Thank you, Sammy. So we're going to do eight questions. Dr. Connor and I will deal with questions that are renal and mostly renal and metabolic. So we can go through this quickly and then give more time for Dr. Connor to go through his topics, which are three topics in a row. So here's your first question. I don't know if you've already scanned your phones to get the QR code. That'll be on the first question. That's on the first question right there? When they get to the answer. OK. So we have a 65-year-old woman with history of hypertension, atrial fibrillation, congestive heart disease, GERD, admitted from the ED, with hypertensive urgency, tachycardia, hyperhidrosis, and headache. She has a palpable abdominal mass and a blood sugar level of 286. She is anxious. Urine metanephrines are positive. She's a little tachycardic at 105 with an irregular and high blood pressure of 189 over 112, breathing at 22 breaths per minute, and an oxygen saturation of 92% on 4 liters of nasal cannula. Which of the following would be the first initial best step in managing this patient? So you see your four choices there. So if you could select your answer over the next few seconds. So then you go to the next slide. And that's where I start doing it. It'll take them a second to log in this first time. So I just give them a minute. So A, furosemide, B, labetalol, C, doxazosine, D, morphine, E, emergent surgical intervention. Any questions? Is the question coming up? No. Question's not coming up? We've already, it's already been started. So it should have come up already according to our supervisor here, said that this one was already started. Is it, it's not coming up, sir? I repressed it. Still not coming up? That's OK, we have the answer. OK, let me just go through it then. So what does this patient have? What endocrine disorder does this patient have? Yeah, OK, got it. You got pheochromocytoma, a neuroendocrine tumor, palpable mass. What was the key to this question in terms of the stem that you probably picked up fairly quickly? It's a catecholamine secreting tumor. So you probably saw that the urine methanephrines were elevated or positive. So that question is a management question. So what should be the first initial step? So furosemide won't be correct. These patients actually might end up being on the hypovolemic side. And so you don't want to do that. If they are intravascular depleted, you give them a diuretic. That will not be a good option. Morphine is also contraindicated as any other opioid analgesic because it can only exacerbate a hypertensive crisis in these patients. Emergent surgical intervention, that's something that will be necessary, but it's not the first step in managing this patient. That's a definitive management, but it's not the first step. And the question then hangs in terms of this very high blood pressure and what to do next. So the correct answer here would have been doxazosin, a short-acting alpha blocker agent. Labetalol, while it has beta and alpha, you wouldn't want to use it right off the bat because it will have unopposed alpha, and that will only trigger more hypertensive crises. So you want a shorter-acting alpha blocker. Now another choice, if I replace doxazosin with another agent, would have also been a correct answer. And what would that agent be? Penoxibenzamine, you're right. The other would be pentholamine, which is also used to reduce hypertensive crises in these patients. And this is your rationale. Alpha blockers are generally started seven days before surgery. You don't want to use a beta blocker until after you have alpha blockaded the patient. Penoxibine would have been a correct answer, but it's a longer-acting agent, and you want something shorter. And that's why doxazosin was the correct answer. And you want to avoid morphine because that can create a precipitating factor for hypertensive crises. These are your references. You see the question here is a glucose-intensive insulin question. A 32-year-old man comes into the ICU following a TBI injury. He necessitates invasive cerebral monitoring. He gets intubated, placed on mechanical ventilation. A generalized tonic-clonic seizure then occurs. He's given anti-seizure medication. And while evaluating the patient, his blood glucose level is found to be elevated at 260, and insulin therapy is started. Based on the current recommendations, which are the following, characterizes the most appropriate course regarding the use of insulin therapy in this patient. Choice A, intensive insulin therapy, is key to improving mortality. B, intensive insulin therapy would increase the risk of hypoglycemic events without improving mortality. C, intensive insulin therapy would not benefit this patient since he does not have associated sepsis. Or D, intensive glycemic control would be no better than loose control in terms of morbidity and mortality in this patient. It seems to be working now. OK. 75. OK, it's falling. Oh, it's going up. Going up. OK, it's leaning 75% of you got the correct answer. While there were very interesting studies about 20 years ago that suggested that intensive insulin therapy to control glucose tightly between 70 and 110 showed a positive outcome that since has been debunked, as you know, with more recent studies that suggested that there actually is no specific subgroup of patients where intensive insulin therapy has been shown to improve outcomes of patients in the ICU. The other thing that's important is not so much that you're controlling the glucose in a tighter way. But it's more important that you don't have so many ups and downs, or what we call a U-shaped curve. So it's more important to control the patient a bit more conservatively. So I think most guidelines now, including the one that was recently published earlier this year in Critical Care Medicine, suggested that you just have to keep blood sugars under 200. And ideally, at least in our practice, we use somewhere between 140 to 180. A loose control has actually been associated with bad outcomes. So you don't want somebody that's being controlled nicely between 140 and 80, and then you're bouncing up and down at 220, and then sliding back down to 140, and then it's 280. So you want something steady, but within the range of somewhere between 140 to 180. It balances a very good way of controlling the glucose levels, but at the same time, avoiding hypoglycemia events, which have been associated with poor outcomes in patients who are critically ill. Not just septic patients, but all other types of critically ill patients. So 75% of you got the correct answer. All right. So the next question, see if we can get this to work. 26-year-old male with a known history of IV opiate abuse was found unresponsive in his floor in his apartment. He had apparently been down for an extended period of time. People were unclear. He got an Naloxone during transport to the ER and had a rapid return to mental status. However, in the emergency department, he was noted to have an AKI. His creatinine was 2.6. He was mildly hyperkalemic. He had a CK of 15,000, and the urine dipstick is positive for blood. But no blood was seen on the microscopy analysis. So he's admitted to the ICU. And the question is, which of the following is the most appropriate management of his AKI? A, administer furosemide. B, give mannitol. Give pentoxyphylline. D, aggressive hydration with isotonic crystalloid. And E, alkynylization of the urine. Let's see if we can get this to work. So, it looks like we're at 100 percent, almost. Give it people a couple more seconds. All right. So, basically everyone got this correct. The answer is aggressive volume expansion with isotonic crystalloids. I won't get entirely into the whole debate of balanced crystalloids versus 0.9 percent sodium chloride. But for this particular patient, the goal is to drive urine output. Independent of all the other questions about which agents are better, we know that balanced crystalloids generate more urine than 0.9 percent sodium chloride in almost all clinical situations. So, you'd want to use a balanced crystalloid here, not because of some question about it being better for shock management. It'll drive the urine output better. So, if you had a choice, you would use LR plasma light over 0.9 percent sodium chloride. There's no real data to support the use of alkalization of urine in large randomized control trials. There were some initial trials that suggested maybe better. Obviously, these patients are probably volume depleted. So, giving them furosemide or mannitol is not indicated. Any questions on that? Next one, 85-year-old female comes into the ICU three days after a hip replacement when she developed severe pneumonia respiratory failure. She was adequately volume resuscitated, or excuse me, male. His baseline creatinine is 1.3, creatinine now is 3.6 on ICU presentation, and the BUN is 86. He is not vasopressor dependent. The potassium and carbon dioxide levels are normal. IV Lasix is being used to maintain a neutral fluid balance and his respiratory status is slowly improving. Two feeds were started two days after ICU admission. His serum creatinine is up to 5.7 and a BUN of 115. His next potassium level is 5.1 and bicarb is down to 21. He's making about 1,500 mLs of urine a day with the diuretics, and his family wants to pursue dialysis. Which of the following statements is most correct? A, if the patient had been started on dialysis when he first came in the ICU, his chance of survival would have been higher. Continue diuretics on ICU day two instead of initiating dialysis because that will reduce the incidence of needing ventilator support. C, delaying dialysis will decrease the risk of catheter-associated complications. And D, delaying dialysis until his BUN is greater than 140 may be associated with higher mortality for this patient. So let's see what you guys think. The writing is so small on the screen, I have to look over here to see which one you're picking. Okay. So seems like the majority of people are picking C so far, which is delaying dialysis will decrease the risk of catheter-associated bloodstream infections. Okay. So we'll talk about this a little bit more in my talk, but the answer is actually choice D here. So let's go through each of these. So if the patient had been started on a dialysis when they first came in and the creatinine was 3.6, we have no data to support that preemptive or very early starting of dialysis clearly improves outcomes. Okay. So that one is not correct. B, continuing diuretics instead of initiating dialysis will reduce the incidence of needing dialysis, excuse me, the vent. This really, in my opinion, it just doesn't make a lot of sense because the idea here is that you're hoping that keeping the volume off is going to decrease the chance that the guy goes on the vent, right? I can keep the volume off with both diuretics or dialysis, so it doesn't really matter. If they are peeing, I would rather them just urinate on their own rather than put them on dialysis, but you're going to accomplish keeping them off the vent theoretically with both of them. You do have a theoretical risk of catheter-associated infections or other complications, but in the studies that have looked at these prospective trials of early versus late, there's really been no clear data that there's a lower rate of complications of CLABSIs in the patients who got delayed onto the dialysis room. Then in choice D, we do have some data that suggests that there is a sweet spot here, that too early dialysis doesn't benefit the patients, but too late dialysis is probably harmful. So there's really a sweet spot and it's really hard to identify exactly when that is. What would I do for this case? I would probably honestly wait a little bit longer because the patient's hemodynamically fine, they're urinating. That's not what the question is, but I'm just giving you my opinion. I'd probably wait a little bit longer on this patient because he may experience a recovery in the next day or so. This is just your rationale. These are the different groups between the different studies. I'll go through a little bit of that in my talk. All right, up to you again. Another endocrine question. A 34-year-old man has Cushing's. He comes into the ICU through the ED after two days of worsening, altered mental status with psychosis, weakness, fatigue. His tachycardic, almost 200 beats per minute, hypertensive, hyperglycemic, hypokalemic. His plasma ACTH is greater than 15, his serum cortisol is greater than 75, and his urinary free cortisol is also greater than 300 micrograms. The endocrine team recommends medical treatment to reduce his cortisol concentrations before surgery for a known adrenocortical carcinoma. Metiropone is started with no effect after six hours of escalating dosing, and his mental status continues to worsen. He is intubated to protect his airway. Which of the following interventions would be most appropriate to rapidly reduce the very high cortisol concentrations on this patient? Is it A, etomidate, B, mitotane, C, ketoconazole, or D, plasma exchange? It's looking like a nice spread of answers, which is good. So this could be a very testable item. So most of you appear to have selected plasma exchange. There's actually no data that plasma exchange reduces cortisol levels. So that would be incorrect. The other three choices, however, are all choices that actually reduce cortisol concentrations. The only teaching point here is that among those three, etomidate would work the fastest, which is why it's the correct answer. It would only take a few hours for that to kick in. Ketoconazole takes a lot longer. Mitotane is a chemotherapy agent that can also reduce cortisol concentrations, but not as fast as etomidate. So the correct answer here is etomidate. There's your rationale here and some references for you about how to treat patients with severe Cushing syndrome. So moving back on to some kidney questions, 73-year-old woman without significant medical history. Sorry, it's not too common. I say that on a 73-year-old in Georgia. Admitted with UTI and septic shock, she requires resuscitation and norepinephrine to prevent AKI. Which of the following interventions is most indicated? A, normalize central venous or mixed venous O2 sat. B, continue to resuscitate the patient with lactated ringer solutions. C, titrate vasopressors to a map of greater than 90. D, add inotropes to achieve a cardiac index, not output, cardiac index of 4.5. And the last one was place a PA catheter. All right. Well, it doesn't seem like too many people have many different opinions on this one. The question writers definitely had selected choice B there. I would just say that they didn't make it very clear in the stem as to how much fluid the patient had already received. So I think a better way to phrase this would be if appropriate, because just continuing to volume resuscitate if you're already resuscitated is probably not the right answer. So if you're already resuscitated and you have a low index or low map, you may have to address that. But nonetheless, we want to continue to use isotonic crystalloids. There has been this whole debate quite a bit about balanced crystalloids versus 0.9 percent sodium chloride. There really isn't any clearly definitive study that clearly demonstrates an obvious survival advantage other than the smart and ideal smart trial. But there is a lot of meta-analyses. There's no meta-analysis out there that suggests that 0.9 percent sodium chloride is superior. So you take that for what it is along the way. The only patient population you need to be careful in is probably the traumatic brain injury patients at which point 0.9 percent sodium chloride is better. Then lastly, I think this is the last ones. An 18-year-old girl with a history of depression was admitted to the ICU after an apparent suicide attempt. She ingested 100 tablets of naproxen, 220 milligrams. She's intubated. She has a limited neurologic exam. She's making a ton of urine. Her serum laboratory results are sodium 150, potassium 3.1, chloride 104, bicarbonate 16, BUN 45, creatinine 1.8, glucose a little bit elevated, phos normal, pH is low, ionized calcium is normal, urinalysis shows a pH of 7.5, urine sodium is 30, and urine creatinine is 72. Which of the following best explains? If I wasn't a nephrologist, I would be screaming at the question writers for this. This is not the type of acid-base question that you as an intensivist need to be able to get right off the bat because your toxicology people would probably help you with this and your nephrologist as well. But let's see if anyone can get the answer. Alright, so it's actually a type 1 RTA. How do you differentiate between those two, do you guys remember? And the urinary pH, right? So the fact that the urine pH is alkalotic is telling you that they're having trouble getting hydrogen ions into the urine, which is a distal type 1 RTA situation, not a proximal issue. That's not going to be, I would be shocked if that's on your boards. If it is, it's only going to be this type of question because you're almost never going to get asked an RTA question on a critical care boards because it's almost impossible in the setting of AKI to diagnose an RTA. It's only in the setting of an ingestion like this that you can really have something to lean on. So just take that for what it's worth. Okay, what were the other choices again there? Oh, FINA, so we'll talk a little bit about FINA, obviously the FINA is a little bit low, but it's not that low in this patient, it's like 0.5, 0.6, all of us sitting here right now have a FINA of around 0.5, 0.6, maybe 0.7 because that's normal. So you wouldn't necessarily be able to do a lot with that and I think that's about it.

hypertensive urgency

pheochromocytoma

intensive insulin therapy

acute kidney injury

Cushing's syndrome

type 1 RTA