 1st 15 to 30 minutes and it can last for up to 5 to 12 hours and if we further increase the dose, all it's gonna do is prolong the duration of action, not necessarily a greater reduction in the urine output. There is really no apparent difference in the EDH effect between the IV and the suck here um route, uh, but we tend to stay away from the nasal administration, uh, in the postoperative period of course due to the impaired absorption which happens due to sec to the nasal congestion. So, uh, up here I, I'm just showing you transDI that can happen after surgery again up to 25% of the cases, permanent DI, uh, which is very rare to happen with, uh, adenomas, much more common actually to happen in supercellular lesions or cranopharyngioma and up to 25% of cases, uh, but I did want to talk about the triphasic response which I'm sure all of you here are aware of, very rare can happen, uh, in about 3 to 5% of cases, but if you really. Sever the connection between your hypothalamus and your pituitary, uh, uh, what happens is you lack, you lose the stimulation of AVP release to the nerve endings and you end up with AVP deficiency. Now what's gonna happen is the gland is gonna start leaking that pre-sored AVP. Um, and you have about a week worth of AVP stored in your posterior pituitary. So, uh, that's when you get into the second phase which is the SIADH or the hyponatremia. So you're getting too much of that ADH dumped into the serum. And then last when you've depleted all your stores uh you're gonna go back to DI or AVP deficiency where you don't have any AVP secretion from your pituitary. So that's here on the left hand side. What I'm showing you here on the right hand side is what we call the isolated second phase or the isolated hyponatremia, which can happen even more often. And that's when you um don't completely sever the stalk but let's say you injure about 50% of the neurons, so you still you only need 20% of your neurons to actually not have DI. So if you sever half of it, uh, you're good. You don't develop DI, but then again those neurons distal to the injury. Uh, this prehistoric AVP will start, uh, being released into the serum, and you will go into a stage or or phase of hyponatremia which when it's done you're not going to end up with DI again because you only need 20% of your neurons. That's very common actually. It's more common than than um triphasic response and it's even more common than DI I mean patients can can do well with DI if they have an intact thirst mechanism. Once they feel that thirst they will drink the thirst and they're not gonna get into much trouble. It's the hyponatremia where we get into trouble, which is actually uh the leading cause of readmissions after pituitary surgery. So what I'm showing you here on the right and the reason why we call it the isolated second phase, uh, is because if you look at the timeline here and those are classic NIH studies, you'll see the na uh sodium levels are occurring in about 7 days. Um, so again incidences may be up to 28% and it usually occurs between day 4 to 14 postoperatively. Most of the time it's mild and asymptomatic and self-limiting. Uh, but again, the moderate to severe hyponatremia is the most common cause for readmission. And up to 7.6% of patients are readmitted following transpinoal resection for the uh delayed hyponatremia. And that highlights the importance of day 7 labs that we instruct all our patients to get after they get uh uh uh discharged from the hospital. A dips ADP deficiency or DI very challenging situation. Uh, you get absence of a thirst response to hypernatremia, and that's usually because of injury to the circumventricular organs. Um, risk increases following resection actually of craniopharyngioma and scellular tumors. It's not that common, but we should expect longer length of stay, and unfortunately the hypodipsia cannot be cured. It's irreversible and spontaneous improvement occurs very, very rare. Um, those patients should be very closely followed up. They usually we do titration of their fluid intake to 1.5 to 2 L regardless of their thirst, really, and we have to weigh them every single day. We have to, um, make sure they have very close follow up with us in the outpatient setting. On discharge, it's important to give patients very clear instructions on signs and symptoms of AVP deficiency, on hyponatremia and adrenal insufficiency. And again, highlighting the importance of day 7 labs and then close endocrine follow-up. I still have some time here so I think um I talked about a lot of things and uh you know the more important uh part here is how we, you know, how do we translate all of this into our clinical practice. Uh, about more than a year ago, uh, we came together in a combined effort, the endocrine division, the neurosurgeon, and the ENT, PCCM, uh, with a great initiative to come up with this pituitary tumor clinical pathway which would serve as kind of a day by day guide for clinicians in order to streamline those patients and to kind of standardize their care after this type of surgery. It was also an initiative to shorten the length of stay um after pituitary surgery because when we looked at our institution really the most critical that we saw was our length of stay after pituitary surgery was certainly longer than the national length of stay, almost double, so most of, uh, uh, you know, nationally most people stay between 2 to 3 days after this type of uh surgery while we're averaging between 4 to 6 days, so. Uh, still in development, but fast forward many, many months later we came up with a protocol and not just that we have actually embedded that protocol in our EMR in the EPIC system which is still not, uh, uh, in there yet but we're hoping for the go live date for the final build very soon in the next couple of weeks. So just to show you here how to use it if you type in pituitary. And the orders, you'll come across this order set, which is the post-op pituitary section. And then under post-op pituitary resection you'll see two different order sets and you can choose which order sets you would like to expand. So if you choose to expand the first one, you can work with that and choose not to expand the second one. So the first one is more so the order set that is a general postop order set that I'm sure a lot of people are familiar with, uh, with certain editions. uh, so if you click on that it'll expand the order set and as you'll see here I'm sure you're familiar with that. The only thing that we have added from an endocrine perspective. Is um if you scroll down to where it says chemistry, now you have uh your cortisol level. Uh, that is, that should be ordered for post-op day one at 8 a.m. and now you have your as needed, um, labs for DI, your serum osmity, sodium, and your urine osmality that should be drawn if your urine output is more than 300 for 3 consecutive hours. We've also added the in the departmental consults, um. A guide here on who really needs to have an endocrine consult. So again we prefer uh all patients get an endocrine consult, but it's very important especially in these situations where you have preoperative adrenal insufficiency or AVP deficiency. If you, um, uh, if all the pituitary tissue has been removed, if there is any concern for aggressive stock manipulation, uh, functional tumors uh really uh need um uh us on board and patients who develop AVP deficiency or require at least one dose of Desmopressin, and you should consider it if postoperative morning cortisol is in that gray zone where it's less than 10 but it's more than 5. And then the rest of the order set is pretty much the same as it used to be. Now if you choose to expand the second order set, this is more so an endocrine focused um order set which will include postoperative hormonal and uh medication, uh, that's related to endocrinology but also will include some of the discharge orders. So if you click this one now you'll you'll see the endocrine postop um order set where again it starts with who gets the consult this is um. The medication part here with some guidance on who should really get Desmopressin so um we all know that a lot of people still get Desmopressin unnecessarily so we're trying to make the criteria very obvious that only those patients who fulfill all those criteria should get a dose. DDAVP otherwise they can drink the thirst and keep their sodium levels in the normal range, and then you'll hear, you'll see here linked you can go ahead and give them the Desmopressin from this order set as well and then the serum sodium and the urine osmolarity that have to follow the the dose of Desmopressin when it comes to hydrocortisone, there's also guidance here on, you know, patients who had, uh, uh, who already have a preoperative adrenal insufficiency, uh, diagnosis, so. Uh, you can choose to give them a hydrocortisone based on this, uh, uh, protocol that we have and then those who do not have preoperative adrenal insufficiency against some guidance here based on their cortisol levels, uh, who needs and uh how much. And then at the end uh we have a discharge part which again you may choose not to use it now but more so when patients are leaving the hospital you can go back to that order set and choose to uh include their discharge labs so we like to do a 7 day um basic metabolic panel to pick up uh uh to see how their sodium is and of course the 5T4 if they're not already being treated, um. And then at the end here, which I think is crucial is discharge instructions. So if you take that, you'll have an auto populated discharge instructions for the patients, which includes everything the patient needs to know from a DI, from a hyponatremia, and from an adrenal insufficiency standpoint. And then, um, discharge medications you can also reconcile them here on in the order set so you can choose to give them the DDAVP on discharge or hydrocortisone based on what the patient will be needing and at the end there's some guidance on uh the follow up for patients um so you know patients do have an established endocrinologist they should certainly follow up with them but at the end here there's gonna be some guidance on if you'd like to refer patients to see us who to call and and what to do and how to get them. Um, in a timely manner to see us. Uh, so highlights of the, of my talk today, I'll say preoperative endocrine evaluation is crucial. Um, perioperative glucocorticoid use in the absence of known adrenal insufficiency is often unnecessary and may prolong hospitalization. Uh, postoperative hyponatremia is often overlooked and it is the leading cause for readmission, and I'll highlight again the importance of follow-up lab testing and phone contacts after discharge, uh, which demonstrates substantial cost savings to the patient. And then at the end I I wanna say the you know the real true value of multidisciplinary teams, uh, which in this case, you know, will include your of course the neurosurgeons, neuro ophthalmologists, your endocrine colleagues, your radi radiation oncologists, just to name a few. And your endocrinologists uh will be of great support for those patients in the out in the outpatient setting we'll we'll give a lot of support to them once they leave the hospital, so I think it's important to have uh that multidisciplinary care for those patients, um, on their way out from the from the hospital. Uh, I did have, uh, at the end of my talk, I just wanted to acknowledge the team here. Thanks for, um, all your efforts, um, and, uh, uh, I'm grateful to be part of this team, and I think this is some baby steps to something that's hopefully even bigger in the future. Um, the order set like I said, is not yet, uh, in the EPI system, but it will be. We expect it to be so in the next couple of weeks, but we'll go ahead and send S bars to everyone just as a notification that hey, you can all start using the order set. So, um, that's all I have today, and, um. I just wanted to, ah, ah, hear any comments, questions from the audience. Published February 27, 2025 Created by Related Presenters Radwa M. Osman, M.D. View full profile
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