Thank you all for hanging with us until the very end of Congress, the very last topic. And similarly to my co-presenters, there is a lot that we could cover in this 15 minutes. And frankly, we could take days to talk about all of it. So I'm going to highlight a few things. It's not going to be everything. It's not going to be every controversy out there. But hang with me. And of course, we'll have some time for questions and answers if you have other things burning on your mind. So I have the topic of adrenal crisis and excess. So we're going to focus in on our steroids here. I don't have any conflicts of interest to disclose to you, similar to my co-presenters. So we're going to start with too much. We're going to start with our crisis management. So what is adrenal crisis? Basically not enough cortisol to handle your stress. There's a couple of ways that this can happen. The most common that our primary care or some of our EM colleagues will see is actually the primary adrenal insufficiency of Addison's disease. We aren't diagnosing this as much in our ICUs. It's usually caught earlier to the patients presenting to us. We're more likely to see either secondary AI, which is hypothalamic or pituitary pathologies like Dr. Reynolds had discussed, or tertiary, which is withdrawal of or insufficient iatrogenic supplementation, probably something we talk a lot about in my ICU because we're very heavy steroid lovers. And the first question I get is when those steroids come off, if the patient gets a little bit hypotensive, is that what's going on? Symptoms here, you think about hypotension can be refractory, can be refractory to your catecholamines. You can see gastrointestinal dysfunction, nausea, vomiting, diarrhea rather than constipation. Some of your electrolyte abnormalities are prevalent hyponatremia, hyperkalemia, very rarely hypoglycemia or hypercalcemia. So I want to talk about a couple of controversies related to this rather than go through epidemiology with you. And one of them is serum cortisol controversy. So the gold standard diagnosis for this test is usually glucose tolerance tests or insulin tolerance tests. This is typically considered inappropriate to do in the critically ill because of the safety profile of these tests. So to diagnose adrenal insufficiency, what are we left with? We have our cortisol stem tests. These are logistically a little bit challenging, difficult to interpret. We also have the random cortisol value. Show of hands in the room, how many of you think that these are great ways to diagnose adrenal insufficiency in your unit? Not seeing a lot of fervor for it. How many of you have seen one drawn in your ICU? Same here. So when someone draws this lab, what are you going to do with it? As the lab steward, let's try to find some way to interpret this result to guide our therapy, recognizing that I think we all know here they're not going to be the gold standard to diagnose. So why not? Cortisol values are considered difficult to interpret because we have a lower level of the protein binding, the corticosteroid binding globulin. We have reduced levels in our critical illness, and we have a higher volume of distribution. So our own society here suggests that we're cautious in using these labs to guide our therapy or diagnose AI, which is good. All of you guys were cautious in suggesting that it would be helpful to you in guiding therapy, but we know that we're going to be presented with these lab values. So there's a couple of studies out there, and I'm going to caveat. These are single center studies, and they're trying to replicate what does a normal stress response look like? Because we know that the normal value our lab is reporting is you or I walking around on the street. It's not what the stress level you'd expect in critical illness is. So what is that stress level? I have two bullet points at the very bottom of the slide. These are both single center studies that try to answer this question. The top one is looking at a vascular surgery patient population, where they underwent, of course, a major surgery, a recognizably stressful event, and then measured cortisol levels daily post-surgery. And we saw that that first random cortisol level post-operatively was 18 mics per deciliter or higher, and that this persisted, this high-level cortisol persisted for up to almost two weeks after the surgery. So this, at least, was shocking to me, the duration of that potential stress response. Arguably, a lot of these patients are probably discharged from the hospital if their operative course was normal. In sepsis, which is a large patient population we treat, you all know that. We've heard a lot about sepsis from the Society, from Congress here. So far, there's a single study that did measure a mean cortisol level during the sepsis state. And there's not a definition of exactly what time point compared to the diagnosis of sepsis. But it suggests that a mean cortisol of 29 might be considered what the stress response is. So we can't exactly give you a value of this is the right level to know your patients responding appropriately to the stress they're being given. But we could say that levels, when measured, less than 18, or arguably maybe even less than 29 in our critically ill patients, might be insufficient based on some of the data that's out there. And again, single studies, very difficult to extrapolate. But as many of you raised your hands, we're being presented with this data. So trying to provide a little guidance of, is there anything we can do with that? So my next controversy is, what are stress to steroids? We've already heard them alluded to. And I'm sure many of you have used this term in your own practice. I know I have. But what exactly is that from a dose, from a duration standpoint, even possibly which drug are you using? Depending on what literature you look at, this actually has a lot of variability. So again, we have primary, secondary, tertiary adrenal insufficiency. You're going to find a little bit of different data depending what type of adrenal insufficiency you're looking at. If we start with our Addisonian crisis, we have pretty standard treatment with our guidelines to suggest that the patient presenting to your emergency department in Addisonian crisis and a severe crisis should receive 100 milligram hydrocortisone IV bolus, followed by potentially 200 milligrams or more per day. A little variability in the studies there, but at least 200 milligrams per day for their maintenance dosing through the course of their stress. These patients are typically prescribed some level of stress dose steroids in the outpatient setting and told to double their regular dose on the sick day rule. So if they're preparing for finals, if they're experiencing a mild respiratory viral illness, they'll double their steroid dose. So I think this is a nice starting point when we start thinking about that tertiary AI where we're talking about iatrogenic suppression. Maybe a starting place can be let's double the dose of where the patient was at. Our sepsis data, I think many of us are familiar with our critical illness related corticosteroid insufficiency. The guidelines put forth by SCCM suggest 200 milligrams per day of hydrocortisone or at least less than 400 milligrams per day of IV hydrocortisone in avoidance of those very high weight-based methylprednisolone doses that the very early literature suggested. So as you can see from all of the regimens here, there's not an exact formula for what's the right dose, the right frequency, the right duration. Arguably somewhere around 200 milligrams a day, less than 400 milligrams a day is going to fit a lot of the types of illness that you'll see causing adrenal insufficiency. And the one caveat I want to give you is that if your patient is presenting on steroids, make sure that your stress dose is higher than whatever their basal dose is. I cannot tell you how many times I see 50 milligrams of IV hydrocortisone Q6 hours ordered as a stress dose steroid in an oncologic or rheumatologic patient who's on 40 milligrams of prednisone daily at home. You're actually reducing their steroid dose, and that's not aiding you in your cause. So recognize when you're encountering those patients who are on chronic steroids and were excluded from many of our critically ill studies that you want to at least increase their basal dose. So now I want to flip sides and talk about too much of a good thing. So we're going to talk a little bit about adrenal excess, and then we're going to give you guys all time to ask us a few questions before we close Congress. So what is adrenal excess? The pathophysiology here is either hyperaldosteronism, which is adrenal hypersecretion. And you can also see the pheochromocytoma, which I'm going to refer to as pheos going forward. And these are truly zebras that you may encounter in your practice. So pheos are that periganglionic tumor of the adrenal gland, so another hypersecretory state. Presentation, it's going to be opposite of what we saw previously, similar to our other disease states with our pituitary. Here you have refractory hypertension, potentially refractory to two or more agents. You can see some mild hypernatremia, hypokalemia, potentially a severe headache, although incidence here is about that of a coin flip. You may be more likely to have some left ventricular hypertrophy, maybe an acute MI, and microalbumin urea. And this is going to be with a very severe presentation. But again, it's not required to make the diagnosis. So to send your diagnosis here, at least we can trust our lab values a little bit more. We'll send our metanephrines, both plasma free and urine free. Now if these are positive, there is a risk for false positive. So we'll send confirmatory tests, clonidine suppression test, chromogranin. There's no difference here from the standard workup you might see outpatient in the emergency department. And then it's recommended to do imaging looking for lesions, looking for that pheo. Your management is going to be similar to how you would approach other hypertensive crises. And it is important to note that this hypertension must be optimized before proceeding to surgery. So you're not going to see emergent pheo resections happen. You're going to see escalation of your antihypertensives until you can get that blood pressure under control well enough to approach the operating theater. The hypertension will resolve post-operatively once you've resected the pheo. And in the surgical ICU, we do receive these patients. And this is a pretty quick, within a day or two, resolution. So once you take that tumor out, you see pretty substantial resolution and no need for resuming those antihypertensives. In terms of which drugs to choose, so you're going to maximize your alpha botcade. And you can see the drug regimens listed here. They're going to be a little bit heavy pill burden for your patients, two, three times a day. High doses escalating up with both your phenoxybenzamine and then adding on your alpha-1 antagonist secondarily. After that, you'll consider calcium channel blockers. You can consider beta blockers, but you have to have your alpha on board. This may be a more familiar term for those of you who approach a cocaine-induced MI where you don't want your unopposed alpha. Make sure if you're blocking beta that you block alpha as well. And then for your patients presenting to us, the ED, the ICU with hypertensive emergency, phentolamine IV, 2.5 to 5 milligrams with repeated boluses. You can also consider an infusion. I have a max dose rate listed here. This is a single case report. So I'm not arguing that everybody titrate your drips up this high. I just wanted to provide this information as an example of the extremes to which you may see doses, much higher than what you might normally consider a max dose. And then after that, think about your afterload reducing agents, targeting reduction in your systemic vascular resistance with either nitroglycerin, nitroproside, agents such as that. I have a lot of references with any of our topics. There's certainly a lot more to delve into.

adrenal crisis

cortisol insufficiency

pheochromocytoma

stress steroids

hypertension management