Thank you all for including your emails. I am actually going to be sending something out either later today or tomorrow, which is a slide deck we showed last week at our PEDS 180 meeting. So just as a prep, if any of you haven't joined or don't know about it, please consider it. So every three months we're going to have a quarterly meeting. There used to be something at Congress called the Section Business Meeting, which was interesting and yet a deterrent because by the name you thought, oh, it's about businesses and finances when it's not. It's about the business of the section, talking about all the subcommittees, the journal, all this other cool stuff that people do. We want you to be a part of it. So we created this quarterly meeting. We're going to start a webinar. You'll get details in your email of the slide deck we showed. Yes. Yes. Come find me. I have the drink tickets, which is what most people want. All right. I don't have question one, so. So once you're done, it'll show you. You have to click something. OK, got it. Perfect. OK, sounds good. All right, perfect. OK. All right, what better way to start than with a sedation analogy is your question? All right, I'll read. Let me know if I'm not doing this the same way you guys did yesterday. But I'll read the question. We'll go through the options. And then you guys will decide. And we'll go through why. All right, a six-year-old, 18-kilo girl was admitted to the PICU with severe status asthmaticus. In the PEDS-ER, she received three doses of albuterol, ipratropium nebulizer, IV methylpred, 40 milligrams, and IV mag sulfate, 900 milligrams. Just before being transferred to the PICU, she was started on continuous inhaled albuterol, 10 milligrams an hour. On arrival in the PICU, she's loaded with IV TURB, followed by a continuous infusion at 0.1 micrograms per kilogram per minute. Despite these therapies, she continues to progress toward respiratory failure. The decision is made to emergently intubate her. Which of the following medications is the best choice for sedation and analgesia in this patient while she is mechanically ventilated? All right, your options are A, ketamine, B, morphine, C, midazolam, and D, propofol. And then I'm going to advance to the next slide. OK. Start, OK. Right here? All right. And then just make sure to move those over. OK. Oh, they need the QR code. That's kind of important, sorry guys. Alright, so your options, we'll give you extra thinking time on this one, so your options were right, ketamine, morphine, midazolam and propofol. And I think they're all just getting the QR code. They need a little time. I don't see how many people answered in the bottom right corner. Okay, perfect. Yeah, and I usually click a note if they, you know, click on it. Okay. And then you press once. It's hard to see. Yeah, it's difficult. It's hard to see what my answer is. Yeah, you can read it better. Oh, okay. Right. I usually. So maybe Jen, you can tell me what it is. What I do is, you know. Okay. And then. I think so. And then you will click that one. Okay, perfect. And you can show me the correct one. Okay. All right. So, wow. Man, you guys are really listening, huh? Okay. It looks like 100%. I don't know if this generally happens, but 100% of people said ketamine. I'm so proud, guys. This makes me very happy. All right. So this one, I also did emphasize it a little bit this morning. But bottom line is, as you go through the options, right, we can read through this. It's very dense. But let's just go through, as you go through any question, why the other ones are wrong, right? So why is propofol wrong? Well, propofol obviously does have awesome sedative qualities, right? But this patient is likely going to be intubated for a significant proportion of time. And remember, we talked about a risk factor for PRIS. For propofol-related infusion syndrome is duration of mechanical ventilation. You're most likely going to have some hypotension associated with this, right? And we know in status asthmaticus, you want a volume load. You want to make sure their preload is sufficient. It's not the best long-term drug. Midazolam, other than the component of being delirogenic, really doesn't add much to the mix compared to ketamine is the right answer here. And again, long-term medication. Morphine? Anyone? Why would morphine be? So the board reason is the histaminergic release. Now, anecdotally and from practice, that may not necessarily be a contraindication in status asthmaticus, but for the purposes of the boards, you don't generally want to administer morphine because of the histamine release. And ketamine, it's a bronchodilator. It provides analgesia. It provides sedation. And they were very clear in the stem, right, that they said, what is the best agent for sedation and analgesia in this question? So that's the most important thing. Do we pause for questions now or keep going to the next one? Oh, yeah. Sure. I think any patient that, you know, septic patients are kind of classically in it, but it also depends, like, how long have they been septic. There's no magic answer. So I would generally say, and again, you have other things to help you if they are hypertensive with either induction or administration. So I would say for the most part, they might ask you if catecholine depletion is an issue. I think we've all universally found that we don't use that as the primary reason not to give ketamine. Yeah. Great. Okay. Yeah. Correct. Yeah. It's not. So if you were to do, I don't remember when the last survey was of what people are doing, but not every institution has access. So I don't think they would expect you. Now they may say, like, if all else has failed, like, what is another option? So remember isoflurane, like going to the operating room and starting isoflurane could be a potential thing. I doubt that that's going to be on the boards because it's just not available widely. Great question. Okay. All right. I think the next one is also mine. A six-month-old, 5.8-kilo girl with trisomy 21 underwent cardiac surgery for patch closure of a VSD three days ago. She left the operating room intubated and the peds ICU team has slowly weaned ventilator settings over the past two days with a plan to extubate the following morning. The bedside nurses say that the patient has been difficult to sedate and is currently receiving fentanyl at three mikes per keg per hour and midazolam at 0.2 migs per keg per hour. Which of the following medications is the best choice to provide her sedation and anxiolysis as well as facilitate extubation by allowing her to discontinue fentanyl and midazolam? A, propofol, B, dexmedetomidine, C, morphine, or D, lorazepam. Okay. Let me start this. QR code? Oh, it's the same one. Okay. Perfect. It's showing them. Okay. All right. So the answer is dexmedetomidine, 83% of you said that. So this one's a little more, it's a little more nuanced and it might take some time to figure out because I think, you know, obviously if she's on fentanyl and midazolam, they're suggesting potentially that you're going to stop it all acutely and then like just start something else. So I have to say, I have some issues with this question, but barring that, let's still go through the process and let's read through this because there's a lot in there that they want you to know. We talked about dexmedetomidine, alpha-2 selective agonist. There are 600 to one alpha-2 receptor agonism compared to, you know, and clonidine, it's much higher than clonidine at eight times. It does have sedative and anxiolytic properties, but it potentially has analgesic properties. So again, this goes back to which of those drugs has both sedative and analgesic properties if you're going to take away both of them and achieve a state of what? Respiratory wakefulness, right? Not have apnea. So the reason they didn't like the other options, for example, propofol, it's probably not going to take away your need to continue the fentanyl. Honestly, the dexmedetomidine in and of itself isn't going to take away your need to give the fentanyl. I'm just going to state that outright, but let's just think through the way they put the question. Propofol, well, doesn't have analgesic properties per our classic teaching and obviously maybe have hypotension associated with it. It's a cardiac hit. That's maybe not ideal. Morphine, again, it's not really going to offer you much other than just replacing an opioid and then the lorazepam, same thing, same class as the midazolam. So they're trying to get you to come to dex. We all know we don't use dexmedetomidine classically in this way, but again, in this situation, it's the best option that you have. So I think it's a good question to illustrate the importance of nuances and ruling out the others and saying they're worse options than the one that you're going to pick. Any questions about that one? Yeah. Just for different institutions, the propofol washout, this could get a qualified in two days, but I was just curious, do you think that's testable? You guys want to hang out for four hours to talk about propofol washouts? So yeah, so as my fellows will probably say, they've heard this. So the term propofol washout, it's really a bridge, right? You're trying to get to a point where you can get the patient spontaneously breathing and safely take out the endotracheal tube. So no, propofol washouts, if they are on the exam, we need to fix that. That's not... They might say, what could you use as a bridge? But it's not a washout because really it doesn't take away your need to deal with the opioid receptors that have been banged on for several weeks and the benzodiazepine receptors and the dexmedetomidine alpha-2 receptors. So the answer is hopefully not. If it is, let me know. I will fight for you. Okay. All right. This is... Jen, were you going to do this one? Do you want me to do it? Either way. No, I think... Oh, okay. Was this the one that you were going to... Yeah, that's fine. I'll... Go. Okay. Let's see. A six-year-old... These are all six-year-olds. Who weighs 22 kilos and 119 centimeters with no significant past medical history, presented five days ago to the PICU with viral pneumonia caused by flu A and respiratory failure. His respiratory status has continued to worsen. Today he's diagnosed with ARDS. He's currently intubated on FiO2 of 80%, PaO2 of 68. ECHO does not demonstrate any signs of RV dysfunction. Since admission, he's also developed significant renal and liver dysfunction, and I'll let you read those numbers, creatinine 2.7, liver dysfunction with all these AST, ALT elevation, total billy 7.8, INRs 1.9. He continues to be hypoxemic despite a fentanyl infusion of 4 mg per kilo per hour and midazolam of 0.4 mg per kg per hour. Who is writing this? The decision is made to initiate neuromuscular blockade. Which of the following agents is most appropriate? Vecuronium, rocuronium, cis-satricurium, and pancuronium. Is the answer going to come up again with this slide? I really want 100% correct answers on this with no help. Okay. Can people put the answers in before you get to that slide? Yeah. Can you, are they able to do that? No? No. Okay. Okay. Maybe it does. Let's see. But we don't have to code. No. Can you do it now? Are you guys able to enter? I have to start it? Yes. Okay. It looks like it's not checked off. Good. Okay. Great. All right, guys. Please. 46. All right. Thank the Lord. Okay, good. Strong work. I don't think this one requires any explanation. Remember, the patient has liver dysfunction and renal dysfunction. So, vecuronium, hepatic. And the one thing, I think someone came up to me afterwards. It is classically going to be, they turned off the VEC, 12 hours later the hepatic failure patient is still paralyzed. Or they might be cold, et cetera. The rocuronium, cis-satricurium, pancuronium, cis-satricurium, pancuronium, cis-satricurium, You really can't see that number in the corner. Okay, we got 46. I know there's a few more people in here. Okay, so we've got a majority answering nafcillin with a couple of lenazolid, macomycin, amoxicillin. Okay, so what were the clues here? So, one of the test-taking strategy take-home points to this is, and I'm gonna go back one, reading the question carefully. Because I admit, when I first read this question, I read right through the fact that it said methicillin-sensitive, and I thought, oh, I have a new culture with Staph aureus. I should make sure that I cover MRSA. And then, when I got to the answer choices and realized, oh, there are a bunch of antibiotics there that cover Staph, including two that would cover MRSA, I better go back and make sure I didn't miss a detail, and in fact, I had. So you know you have methicillin-sensitive Staph aureus, right, so now you're thinking, okay, what's my best drug of choice for methicillin-sensitive Staph aureus for a life-threatening infection? And there, you want something that is bactericidal and not bacteriostatic. And so your answer choice here really is nafcillin for something that's gonna be truly bactericidal. So that's really thinking about, particularly for your antibiotics against Staph, that's gonna often be a relevant detail to remember. And that's really what's in the rationale here, is that you have methicillin-sensitive, and so you don't need something to cover MRSA, and in fact, both lenazolid and vancomycin are bacteriostatic, and so you want nafcillin for that. Questions? Okay. So you can say antibiotics and start with bowels don't actually work. Let's see, this one's not mine, but. Three-year-old girl who recently immigrated from Vietnam is admitted to your PICU for neurological monitoring because her chief complaint on admission was increased sleepiness. And originally, this was attributed to her anti-convulsive medication. She underwent lumbar puncture. CSF showed a protein of 190, glucose 45, and white blood cell count 220, with a predominance of lymphocytes on the differential. Patient underwent repeat CT imaging on day three of admission, and this showed moderately dilated ventricles, but no interval change in size from admission, and her neurologic exam was unchanged. On day six, she clinically worsened, and now is arousable only with painful stimuli, with a Glasgow Coma score of nine. There's the vital signs. The blood pressure is 146 over 88. Heart rate is 68. Pulse ox is 98%, and breathing rate 20. Which of the following is the most appropriate course of action at this time to improve her outcome? A, mannitol, B, hypertonic saline, C, lumbar puncture with moderate sedation, D, emergent decompression of the ventricles, or conservative management with serial brain CT imaging? You have to click on the start. One more? No, no, no. Start menu in the middle right. Here, I can't see. You gotta scroll to that start menu. OK, we have a variety of opinion. Third to 40% say hypertonic saline. Another 17% emergent decompression. Nobody likes mannitol anymore. So let's. So here is the rationale. So what's the diagnosis for what are they getting at? Tuberculous meningitis, based on what the CSF looked like. And we can have some controversy about this. Mannitol and hypertonic saline both can help temporarily decrease ICP. However, an emergent decompression of the ventricle is needed and is the safe and most effective strategy. Lumbar puncture would be a big no-no, because you would risk brainstem herniation. So the patient has signs and symptoms of increased ICP, but maybe is not acutely decompensating. And so you wouldn't have to give the osmolar therapy. I think that's what the thinking is here. And the patient can await to undergo surgical decompression of the ventricle. Depending upon exactly what the clinical situation is, you could make the argument that we need to do something while we're waiting for the neurosurgeons, arguing with the neurosurgeons that something needs to be done. And that might be mannitol or hypertonic saline. Hypertonic saline gets the nod, mainly because the research around it is just the quality of evidence is better. So I don't know if you don't mind pointing out, there's a little bit of a test-taking strategy on this one too, where generally speaking, you have a list of choices. And if there are two choices that are going after the same mechanism, it's perhaps less likely to be that, unless there's a really, really, really strong reason why, specific to the stem, one is wrong and one is right. So that's one. The other one is in the actual question, where sometimes it'll say, what's the next best thing? And sometimes it'll say, what's the thing that will improve the outcome? The improve the outcome, for me, says more definitive therapy, usually, versus what's the next best thing? Because I looked at this and I'm like, well, it's not unreasonable to try hyperosmolar therapy to temporize while you're waiting for your neurosurgeon. So why is it emergent decompression? For me, that's how I interpreted that from a test-taking strategy perspective. Yeah, so I would say, at this time, the patient does show some signs of Cushing's triad. And I probably would want to do something now. But then seeing these two options, A and B, you could do either one and you have to choose one. I don't know why you choose one over the other. So it's not the best question. A previously healthy eight-year-old girl is evaluated in the ED with a one-week history of polyuria and polydipsia. And now, for one day, a history of lethargy. In the ED, the serum glucose is 728. The arterial blood gas shows a pH of 6.92. The bicarbonate is 4. And the urine is positive for ketones. The patient has an IV placed and receives a 20 mil per kilogram bolus of saline. And after this, she becomes markedly less responsive. Now, she responds to pain from nail bed pressure, withdrawing all extremities. With a sternal rub, she moans, opens her eyes. The vital signs are temperature normal, heart rate 120, breathing rate 36, and blood pressure is 106 over 83. The oxygen saturation by pulse oximetry is 98%. And a repeat glucose is 550 milligrams per deciliter. So at this moment in time, which of the following is or are the most appropriate next steps in the management? You have to choose one. Non-contrast head CT, a bolus of intravenous sodium bicarbonate, rapid sequence intubation and mechanical ventilation, a bolus of mannitol, or a IV infusion of insulin. The reason why I had CT imaging is incorrect is that this patient is falling apart and you don't want to be in radiology. Okay, so here is the rationale of the answer is mannitol. You may have noticed that the glucose fell pretty precipitously with initiation of therapy. So the patient is demonstrating signs of increased intracranial pressure. So what are you going to do about it? So, you know, imaging is good, but the patient's already deteriorated and you don't want to waste time getting imaging when the patient really needs some form of treatment. The patient has a DKA with neurologic changes. Mannitol and hypertonic saline, either one would be appropriate in this situation. In the setting of DKA, the most quality evidence is still around mannitol. Specific studies using hypertonic saline have not been done, but either one would work for the same reasons, to improve cerebral blood flow. You know, the patient might require intubation and mechanical ventilation, but that is just, man, that's just asking for trouble. This patient is protecting her airway, breathing adequately, and the initial intervention should try to be to reverse the cerebral edema that you see manifesting before your eyes. Sodium bicarbonate. There is no evidence for the benefit of this therapy, and lots of retrospective cohort descriptive data indicating that it is a risk factor for cerebral edema, so that is a no-no. And bolus insulin is not used in pediatric patients in DKA, but did you know that it still is used in adult DKA? I saw an article. Yeah. Yes. Intubated and mechanically ventilated in DKA. So, I just wanted to clarify why, so, you know, you also, every option, you have to think of what's the worst thing that could happen, right? So, the reason, just to cut to the chase, is that it is almost virtually. It's very similar to asthma, right? You let it go until the bitter end, until there's absolutely no interruption. So that's why it's really important to take that one off the list. Bob Tasker has written about this. Robert Tasker from Pediatric Critical Care has written about it. The brain, our brains, this person's brain is optimizing every aspect of ventilation to the correct way. The patient has no lung disease, so. All right, anybody else, any question? Way in the back, speak up loudly. Great question. It's almost never going to be a cut and dry GCS and say, you must intubate situation, right? So yes, in any other circumstance, you might be considering, even if airway refluxes are intact, mental status is decreasing rapidly. But all of the other things, there's more risk at this point than benefit to intubation and mechanical ventilation. Now, if she gets worse and her airway refluxes are back, and she stops breathing in a way that facilitates this amazing pH of 6.98, then we need to take over. And the other thing about GCS is that the But the kid's not a trauma patient. Right. They're trying to trick you a little bit. Yep. Absolutely. I think somebody with a GCS of 7, you have to watch. You need to be at the bedside watching because anything could happen. I hear what you're saying, and it makes sense. But this administration of – and what you would do is if the patient now blew a pupil on top of it, you'd put the bag and mask on and start hyperventilating. Give the mannitol. The treatment of cerebral edema, the patient's Glasgow Coma score could change to the better fairly quickly with an osmotic agent. And the question is what's the next step? Yes. Okay, a previously healthy 7-year-old is admitted to the PICU after presenting to the ED with dizziness, headache. Here are the vital signs. The temperature is 37.6. The heart rate is 125. Breathing rate, 20. Blood pressure, 178 over 126. That's notable. And an arterial saturation on pulse ox of 99% breathing ambient air. Diagnostic evaluation is significant for elevated urine and plasma metanephrines. Right out of the blue, there it is. All right. Tumoral imaging reveals a 2-centimeter mass on his left adrenal gland. And echocardiography is significant for significant left ventricular hypertrophy, but still normal systolic function. So surgery is scheduled to remove this tumor. So which of the following antihypertensive agents is most appropriate as a first-line therapy in the preoperative period? So what does this patient have, and how would you treat the hypertension? Is statin the only one that gets 100%? Got to step up your game, Jerry. Okay, so this patient has a pheochromocytoma, as evidenced by the increased metanephrines, nor-metanephrines in the screening test that diagnosed the pheochromocytoma. So this tumor is producing catecholamines, as evidenced by the high blood pressure that this patient presented with. So the patient needs to undergo surgery for removal of this tumor, and you want to get the blood pressure under control to prevent rebound hypertension when the surgeons are putzing with the tumor, moving it around, whatever. And historically, the teaching here is you undergo alpha blockade first. If you go too far with that, you still have beta to drive your heart rate. So alpha blockade first with something like fentolamine. When you get that under control, which is usually a few days with fentolamine, then you add your beta blockade. And if there is time, you can use something with combined alpha and beta effect, like labetalol. So alpha blockade first, then beta, and then surgical resection. Sapna, as an anesthesiologist, any? I think that's the classic ABA board certification exam question, too. So it's always going to be exactly what they said, alpha adrenaline blockade. And they will try to trick you and say, oh, well, labetalol, it's a dirtier beta blocker. Maybe it's going to be fine, but it's never going to be beta blockade as first line. OK. So now we have a three-year-old. It's been in your ICU for two days. Day 38 after stem cell transplant for ALL. Has respiratory distress due to abdominal distension from VOD slash SOS. Despite treatment with defibrotide, has increasing abdominal distension due to ascites, confirmed by ultrasound. Requiring now high-flow nasal cannula with FiO2 of 0.9 to maintain oxygen saturations above 92%. Chest x-ray shows small lung volumes and bilateral pulmonary edema. Urine output has decreased to 0.1 ml per kilo per hour, urine as a vital sign. Despite receiving continuous furosemide, BUN has increased. Creatinine has increased, as you see there. Interabdominal pressures measured through the Foley catheter are 22 to 28. Which of the following is the most beneficial intervention? So A, non-invasive ventilation with CPAP. B, abdominal paracentesis with drain placement. C, adding TPA to the defibrotide. D, adding chlorothiazide. Or E, sedation, paralytics, and intubation with mechanical ventilation. So we are nearly 100% at what is, in fact, the correct answer. So what does this patient have in addition to VOD? Abdominal compartment syndrome, right. And more importantly, what is that abdominal compartment syndrome from that was confirmed on the ultrasound? It's from fluid, right? So you can go after it. So this is a little bit of a tricky one because it, you know, not uncommonly when you're approaching these questions, you'll get to the answer choices and you're like, well, I would do two or three of those at the same time. Like how do I pick which one? And so again, from a test taking strategy perspective, you have two things that might address your respiratory function and only one thing that really gets at the underlying cause of all of it. And so that can be a little bit of a clue. And the clue that it gives you, you have symptomatic abdominal compartment syndrome. That's your priority. And you need to take care of that as quickly as possible because remember what the mechanism of abdominal compartment syndrome is, it's ICU medicine is physics, right? So it's the pressure that is keeping the blood flow from going in to supply your abdominal organs. And it's like any shock state, the faster you reverse that, the better you're going to be able to preserve your organ function. So that is a true medical emergency needs to be taken care of right away. Now in real life, would you also support the respiratory function while you're doing it? Of course. But for test taking purposes, go at the thing that is, it's giving you, this is a medical emergency. Did you recognize it and do you know how to treat it? Questions? Okay. I'll just add one thing to the intubation mechanical ventilation paralysis situation. So again, the patient's not doing a great job, right? With respiratory stuff. So you might say, okay, let me help out. How old was this kid? Two or three. Two or three. Okay. So you might say, okay, like how's the kid going to tolerate that procedure without some deeper sedation? The sedation may put them at risk for more respiratory compromise. I think that the key here for me to rule out E was actually that we're going to immediately paralyze the patient, right? Because right now, again, remember anytime you want to intubate someone, you have to think about reasons not to intubate them. And in this case, this patient's negative inspiratory breathing might be the best thing they have going for them. And if you were to intubate and paralyze them, overcoming their abdominal compartment syndrome with positive pressure might become really difficult and actually make his respiratory situation worse. So if you needed a reason to rule out E, that would be my primary reason. Because you might actually need to intubate him to do this safely. You know, that's questionable, but the paralytic is the big thing. Right, exactly. So he's high risk for potential arrest or decompensation during the intubation itself. Sometimes this is a little bit of getting in the mind of the question writer, too, because it is a true statement that sedation and paralysis would decrease your abdominal pressure some, but it's not going to be enough to fix the problem. And so sometimes you can think of, you know, this is maybe part of the answer, but not the full answer. And you have the full answer in front of you, too. Okay. I'm going to take credit for that one, the 96%, because you realize this was a secondary process going on and not a primary process going on, right? Out of curiosity, how many of you guys know how to set up an intraabdominal pressure monitor from a Foley? Yeah. So if you don't know how, because we don't actually have an IAP device that's globally available yet, work with your nurses and learn how to do it. Because it's good to do those, learn how to do those things, but it's also something that we don't normally do. But as we start getting more sophisticated devices, it'd be interesting to know what we do with the data. But it also relates, Anjali, I think you were asking this question about the isoflurane, right? One of the things that I think about for boards is these boards, while many of you in this room are early career faculty coming out of your training boards, are also for people to do research and out in the middle of wherever they are. So testable material is not going to be some esoteric stuff, right? So if you're in the middle of nowhere, blank state, you probably don't have isoflurane as a ventilated asthmatic option. So all right, here we go. An eight-year-old with septic shock in MADS is being ventilated and has hemodynamic support using epi, vaso, and milrinone. His heart doesn't work so well, has an EF of 21%, and he's not peeing and has AKI. Blood pressures have been going down despite going up on the vasopressin. The trainees ask about CRT, reversing milrinone accumulation. Which one of the following is the most accurate response? And this is one of those you kind of know or you don't know. And if the answer is not 100%, I'm not going to take offense because, again, this is one of those. I like how it's dark pink and white pink. Who's that? Alright. Some people abstaining. That's okay. What's up? It's important to know what you don't like. Move your mouse off that answer. I like everything else. Aha! Ha! Very good. Red. I don't need C or red. Milrinone, the effect of CRT on Milrinone and some of the other infusions is pretty minimal. And so cardiac meds, inotropes, vasopressors, vasodilators are not generally cleared off. Okay. An 8-year-old is brought to the... Are you doing this one? I can do either one. Yeah, well, I'll do it. It's fine. 8-year-old is brought to the ED. Has a history of polyuria, polydipsia, weight loss. On exam. She doesn't look so well. She's anxious. Has deep and rapid respirations. Your ABG, as you see, is right there. And your BMP shows sodium-135, potassium of 2.6, elevated glucose, spion, creatinine is shown. Which of the following is present? Sorry. Oh, OK. I defer to the expert here. Just DKA. Yeah. No, but she's asking for the, generally speaking, like the overlay of HHS and DKA, right? That's what you're asking? They don't overlap. Oh, they do overlap. Oh, for the board, I'm sorry. Yeah. I doubt it. All right. Who answered yellow, the metabolic acidosis and alkalosis? Because that's the answer. So this is a kind of a phenomenon where you do have to do some math on it. You can't just look at the pH. So if you look at the pH, you're going to say there is no problem, but there is a problem. So the anion gap is actually 28 if you do the math, and it should be associated with a decrease in your bicarb. But if it's an appropriate bicarb, then you figure this out by adding, if you're, you know, the decrease in HCO3, equal to the increase in anion gap above normal, the increase is added to the bicarb. So then it's 38. The anion gap was, you know, the serum bicarbonate was 20, right, I think? Yeah. Yeah. So the difference between kind of the measured anion gap and what's normal, if we assume normal is 10, is 18. So that's 38. This is greater than the actual anion gap. So the patient has a concurrent metabolic alkalosis. So it's both acidosis and alkalosis. I don't like this question. I don't know if I have used the Winter's equation myself, but the other clue in the stem was that the chloride is 87. So there's your metabolic alkalosis. That's not the end You have a baby And she has no medical to problems But she shows up with altered mental status and seizures She's intubated She gets some sedation meds. She's gotten a CT which shows no problem After you intubate her and she's in the ICU you see that she has a heart rate of 147 her blood pressure is 70 over 45 Her hemodynamic exam, she's got good pulses, good cap refill, a regular pericordium exam She has fed formula, reported feeding well, and then the electrolyte panel is as you see it. Which of the following is the best description of the kid's problem? Yes, we can. Despite the baby with the seizure, there's no ammonia mentioned. So this is not liver failure. This is not metabolic question. Okay, how many people? You're not allowed to abstain. We're getting close. Close to 50. Good. Majority of you got it. Euvolemic hyponatremia. So, you know, volume status must be the first thing and you can tell based on the kid's hemodynamic exam with good pulses, good refill and all this stuff that the kid is likely euvolemic, but obviously hyponatremic and the clue of the formula and feeding is not just random. It is in there for a reason. And it's to key you in that this kid was doing well. And this is a formula related issue, probably from mixing issues. So the issue is euvolemic hyponatremia. And as Dr. Zimmerman pointed out, understanding the table of what's the problem? Is it a sodium problem? Is it a water problem between SIDHDI and cerebral salt wasting will get you at least two points on the exam. Um, yeah, I don't think so. Yeah. I mean, I think this key here with a pretty solid physical exam is probably obviates a need for that. Yeah. Okay, I think this might be the last one. No. Is this one mine? Yeah. A six year old boy with a history of progressive darkening of the skin, the oral mucosa, the tongue and the nail bed. Bing, bing, bing, bing is admitted to the peds ICU from the ED with nausea, vomiting, ongoing fevers, severe abdominal pain, tachycardia and hypotension. On physical examination, the patient is severely dehydrated. The initial blood pressure is 60 over 50. And so he's not normal. He is given three boluses, 20 mils per kilogram of saline. His vital signs on admission to the PICU now include a heart rate of 140, breathing rate of 26, and pulse oximetry breathing room air is 98%. An abdominal examination is concerning for generalized tenderness, though no guarding or rigidity is noted. His mental status examination is normal. Laboratory study evaluation reveals the following the sodium is 120, chloride 105, potassium 5.4, bicarbonate 16, creatinine 0.4, BUN 20, glucose 60, lipase 500. So based on all of this, which of the following is the next most appropriate step in stabilizing this patient? A, CT of the abdomen. B, IV hydrocortisone. C, hypertonic saline or D, epinephrine. All in? So what is described here is a patient with cortisol deficiency, chronic, with a discoloration of the skin. He also presents with acute pancreatitis and with the elevated lipase, the abdominal pain. And so this needs evaluation, but right now, you see that this patient has a low glucose, a low sodium, and a slightly elevated potassium. And with all of that laboratory evidence, as well as the skin darkening, this has adrenal insufficiency all over it. So the intervention is stress dose hydrocortisone, 2 milligrams per kilogram loading dose. That's what you would do. The patient really starts to crash and burn, you know, epinephrine. But in terms of using all the evidence from the clinical stem, hydrocortisone is the right answer. Okay. One more to go. You have a little girl who shows up with no medical history, who has a couple days of stuff coming out of the wrong sides. Her initial vital sign in the ED is noted that she's febrile. Her heart rate's 135. Her blood pressure is 140 over 90. She's breathing about 22. Draw CBC. Her white count's 22,000. She's anemic. Her amatogrid is there. She's thrombocytopenic. And you see her electrolytes, sodium 124. You notice that her BUN 60, creatinine is 0.88, FOS is 4.9. LDH, which is drawn, is 1817, and CRP is 6. She's arousable but sleepy. And then she starts seizing. And then she's intubated and brought to you. Which of the following would be most important to you to determine the course of therapy? Is it a complement factor, C5A, Adams TS-13, a peripheral smear, or serum haptoglobin? No one likes haptoglobin, huh? Man, how the mighty have fallen. I don't think anybody calls haptoglobin mighty. Anyway, okay, well, about three-quarters of you are correct. The ADAMS-TS13 activity is the answer. Why is that the answer? What does this kid have? Yeah, very good. So this is something actually that was mentioned yesterday. The findings are very consistent with the umbrella diagnosis of TMA. So thrombotic microangiopathy, as we pay attention to it more, rears its head in different organ systems. And certainly this kid has every indication that that is what's happening for her. But ADAMS-TS13 is very helpful to rule out HUSTTP in this situation. So you want to be able to rule out other causes of AKI like HUS or atypical HUS. So C5a is important in the complement cascade, but it's in that terminal complement complex, C5a through C9. It's not exactly that helpful when you're diagnosing TMA. So this is one of those, you read the stem, you kind of know what it is, but you need a confirmatory test. So sensitivity, you need a specific test for this. So a peripheral blood smear is not going to help you because you kind of already know from a sensitivity standpoint, this is some kind of microangiopathy. It's not specific for TMA. Yes. So would that, instead of ADAMS-C-S- Instead of ADAMS-T13? Uh... So, I think, so, one of the clues that they give you that per traditional diagnostic criteria differentiates this as TTP. Yeah, sorry. So, one of the clues that it gives you that from a traditional diagnostic categorization perspective differentiates this as TTP as opposed to HUS is the neurologic symptoms. So the fact that she has seizures says, oh, this is TTP and your ADAMTS-13 is going to be the right test for that. I think it would be challenging and I can't imagine that they would give you the correct complement test plus ADAMTS-13 as choices. Yeah, and I agree. Your terminal complement typically is what you're going to look for for your complement-mediated TMAs, which again, it's a spectrum. And so, some of this is board exam plus real life or there's more nuance, right? So, TTP itself is probably on that spectrum and some TTP may in fact be complement-mediated. And so you might do both, but your immediate answer is going to be that ADAMTS-13. And then you might get a question about the management of, right? So, if you're at a place where you don't have easy access to an ADAMTS-13 or it's a send-out lab and you're going to get it back in a week, you're not going to be able to use that to guide your therapy. And so, what therapy would be used for this patient if you didn't have your ADAMTS-13 just based on the clinical scenario? Yeah, for plasma exchange. Yep, yep. Great. Okay, I think that's it, right? Great. Lunchtime. Lunchtime. Good luck to everyone.

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