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okay behind the knife ab site review today's topic is adrenal i'm here with kevin patrick this is jason so let's dive right in with some high yield anatomy so Kevin, our resident vascular surgeon, can you please describe for us the vascular supply to the adrenal gland?
Yeah, for such a small organ, it has a lot of blood flow. So the superior adrenal artery branches off the phrenic artery, the middle adrenal artery branches off of directly from the aorta, and then the inferior adrenal artery branches from the renal artery. And of course, you need your venous outflow. So you have the left adrenal vein, which drains directly into the left renal vein. And then you have your right vein that drains into the IVC.
Okay, so Patrick, let's talk about the layers of the adrenal gland. So we break it up typically into the medulla and the cortex. but they'll break down any further so walk us through the cortex yeah so we start with the zona glomerulosa that's the salt memory of salt sugar sex we're starting with salt The zona glomerulosa regulates aldosterone. Move on to the zona fasciculata. This is sugar, which produces glucocorticoids. And the zona reticularis, sex.
Apparently it's the androgens and estrogens. Okay. So GFR, salt, sugar, sex. The deeper you go, the sweeter it gets. It's a way to remember that. Back to you, Patrick. So down to the adrenal medulla. What's significant about that? Yeah, this is where the neuroendocrated chromatin cells live. This produces epinephrine and norepinephrine. Okay, great.
So that's a little bit of anatomy and physiology. Like I said, with all of these endocrine organs, it's important to understand what they do, which will help you understand the pathology and help you answer these questions. One thing that we see very commonly, and I'm sure, Patrick, you see this a lot in the trauma world, is what we call adrenal incidental illness. So we'll stick with you, Patrick. Can you describe the epidemiology of incidental adrenal masses and what's your initial workup?
Yeah, so the incidence is 1% to 2% of CT scans, essentially, on our patients, which is really quite common. So as you mentioned, when we're getting all these trauma scans, we do see adrenal incidence quite commonly. And in regards to the workup, you want to evaluate for concerning imaging features, right? And we'll try to determine if this tumor is functional. So that means we're getting labs and a CT scan, specifically a CT scan, adrenal protocol.
Yeah, that's great. Exactly. So you want to be sure that you get that adrenal protocol CT. And what that is, that's a three-phase thin-sliced scan. So the three phases you're looking for is a non-contrast, a arterial, and a delayed washout in 15 minutes.
and that will help you kind of classify because the two big things you're worried about with this incidental illness is well one is it malignant or non-malignant and then we're going to talk about whether or not it's functional versus non-functional because that's going to guide our management So concerning findings on our CT adrenal would be its size. So it's greater than four centimeters. That adds a higher malignant potential.
Anything that's greater than 10 Hounsfield units on a non-contrast scan is more concerning. Typically our benign lipid-rich adenomas are less than 10 Hounsfield units. or a delayed washout, so less than 30% washout at 15 minutes would all be concerning findings on our CT scan.
So, Patrick, in addition to the CT, I said we want to worry about malignant versus non-malignant, but we also want to worry about functional versus non-functional. So, what kind of labs can you get to help you figure out whether this thing is functional or non-functional?
Yeah, so we're going to order urine metanephrines, a VMA, catecholamines, and also do a low-dose dexamethasone suppression test. And then the classic or standard labs, I would say serum potassium in addition to renin and aldazine. Yeah, this can be somewhat institution-specific. Some places will start with aplatis of metanephrin and get the 24-hour urine as a confirmatory test.
The one I would add in there as well is the DHEA sulfate. That's one that's pretty standardly obtained to look for function as well. And we should go back to say that, of course, With all these, you know, you're going to ask a history and physical. And so on the outside, you might see that in a form of a patient with Cushing's or a patient that's concerning for pheochromocytoma, and that can help you guide your management.
Additionally, you want to ask about or know about any history of prior malignancies because there can be some tumors that will metastasize to the adrenal gland, most commonly long, and that's going to affect your workup and your management as well. But getting back to some different pathologies of the adrenal gland, one thing that we probably all studied in medical school and haven't thought about since then is congenital adrenal hyperplasia.
So Kevin, can you talk to me about the etiology of congenital adrenal hyperplay? Yeah, unfortunately. So there's the 21 and 11 beta-hydroxylase. And what these do is they convert cholesterol to aldosterone, cortisol, and testosterone. Okay, so what hormonal abnormalities, you know, there's three types of congenital adrenal hyperplasia. What are those types and what abnormalities do we see with them?
I just want to know when I'm not going to be tested on these again. So you have the 21-hydroxylase deficiency, which is the most common, and that increases your testosterone and decreases your aldosterone. You have your 11 hydroxylase deficiency. This increases your testosterone and increases your aldosterone.
And then finally, you have your 17-hydroxylase deficiency. This decreases your testosterone and increases the aldosterone. Okay, so I have good news from everybody. If you look at our abcycopanion, there's a really easy way to remember these different congenital adrenal hyperplasias.
that are going to get you 99% of the answers correct on any test you'll ever take, unless you become an endocrine surgeon. It's a table, and it's a little bit difficult to explain, but essentially if you take those numbers, 21, 17, and 11, and you replace the one with an up arrow and then you create another comment column one that says hypertension and one that says burialization
and you plug in those numbers, it's going to tell you what's high and what's elevated in each syndrome. Like I said, it's difficult to explain, but just take a look at the table in the Abcite Companion, and that's all you need to know for congenital adrenal hyperplasia for the Abcite. So coming back to you, Patrick, let's talk a little bit more about some more pathologies. So hyperaldosteronism, otherwise known as Kahn syndrome. So how do these present?
These patients are often hypertensive. That's the key sign. They'll have elevated sodiums and low potassium. Yeah, that's exactly right. And they're going to give you that in the prompts, too. You're going to have a patient that typically has poorly controlled hypertension, typically on three different agents, and their labs show elevated sodium and a low potassium. What else do you see? Yeah, so for primary hyperaldosteronism, you're going to see low renin.
versus secondary hyperdicinism in which you're going to have high renin. And typically, the plasma aldosterone to renin ratio is going to be greater than 25. Great. Yep. And that's in all those labs that you said you're going to get. You're going to look at that aldosterone to renin ratio, and that's going to clue you into that diagnosis. So what other workup does a patient with a suspected hyperaldosteronism get?
Yeah, this would be the salt load suppression test. And so we're going to check urine aldosterone after the patient is salt loaded, and this is going to remain elevated. we can also perform imaging so we're going to want to localize the lesion with a ct scan mri or np59 scintography you could also if needed to try to
determine the sightedness and do adrenal vein sampling. Yeah, we're going to get back to that in just a second because that's an important caveat for these hyperaldosteronism is that adrenal vein sampling. But let's first move into, okay, let's say we make the diagnosis. We have a hyperaldosterone patient. What's the management?
So bilateral idiopathic adrenal hyperplasia is, first and foremost, the most common reason in which these patients have hyperaldosteronism. This makes up about 65%. In this case, we're going to manage... Medically and that includes meds like spironolactone ACE inhibitors, and calcium channel blockers like nifedipine. We're also going to make sure, as we mentioned earlier, that these patients have low K. We want to make sure their potassium is replaced.
And if we can localize it, we're going to perform an adrenalectomy. If the patient has bilateral lesions, then they're going to need flujicortisone supplementation postoperatively because we're going to be messing with both the glands. That's great. That's a great overview.
You know, I will say that there are some places that are doing subtotal adrenalectomies for bilateral adrenal hyperplasia, but that's a little in the weeds for the ab site. But what I think is pertinent is, Kevin, let's say... That you have a two centimeter adrenal mass and the patient has hyperaldospirin. Let's say it's less sided. So what are you going to do? So.
You have a left-sided adenoma and there they are, it's functional with hyperaldospin. I'm going to remove it. Okay, you do that and they still have clinical hyperaldospinism. What happened? You screwed up, man. Oh, so you still do the adrenal vein sampling? Exactly.
So aldosteronomas tend to be very small. And it's getting less and less common with CT scans as CT scans get more and more sensitive. But the functional... aldosterone adenoma tends to be very small so what most likely happened was that two centimeter incidental loma was a benign adenoma and your functional tumor was actually on the contralateral side
So hyperaldosteronoma is one thing where most people in most places are still doing a selective or doing venous sampling to localize prior to surgery. You don't have to remember that for the other ones, but for aldosteronomas, you need to be sure to remember that. Okay, so Kevin, we're going to stick with you, and we're going to talk about Addison's disease, or hypocortisolism. Can you describe the presentation, workup, and management of hypogorisolism?
Yeah, so it can present in a couple different ways. Kind of the more chronic presentation is when they have weakness, fatigue, nausea, anorexia, weight loss, and hyperkalemia. They can also present an acute adrenal crisis due to sudden or complete loss of adrenal function and this would be with refractory hypotension, fevers, lethargy, pain, nausea, vomiting. All right, Jason, you seem to be our relative endocrine expert here. So I'm going to bump it back to you for the workup.
Sure. So with a work of AdSense disease, what you're trying to distinguish is between primary and secondary AdSense disease. So you're trying to figure out whether the problem is a pituitary gland or whether the problem is the adrenal. so you'll start by measuring your am cortisol okay so if that's well okay you know that there's a problem you still don't know where it is so what you do is you give cosentropin and if the adrenal gland is functioning you should see a rise in cortisol
Okay, but let's say you don't. Well, you still need to kind of confirm that the pituitary is functioning okay. And the way you do that is measuring the ACTH. So you stop and think about it, think about your feedback mechanisms. If your cortisol is low, your ACTH should be high. So if you have low cortisol... that doesn't respond to a cosentropin stimulation test.
Okay, now there's a problem with the brain gland. Now, is it pituitary functioning? Well, if your ACTH is not elevated, in other words, if it's normal or low, then you have to consider there's a component of secondary hypocortisolism. Does that make sense? I think I got it. Okay. Well, I'll kick it back to you then. Let's say we made the diagnosis. How about management? So chronically, you give them corticosteroid replacement. In the acute setting, you're going to use high dose.
drugs like dexamethasone and hydrocortisone and IV fluids of course and then we're always going to worry about this if we're stress dosing patients for elective surgery and those type of things as well okay so Okay, moving on to Heifert Cortisolism, so Cushing Syndrome, Patrick. can you describe the pathophysiology workup and management for a patient with suspected hyper cortisolism yeah most like so what's the most common cause just first of all
Yeah, so these are exogenous steroids. So Kevin, I'm sorry, you don't have Cushing. syndrome, right? It's all the steroids you've been doing. It's been all those wrong websites. That's right. How about the workup? Yeah, so I want to try, okay? And this is something that everyone needs to take some time to wrap their head around for the test. You will have a question on this.
and so initially we're going to perform a 24-hour urine cortisol and or a late night kind of evening serial cortisol check now if this is high and it matches up with our clinical presentation then we have concern for cushing syndrome So next we're going to check the ACTH. Okay, so this is low than I'm concerned for an adrenal source. So primary hypercortisolism. If ACTH is high, then I'm concerned for a secondary source like pituitary, which would be Cushing's disease or an ectopic source.
Now, to further determine the difference between, you know, the secondary source of pituitary ectopic, we're going to perform a high-dose dexamethasone suppression test. This will inhibit the pituitary gland. It will not inhibit our ectopic source. i gotta go searching now for where these things are so if i'm worried about a primary primary hypercorrhizalism i'm performing an adrenal ct scan try to find the sidedness here and identify which gland is involved
If I'm worried about a pituitary source, we're going to do a brain MRI. And if I'm worried about an ectopic source, we're going to do a CT scan of the chest, the abdomen, and the belt. Great. I think it's a great overview. You know, I feel like we maybe skipped ahead a little bit. We didn't talk about how these patients present. So let's backtrack just a second. And Kevin, what do we see and what's your standard, you know, Cushing's patient?
Yeah, they're generally overweight and have abdominal stria and... Yeah, so these are your patients that are diabetic, they have poorly controlled insulin, they typically have hypertension. So don't confuse them with, you know, they can present some more to patients with hyperaldosteronism as far as hypertension goes.
The buffalo bone hop, abdominal strea, obesity, you know, all the peripheral wasting, all those things that we see with Cushing's syndrome. And like Patrick said, you got to figure out if their cortisol is high, if their cortisol is high, you got to figure out what the cause of it is. It's the adrenal gland.
if it's too much acth from the retubutary and you use your various cortisol test and your low and high dose dexamethasone suppression test to parse that out and then you move to localization with imaging so how about management matt patrick yeah so if it's a cortisol producing adrenal tumor we're going to perform an adrenalectomy if we have cushing's disease again a bitutary mass that's producing acth
then we're going to move forward with trans sphenoidal resection and if we have an ectopic acth producing tumor most commonly metastasis or small cell lung cancer then we're going to try to identify where that's at and perform resection Okay, moving on, working through our functional adrenal tumors, let's go with the ever-popular pheochromocytoma. So, Kevin, we talk about FEOs. We frequently hear about the rule of 10 for FEO CROBO. So I talk about what was the rule of 10?
Yeah, so that's the 10% are malignant, 10% are bilateral, 10% are in children, 10% are familial, and 10% are extra adrenal. Great, okay. So our field patients, these are the ones that show up with impending sense of doom. You know, they have palpitations, they have very poorly controlled. hypertension. So these are the ones that we're suspecting as having a pheo. Now we talked a little bit about it before, but what's the workup for a patient with a suspected pheochromocytosis?
So you're going to start with plasma-free metanephrines as the initial test. And then you'll get your urine metanephrines. These are more specific but less sensitive and good for confirming the diagnosis. I'll pause you right there. So I will say that's a little bit controversial. I remember this question showing up on the outside. It always made me angry. So the way it'll be worded. He'll ask, what's the best test for a pheochromocyte telomone?
And multiple right answers. Yeah, I think that's not fair because it best are you looking for more sensitive or more specific? And I still don't know exactly what they're going for. If it was me answering that question. i'm going to put plasma free metanephrines because it's more sensitive most places are using that as their initial screening test and then when the 24-hour urine is their confirmatory test
But I guess it's how you interpret the question. If in your mind, you think best means more specific, then the question is probably a 24-hour. Good luck. Yeah, so... That's the best advice I have. I remember seeing that question four or five times throughout my time taking the app site. And every time I felt like I was gambling. Okay. So how about some imaging? Yeah, so this is where you get your dedicated CT adrenal scan and MRI.
Okay, great. And what about you don't see anything on CT adrenal or MRI? This is where you get your MIBG scan. Yeah, so your VibG scan. Again, going back to your rule of 10s, you know, 10% are extra adrenal. And the most common site for an extra adrenal, anybody? No, you're an organ and a soccer candle. I remember this. Oh, the aortic bifurcation? Yeah, aortic bifurcation. You should work around that area. Yeah. Yeah, so...
We'll get them really deep into the weeds, but it's described as either the aortic bifurcation or the takeoff of the IMA. But I think most people consider it the aortic bifurcation. Okay, so there's a lot to talk about here. So are you going to rush these patients off to the OR for their adrenalectomy? No. Why not? You need to get them optimized before you take them to the OR. Yeah, these can be very hemodynamically labile interoperatively. So how do you get these patients ready for the OR?
So you start with volume replacement as they chronically become more or less dehydrated. And then you start an alpha blockade on them with phenoxybenzamine or prosazin. Yeah, phenoxybenzamine is probably the main answer on the test. In reality, it's cost prohibitive for phenoxybenzamine. So again, typically prazosin. So how do you know when you've had them adequately blockaded?
I think you look at their blood pressure and their heart rate. Yeah, so while you go for, you want them to be orthostatic and also dry mucous membranes are your indicators that you have them appropriately off the blockade. And then you can add a beta blocker too if you need to, but you want to make sure they're alpha blockaded before you beta block them.
Okay, a beta blockade universal after the adequate alpha blockade? Not everybody will need that, but if you do need it, you can add it. You just want to make sure that you add the alpha blockade so you don't get unopposed to alpha agonism. Sure. Okay, so Kevin, what's the management?
So the management is an adrenalectomy. Okay. And how do you want to, you're in the OR, you're staring at the adrenals, you got the artery, you got the vein isolated. What do you want to make sure that you're one, communicating to your anesthesia provider and two, what order are you going to take? Yeah, so we're going to let them know that they were about to ligate some vessels, and you might see a drop here in their catecholamine, so you might need to give them some volume ASAP.
So I'd like you to get the adrenal veins first to avoid a catecholamine crisis with tumor manipulation. Perfect. Okay. So let's wrap that up with Ferfito and move on to now adrenocortical carcinoma. Okay, Patrick, so what can you tell me about adrenocortical carcinoma? It's a rare malignancy. Unfortunately, it often presents in advanced stages.
And most typically presents in the fourth or fifth decade of life, these patients will often have Cushing's syndrome, size of virilization, and hypertension. Okay. Can you describe the management to me? Yeah. So you want to take out as much as you can. So radical adrenalectomy with debulking as needed for patients who require adjuvant treatment. This is somewhat unique in that we get mitotain. And you can consider external beam radiotherapy as well. And this would be indicated for patients.
who are at high risk for local recurrence and some of those factors are certainly a positive margin, vascular or capsular invasion, intraoperative tumor spillage, and a KAI 67 of greater than 10%. Great. So, Kevin, I'm going to throw a little bit of a curveball at you. But let's say you're laparoscopically taken out an adrenal gland for a presumed functional aldosteronoma.
You get in there and you see that the adrenal mass is invading into the abdominal side wall. What's your first step? I think at that point, I would just biopsy it and stop. Wrong. So what you would do is you would convert to an open procedure because renal cortical cancer is one of the few that has a theoretical risk of spread through aerosolization.
So that's doubtful. That was pretty theoretical. Well, there are some advanced centers that are doing laparoscopic resection of retocortical cancers, but the board answer is still convert to an open procedure. Unlikely to show up on the app site, but you can... file that one away for your oral boards, potentially.
I like picking on Kevin because he's a very smart vascular surgeon. So whenever we talk about topics that I know more about than him, I like to tease him a little bit. Okay, so back to you, Patrick. So your patient has completed his treatment for his adrenocortical carcinoma. What's the appropriate surveillance? Yeah, so for this one, remember, it's pretty aggressive, right? So it's quite frequent. You get CT scans of the chest, the abdomen, and the pelvis every three months.
Okay, so just one last thing to mention before we get into our quick hits, and that's the adrenal myolipoma. So this is a benign tumor of fat and bone marrow. They can be small, but they can also be very large, sometimes greater than 10 centimeters. The important thing to remember is that they have a very characteristic finding on CT scan and they can often be diagnosed on CT. So when we talk about those
size cut-offs that are greater than four centimeters, a higher risk for middle agency. That does not apply to these. So you can typically observe these. So if you get a question that very clearly describes adrenal myelolipoma, it's okay to watch those unless they're symptomatic or, you know, very large, say over, you know, 7 to 10 centimeters in size.
Okay, so I think that wraps up a good discussion of our adrenal tumors. Again, incidental lomas, your two main questions are... benign versus malignant and we talked about ways of distinguishing these two and then parsing out functional versus not
You always want to do a resection for anything that's concerning for malignancy or that's functional. And there's various things to consider depending on the particular pathology or physiology and pathophysiology of that tumor, getting that patient ready for the oar. So you guys ready for a quick hits? Ready. All right, let's do it. So Kevin, most common etiology of Cushing syndrome. Exogenous steroids.
Okay, great. Patrick, most common ideology of adrenal insufficiency? Globally, it's tuberculosis, and developed countries is autoimmune. Perfect. Okay, Kevin, screening test for adrenal insufficiency? And serum cortisol. Great. Patrick, a patient's undergoing a resection of a pheochromocytoma and becomes hypertensive. What would you want your anesthesiologist to get?
So first line would be nitroprusside, among other antihypertensive agents. Yeah, it's very important to be communicating with your anesthesiologist throughout resection for a FIBO, because those patients are... incredibly labile, and you need to be prepared for everything. Okay, Kevin, the most common primary cancer site for an adrenal metastasis. that's the lung yeah so if you're concerned about metastasis
We didn't really talk about it, but if you're concerned about metastasis, that's one of the few indications for a biopsy of an adrenal mass. You do not want to biopsy most of these, and certainly if you're thinking about biopsying, it's something you want to rule out a pheo before you stick a needle in it.
But long is the most common, and so if you're concerned, you should include a CT chest in part of your workup. So last one, Patrick. A patient with suspected pheochrobocytoma has normal plasma and years of urine metanephrine. What additional tests can be performed? This is, of course, the clonidine suppression test. Exactly. Clonidine suppression test for confirmation of a questionable theta. Okay, that does it for Adrenal. Hopefully you guys found that helpful, and thanks for listening.
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