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ABSITE Review: Adrenal (Podcast)
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>> Ok and welcome back to another Behind the Knife ABSITE review. Today we have Jason Bingham, Woo Do, John McClellan and myself bringing you adrenal gland. Wanted to let you guys know we finally got the podcast onto Spotify. It took a lot of work but now if you guys are Spotify listeners you can go on there and listen to Behind the Knife on Spotify. So tell your coworkers a little easier sometimes than ITunes and it streams rather than downloads. So save some data; use some Spotify. Alright Jason take adrenal away.
>> Alright, Behind the Knife ABSITE and board review. I hope everybody is studying out there, I hope everyone is dominating their study out there. Let's talk about some adrenals. So we'll start with some high yield anatomy. So John, what's the arterial blood supply to the adrenal gland? >> So working from top to bottom so at the superior part of the adrenal you get branches off the inferior phrenic. You also get branches directly off the aorta and more inferiorly it will get branches off the renal arteries.
>> Yeah so it's got a couple different arterial feeds into it. The more interesting and the more tested thing Woo is however the adrenal venous drainage. It's a little different on the left than on the right, isn't that right? >> Yeah, that's correct. So on the right side the vein is shorter and drains directly into the IVC. And on the left the vein is longer and drains into the left renal vein. >> So John the adrenal gland is broken up in two anatomic functional units; the adrenal cortex and the adrenal medulla. Now the adrenal cortex is broken up to three different zones that also secrete a particular hormone.
What are those three zones and what hormone do they secrete? >> So I think about this from the medical school acronym GFR or salt, sugar sex. So the first one is zona glomerulosa which secretes aldosterone. Zona fasciculata which secretes cortisol and zona reticularis which is secretes your androgens. >> Right, right, right salt sugar sex the deeper you go the sweeter it gets is the mnemonic I remember from medical school. Ok what about the adrenal medulla Woo, what is the origin of that and what does it produce?
>> So the medulla comes from neural crest origin and it produces catecholamine's so your epinephrine and norepinephrine. >> So moving on to a little bit of physiology John, so the something often comes up when we talk about the adrenal gland is the renin angiotensin aldosterone pathway. Walk us through that. >> The renin angiotensin aldosterone pathway it stems from a decrease intervascular volume and decreased sodium concentration in the blood. So this will stimulate renin release in the juxt to marrow apparatus.
Then the renin which is now circulating stimulates the conversion from angiotensinogen to angiotensin I. The angiotensin I is then converted to angiotensin II by the angiotensin converting enzyme ACE in the lung. >> Yes, so it's a good one you need to know that. So those are -- those are testable things. So renin from the JXA or the justaglomerular apparatus. Renin converts angiotensinogen to angiotensin I, angiotensin I then goes to the lung and -- where it's converted to angiotensin II by the angiotensin converting enzyme.
What are some of the actions of angiontensin II after it's produced? >> So this will cause vasoconstriction and the release of aldosterone from the zona glomerulosa. >> Yep, that's -- so that's where it comes into the adrenal gland. After all of that happens angiotensin II responds by vasoconstriction and traveling to the adrenal gland causing the reduce of aldosterone. And aldosterone then does what John? >> It will cause sodium retention and potassium excretion in the renal tubules. >> Yep, so that' -- that's again these are all feedback mechanisms and response to decrease to vascular volume.
It's a very important component of the adrenal gland and its functional capacity. Another thing is the cortisol pathway Woo, walk us through how the adrenal fits into all that. >> So for the cortisol pathway, think back to the hypothalamic pituitary axis. So the hypothalamus releases corticotropic releasing hormone or CRH which then in turn stimulates ACTH release from the pituitary gland and that ACTH stimulates cortisol synthesis and release from the zona fasciculata of the adrenal gland.
>> Right and so -- and then what is the role of cortisol, what does cortisol do? >> Yeah so the end affect of cortisol is to inhibit the release of CRH and ACTH in a negative feedback loop. And downstream the cortisol has effects on hepatic gluconeogenesis, glycogen synthesis, protein catabolism, lyposysis of fat. Additionally cortisol has effects on hyperglycemia, impairing wound healing, leads to collagen loss and bone loss. >> Yeah, so I know we all became surgeons so we didn't have to worry about this confusing physiology, but it's really important to understand the underlying mechanisms so that way you can understand the pathology.
It makes understanding some of the different primary disorders of the adrenal gland easier which we're going to move into right now. So some adrenal disorders, John primary hyperaldosteronism tell us a little bit about that. What are some just kind of key, basic things we need to know? >> So on the ABSITE if you see a patient that they're presenting to you as hypertensive with hypokalemia this is what you need to be thinking of off the bat. Primary hyperaldosteronism is more common than previously thought. Up to 10% of hypertensive patients now have it.
>> And I was surprised, I was surprised by that. That's pretty common, up to 10% of hypertensive patients are due to a primary hyperaldosteronism. Good news for us who like to operate because we'll get to that here in a little bit. But how do you make the diagnosis? >> So you first want to measure your serum aldosterone and measure the plasma renin activity. You can also confirm this with a salt load test and you're aldosterone to renin ratio should be greater than 20 to 1.
>> Right, so that's an important thing you need to know. The aldosterone to renin ration of 20 to 1. And if you go back and you think about your pathway that'll make sense. So after you get your biochemical -- your laboratory confirmation what kind of imaging do you want to get? >> So I directed CT adrenal protocol with thin cuts. >> Yeah and that's an important thing we'll get to here in a minute. These are typically very small -- the cause, when it's caused by an adenoma. The adenoma is typically very small.
So let's say under CT scan you see a -- you first off you have all the things. You have the laboratory confirmation of hyperaldosteronism and your CT scan shows a unilateral macroadenoma greater than one centimeter. What do you want to do? >> So these patients would be consented for a laparoscopic adrenalectomy. >> Ok and what if you either see something less than a centimeter or you don't really see anything at all, what do you want to do? >> So then your next steps would be adrenal venous sampling to distinguish unilateral macronoma versus a bilateral hyperplasia.
>> Yeah and believe it or not some texts will actually say you need to adrenal venous sampling on all patients even if you see a macroadenoma because it's possible to have a nonfunctioning benign adenoma. And you actually have a contralateral functional microadenoma that's an aldosteronoma. That's in some texts; I don't think that most people are practicing that way. So typically I would go tumors that are greater than one centimeter resect, if they're smaller than that then you go with the selective venous sampling.
What about if you see hyperplasia? >> So hyperplasia is managed medically with sodium restriction, potassium supplementation as well as spironolactone or eplerenone. >> Ok, Woo another common clinical syndrome associated with adrenal gland we talked about the renin aldosterone pathway and how that can go wrong. Let's talk about the cortisol pathway and how that can go wrong. What's Cushing's syndrome? >> Yeah so the symptoms of Cushing's syndrome include obesity, muscle weakness, fatigue, moon faces, your buffalo hump, striated skin, hirsutism and osteopenia.
For Cushing's syndrome think about three different discreet categories. So first you have your ACTH secreting pituitary tumor, this is the most common comprising 65 to 70% of Cushing's syndrome. Second think of your ectopic ACTH secreting tumor and these are most commonly small cell carcinoma of the lung. And third, think about cortisol producing adrenal tumors and this is most commonly in adenoma. >> Yeah, so exactly so you went through the clinical syndrome there, there can be some different causes.
So how do you go about working that up and sorting these out? What's your goals of your evaluation? >> Yeah there are a couple goals in the diagnosis of this. So first you want to determine that a state of increased cortisol production exists. Second you want to determine whether the state is ACTH dependent or ACTH independent. And if it's ACTH dependent than it's going to be pituitary or ectopic. And if it's independent it's going to be an adrenal source. >> Ok, so how do you go about doing that? What kind of test do you want to run?
>> Yes, so first you want to start with a 24 hour urinary free cortisol collections. >> And that's going to tell you that the first goal of therapy like you said is going to determine whether or not there's a hypercortisol state. So that's -- that's you way of doing that. The 24 hour urine not a serum cortisol because it fluctuates throughout the day, you need a 24 hour urine cortisol for that first goal of therapy. Ok. >> Exactly, so after that once you have your 24 hour collection that's elevated, you want to move on to a low dose dexamethosone suppression test.
If both these are elevated then the next step is to measure the serum ACTH level. And if the ACTH is suppressed then you know that it's an adrenal source because the axis is intact, it's in the adrenal. If the ACTH is elevated despite the suppression test, then you want to move on to do a high dose dexamethasone suppression test. And here the high dose dexamethasone will suppress an ACTH produced for most pituitary adenomas. But if it's an ectopic source such as the lung the high dose dexamethasone will not suppress that.
>> Right, so it's just going back to your axis, you're doing your confirming your excessive cortisol level with a 24 hour urine test. You're doing your dexamethasone suppression test. If you measure your ACTH and its suppressed then like you say you know your axis is intact and your source is from your adrenal gland. If you ACTH is elevated then you got to sort out where is it coming from? Is it coming from the pituitary? Is it coming from an ectopic source? If you do a high dose dexamethasone test that will suppress most pituitary tumors but it won't suppress if it's coming from the lung.
So just again you've got to understand the axis and once you do that you understand how you suppress different things. You just got to -- it's difficult to just rogue memorization. But if you understand the process you're going to be able to answer these questions. So, ok so let's say you do that Woo and based on all those tests you suspect that you're excess cortisol is coming from an adrenal source, what's the next step? >> The next step would be to get a dedicated abdominal CT scan. >> Perfect. And it's -- you want to make sure it's a triple phase adrenal protocol CT.
It really finds those smaller adenomas. Let's say that you after you run your dexamethasone tests you suspect a pituitary source, what's the next step? >> The next step then would be a pituitary MRI. >> Ok. And let's say you suspect an ectopic source. >> So then you want to get a chest CT. >> Yeah, if you're looking for a lung cancer. And what type of lung cancer produces ACTH? >> Small cell.
>> Small cell lung cancer, perfect. >> Ok, so moving on another common board scenario that you're unlike -- that most of us are unlikely to encounter in actual clinical practice is congenital adrenal hyperplasia. I really like to ask questions about this and it's a very complex topic. I know at one point I spent a long time trying to memorize the hormone pathway and how different things get broken down and what's high and what's not high. And then I found a very easy simple to use mnemonic that's gotten me almost every question right on the boards since that time.
So it's a little bit hard to describe so what we're going to do -- I'm going to try but first what we're going to do is I'm going to point you to a very useful two minute YouTube video called, Easy Congenital Adrenal Hyperplasia Mnemonic that's going to get you most of the answers right on the ABSITE and the general surgery boards. Now we're going to put a link to that in our show notes. So I'm going to try and describe this table to you to help you visualize. So the three most common ones you need to know are 21 hydroxylase deficiency, 17 alphahydroxylase deficiency and 11 alphahydroxylase deficiency.
The key things we're worried about with these syndromes are aldosterone levels and testosterone levels. If you have an elevated aldosterone level we know what aldosterone does, we know the pathway. So it's going to give us hypertension and hypokalemia. If you have elevated testosterone it's going to give you virilazation. So you think about the numbers; 21, 17 and 11. You make two columns the first column is aldosterone, second column is testosterone. You think about blood pressure and sex. Your blood pressure comes up before you have sex.
Aldosterone and testosterone. Use the numbers 21 and under those columns 21. Every time you see the number one it's and up arrow, think of it as an up arrow. That's going to tell you what's elevated. So a 21 hydroxylase aldosterone is going to be normal and Woo your testosterone is going to be? >> Up. >> Up, so two -- one, two normal one elevated. Seventeen is going to be one seven, aldosterone testosterone what's elevated John? What's normal?
>> So aldosterone would be elevated. >> Aldosterone's elevated. Testosterone's normal so those patients are going to have hypertension, hypokalemia and no virilization. Your 21 hydroxylase is going to have normal blood pressure, normal potassium and virilization. What about 11 Woo? >> So for 11 you have one in the aldosterone column and one in the testosterone column so both are elevated and these patients will have hypertension, hypokalemia and the virilization.
>> Right, and they're going to give you those clinical scenarios, they're going to ask you what -- which they're going to list those. It's going to be A, B and C you've got to pick them. So go watch that YouTube video, draw that out, you'll never miss another question on congenital adrenal hyperplasia on the boards. Ok so let's move on to adrenal insufficiency. What are some causes of primary adrenal insufficiency Woo? >> So the most common in western societies is auto-immune. In the developing world the most common is tuberculosis.
And additionally you want to think about bilateral adrenal hemorrhage and adrenal metastasis. >> Ok, John what about -- so that's primary adrenal insufficiency. Again auto-immune most common in the United States and western societies. The world wide you've got to think about tuberculosis, something we often don't think about. Ok what about secondary adrenal insufficiency. >> And so the most common reason for adrenal insufficiency in the United States is actually suppression of ACTH secretion but from exogenous steroids.
>> Right, these are your patients that are on prednisone for whatever reason; for rheumatoid arthritis, for lupus whatever and they're coming in to have a surgery and they're adrenally suppressed. What are some signs of chronic adrenal insufficiency Woo? >> So you get fatigue, anorexia, abdominal pain, nausea, diarrhea and that classic skin hyperpigmentation. >> Yeah and so the big thing we're concerned about when these patients that come in with adrenal insufficiency is this is a surgery test, we're going to be operating on them.
We're going to be putting them through stress. The concern of pushing them into an Addisonian crisis. So that's in patients who have a decreased adrenal reserve, who are adrenally suppressed and during time of stress such as surgery or trauma. What are some signs that we'll see with Addisonian crisis John? >> So you'll get cardiovascular collapse, they'll be hypotensive, tachycardic. And you'll get refractory shock. >> Yep, refractory shock so what's the classic? You see a patient in the ICU what's the classic thing that tells you that they're adrenal insufficient?
>> So a patient that's in the ICU on multiple different pressors and you're still not having a response. >> Right. Hypotensive, unresponsive to pressor that's classically what you're going to see. What do you want to do with those patients? You want to send off your cortisol test, your dexamethosone or your ACTH stimulation test. What do you want to do? >> So the internal set off, then you send off your cortisol level. But you also want to be a -- start treating these people imperically. >> Right, and that's the key thing right there.
You don't wait for your test. You treat them imperically and what do you want to treat? What typically -- what's a good answer to treat them with? >> So you want to treat them with hydrocortisone 100mg. >> Yeah, yeah. So again you send off your test sure. But the key -- the key concept there is you don't wait for your test, you treat them. You treat these patients. And so we're talking about the ACTH stimulation test, Woo what is that?
>> So for this test you administer a synthetic ACTH and you measure cortisol levels at zero, 30 and 60 minutes. So if you see that the cortisol level is greater than 18, that's a normal test. >> So John you mentioned that you can treat with hydrocortisone which I think what a lot of people would treat suspected renal insufficiency with. What's the problem with that when it comes to the ACTH stimulation test? >> So it actually will interfere with your test and give you false results. >> So what's an alternative steroid that you can use that doesn't interfere with the ACTH? >> Then you can use your dexamethasone and this won't interfere.
>> Right. We're getting a little bit into the weeds I doubt any of that's going to show up on the -- on the boards. But certainly Addisonian crisis and treating and all that stuff will. Ok so we're moving into some lesions, some adrenal lesions. So something we encounter a lot hear a lot about and we talk a lot about is the adrenal incidentaloma, Woo what's the definition of an incidentaloma? >> So this is something that is found incidentally as a victim of modern imaging technology.
>> Right, so you have everybody that trauma patient, every trauma patient gets pan-scanned, everybody with belly pain gets an abdominal CT. We're seeing more and more small, little adrenal lesions that are very common that we would have never seen before. So then we're stuck with what do we do with this? So how do you approach these patients Woo? >> So first you want to start with a laboratory work-up to determine if the tumor is hypersecretory in any nature. So test for cortisol levels, catacholamines, aldosterone to renin ratio and a DHEA sulfate levels.
>> Yep this is -- I've said it multiple times in this podcast already but if you understand the physiology you don't have to memorize what you send off, you just know. So you -- do you think about what does the adrenal gland secrete? Those are the things you test for to see if it's hyperfunctioning tumor. So what about if your laboratory work up is negative? How do you approach these incidentalomas? >> Then your management is going to depend on size and imaging characteristics. So let's start with the small lesions.
So small lesions less than 4cm with benign imaging characteristics namely they're smooth in appearance, they're homogenous, they're less than 10 Hounsfield units and they have greater than 60% wash out on 15 minute delay phase CT. So for these select lesions it's OK to observe with repeat imaging in four to six months. >> Right. Less than 4cm this is what you do. You look for those benign imaging characteristics and specifically that less than 10 Hounsfield units and the greater than 60% wash out.
Those are things that are going to show up, those are things that you need to know. For those repeat imaging six months. OK, what about lesions that are larger? Let's say larger than six centimeters. >> Yeah, so six centimeters is a good cut off. Or you want to kind of lump into this category any functional lesions. Or any of those worrisome imaging characteristics. So for these think about heterogeneous greater than 10 Hounsfield units, less than 60% wash out on delayed phase.
So for all these patients they should move on to adrenalectomy. >> Ok what's an important caveat though? Because you said you know anything that doesn't meet those characteristics, anything greater than six centimeters. There's one important thing that you have to think about. >> Yeah the exception to the rule is the clearly benign cyst or myelolipoma. >> Yeah so myelolipoma it has a pretty characteristic appearance on imaging. And these can be pretty large but they don't need resection. Same thing with adrenal cysts.
If it's characteristic on imaging as a myelolipoma and asymptomatic even if it's 10cm it does not require dissection. Ok so we covered lesions that are less than four centimeters, we covered lesions that are greater than six centimeters. What about that in between that four to six incidentaloma, what about those? >> So there has been a trend towards taking out smaller and smaller lesions in young and otherwise healthy individuals. But in this kind of grey area it should really be individualized therapy based on the patient age and comorbidities.
>> Right and again these kind of grey areas are unlikely to show up in board type scenarios but just know that there's clear recommendations for less than four, there's clear recommendations for greater than six. The four to six is kind of individualized. If it's a young, healthy patient that's a surgically fit patient and doesn't want to undergo serial imaging it's perfectly acceptable to do adrenalectomy. What's the role of biopsy for an incidentaloma? >> Generally you don't want to biopsy these lesions; they have low diagnostic value and a high complication rate.
So namely bleeding initiating a hypertensive crisis if this happens to be a functional pheochromocytoma. That said you might consider it if it's a suspected metastatic disease and you need tissue diagnosis prior to initiating therapy. But generally you're not going to biopsy these lesions. >> Ok great so that covers our incidentalomas and obviously we had already talked about aldosterone, the cortisol producing tumors anything that's functional we want to resect those. So moving to the other extreme we've talked let's talk about adrenocortical carcinoma.
John what do we need to know about these? >> ACC is a rare aggressive tumor, typically very large at time of presentation, greater than six centimeters and in 60% of them are hyperfunctioning. >> Great, Ok so what's the treatment for adrenocortical carcinoma? You'll give -- I'll tell you you'll be -- to get the diagnosis on the exam and you'll be given laparoscopic adrenalectomy, open adrenalectomy, retroperitoneal periscopic adrenalectomy what's the answer? >> So the answer is open adrenalectomy and that's what you should be using for all your board and ABSITE at this time.
Not a retroperitoneal approach. Laparoscopic resection is still controversial but the right answer on any board exam or an ABSITE test at this time is open. >> And why is that? Why is it not retroperitoneoscopic? Why is it not laparoscopic? What's the key surgical principle there? >> So the basic is not tumor spillage, you don't want to violate the tumor capsule and create more disease.
>> Yeah, yeah exactly you don't want it's very, it's covered in fat, it's very easy to violate the tumor capsule. So there are people out there that are doing laparoscopic adrenalectomies and you may have in fact worked with some of these people. But just know that's at specialized centers and the answer on the board is going to be open adrenalectomy. There's also a theoretical concern about aerosolization of the tumor cells, the laparoscopic technique that you want to avoid. But I think that it's mostly theoretical at this point.
How about for treatment of patients that are deemed to be unresectable what's the adjuvant therapy for adrenocortical carcinoma? >> So this is where you might think of a mitotane. It's cytotoxic for all the adrenal cells. >> Yep, mitotane that will definitely how up on your boards. Mitotane is cytotoxic to adrenal cells it is the adjuvant therapy for unresectable adrenocortical carcinoma. Alright let's move on to pheochromocytoma this is a lesion of the adrenal medulla so Woo what are some key principles of pheochromocytoma?
>> Yes remember that the adrenal medulla is the sources of the catacholomines. The subsequent catacholomine surge that is characteristic of pheochromocytoma results in paroxysmal tachycardia, headaches, palpitations, flushing and sweating as well as a sense of impending doom. >> OK we often hear about the rule of 10's associated with pheos. John what's the rule of 10's? >> So 10% are extra-adrenal they -- if they're extra-adrenal they will secrete norepinephrine not epinephrine. >> Why is that?
>> When they're extra-adrenal you'll lack the enzyme PNMT. >> That's the phenylethanolamine N-methyltranserase I believe, PNMT. So that's only found in adrenal medulla. So that is responsible for the conversion of norepinephrine into epinephrine. So you're actual adrenal fields are the only ones that have -- that secrete epinephrine. Anything extra-adrenal is going to be norepi only. OK So what's the rest of the rule of 10's? >> So just running through them; 10% are bilateral, 10% occur in children, 10% are familial associated with MEN 2A and 2B von hippo lindau and neurofibromatosis and 10% are malignant.
>> Great those easy things that are broken off into 10's those are all things that you want to remember. Those are all things that are can potentially be asked. So let's say you have a patient that fits this clinical scenario, you're concerned for a pheo Woo how do you make the diagnosis? >> So you want to start with your initial screening tests of a plasma fractionated metanephrine. This is a very sensitive test it's much simpler to perform than a 24 hour urine test. But just be aware that it does have a false positive rate.
>> Yes, and this will come up often. Like they'll ask you what's the -- you know how do you want to make the diagnosis? And I think that and I've seen several different things. You'll see it written in different review books but I've combed through the literature I think right now the correct answer is going to be the plasma metanephrine as your initial test. It's got high sensitivity; it's not as specific so that's why you wanted to follow up with the 24 hour urine collection for catacholamines and metanephrines.
But the first initial screening test is going to be the plasma metanephrine test. Ok take us from there Woo. >> So once you have these tests back you're going to move towards an abdominal CT, it's generally your first imaging modality and this helps you with localization. After that you want to do an iodine labeled MIBG. >> What is that? What's that good for? >> So this is actually the best localization study. It's especially helpful for localizing extra-adrenal tumors that may not be seen on standard cross sectional imaging.
>> OK great. So John what's in principles of treatment for pheochromocytoma? >> So a lot of the questions that stem from pheochromocytoma and treatment actually is how you prepare the patient pharmacologically before the operation. So the first thing is if you have a patient who's hypertensive and has a pheochromocytoma you want to treat them with an alpha blocker. So the answer would be phenoxybenzamine which is a non-selective irreversible alpha blocker. So you want to titrate this into the patient as mildly orthostatic.
And then a beta blocker may be added on but only after, like I mentioned, that you have your appropriate alpha blockade. >> Right so those are some very important principles. So you want a -- your initial treatment is going to be control the blood pressure. There's going to be people who are very hypertensive so a non-selective irreversible alpha blocker phenoxybenzamine, that's your answer. Sometimes you'll be asked how do you know when you're -- you've reached an appropriate dose? The patient's mildly orthostatic and dry -- I think dry nasal mucosa.
Like they dry up nasopharyngealy are going to be answers there. But usually the mildly orthostatic. Don't ever pick a beta blocker first because you'll get unopposed alpha stimulation and which is a big, big, big problem. So make sure that they're adequately alpha blocked first. If you still need help controlling beta -- controlling the blood pressure it's ok to add a beta block later. But never pick that first. Ok and then so after you have appropriate pharmacological control what do you do?
>> So then after you can proceed to surgery at this time so a laparoscopic adrenalectomy or retroperitoneal approach is appropriate. You need close intraop hemodynamic monitoring and management. And these patients peri-operatively you should try to keep them hypervolemic during the operation because after the operation they're going to lose a lot of sympathetic tone. >> Great OK so that -- that's a good kind of general overview of adrenal disease before the boards. Let's move on to our rapid fire segment.
So Woo we covered this already but where is the only place in the body where epinephrine is produced? >> The adrenal medulla and that's because that's the location of that enzyme PNMT. >> John what's the most common site of an extra-adrenal pheo? >> So that's at the aortic bifurcation the organ of Zuckerkandl. >> Yep, some -- some sources that you read say actually that there's a just below the diaphragm in the periaortic reason that the most common place of an extra-adrenal pheochromocytoma but at this -- I think I would still answer the organ of Zuckerkandl on a test.
I think it's for some reason that sticks out in people's mind. Ok Woo patient has long standing rheumatoid arthritis admitted to the ICU with urosepsis despite fluid resuscitation, antibiotics and vasopressor support the patient remains hypotensive, what's your diagnosis? >> An acute adrenal crisis. >> And what's your management? >> So you're going to start with imperic steroids, hydrocortisone 100mg IV q eight hours. >> Yep, and how -- how do you want to manage that?
What's the acute insult, the sepsis is over? >> So you actually do a rapid wean to a home dose level over the first 48 hours once the acute insult is taken care of. >> Great. Rapid wean over 48 hours is what you want to do. OK, John you have a patient with long standing rheumatoid arthritis who takes 20 mg of Prednisone daily for the past six months. She develops intractable biliary colic and is being prepared for laparoscopic cholecystectomy how do you want to manage here steroids perioperatively?
>> So you want to continue the 20 mg the patient is already taking and then you can supplement with hydrocortisone 50 mg IV. If the patient develops signs of an adrenal insufficiency. >> In another words you don't want to stress dose them? >> Correct. >> Ok yeah if you just continue their home dose, should be fine. Supplement if needed. Woo you have a patient with a recurrent upper respiratory infection who was treated with a five day medrol dose pack.
She develops acute appendicitis and is set to undergo appendectomy how should you manage these perioperative steroids? >> Nothing further, you don't need a dose -- a stress dose of steroids. >> And why is that? >> Because you're unlikely to have any HPA axis suppression for steroid use of less than 20mg. >> Twenty milligrams taken for. >> Less than 20mg of prednisone equivalent for less than three weeks in duration. >> Exactly ok. John you have a patient who has clinical and laboratory evidence of a pheochromocytoma what imaging do you want to get?
>> So you want to start with the either abdominal CT or MRI. If you can't see it on that then you'll want to do your iodine labeled MIBG. >> Yep, your MIB-G. Ok Woo you have a patient undergoing laparoscopic adrenalectomy for a 7cm incidentaloma. Intraoperatively you found to have adjacent lymphadenopathy and a tumor invasion into adjacent abdominal wall. What's your next step? >> So you convert to an open procedure here your suspicion for ACC is heightened and so you want to avoid any risk violation of that tumor capsule through that laparoscopic approach.
>> Correct. Ok last one John what's your most common cause of hypercortisol? >> In steroid use exogenous administration of steroids. >> Yep, exactly. Alright well that does it for Behind the Knife's review of the adrenal gland for the ABSITE and the boards.