We're going to go through a potpourri of questions here in the next half hour or so on questions on nutrition, obstetrics, heme, onc, and ethics questions. So we have a great panel here to answer these questions and go over some of the rationales with you. I'm Steve Pastoris from Critical Care Medicine at Memorial Sloan Kettering Cancer Center in New York City. So this is our first question. A 65-year-old male with chronic lymphocytic leukemia is initiated on infusion pump therapy with fludarabine as an outpatient. Lab data shows a hemoglobin of 11.4, very elevated white blood cell count of 90,000, 95% of which are lymphocytes. You see the platelet count there, the creatinine, see the BUN. The uric acid is elevated at 7. The LDH is also very high at nearly 600. After starting treatment, he has massive spenomegaly. He has bulky adenopathy. He now comes in four days after his chemotherapy. And he presents to the hospital with flank pain, weakness, nausea. And you can see his creatinine has now jumped to 2.4. His BUN is now elevated to 55. His uric acid is extremely high at 18. And his LDH has tripled to 1,800. He is hyperkalemic, nearly 6 millimoles per liter. In addition to IV fluids, which of the following interventions should be initiated? What would be the first thought that what this patient has is a syndrome? Tumor lysis syndrome, right. So the question is, after you give fluids to this patient, which is obviously very important, what would be the next best step to try to treat this patient now? And these are your four choices. A, resveracase. B, immediate hemodialysis. C, immediate CRRT. D, urine acidification. Or E, IV furosemide. You could just zoom in into that QR code, get it on your phones, and start making your selections. Okay. Most of you got the correct answer, resburicase. We'll talk a little bit more about this in the lecture. But the patient is not in any immediate life-threatening acute kidney injury despite the potassium of nearly 6. So dialysis and CRT would not be the initial interventions to think about this. In this scenario, patients tend to be volume depleted, and even though you're resuscitating them with fluid, there's a danger of giving them IV diuretics too soon and make them even more fluid deplete. Urine acidification would actually not be a good answer here because uric acid actually will dissolve more in an acidic medium. Alkalinization, however, of the urine has been tried, and although it might make uric acid initially more soluble, it has the risk of letting the calcium and phosphorus precipitate. So it's actually not a good option, and it's still controversial and not usually advocated. So the correct answer here is you've got to bring that uric acid that's very high down as quickly as possible. If this was a question 10 years ago, allopurinol would probably have been the choice, but resburicase is much more effective as a recombinant uric acid inhibitor, and therefore now is the treatment of choice. The correct answer is resburicase, and you can see the rationale there. We'll go over a little bit more in the lecture. I mentioned that dialysis, if it comes to needing hemodialysis, it would be preferred over CRRT because you need to correct the hyperkalemia and hyperuricemia and other electroabnormalities a lot faster, and you can achieve that with dialysis much more efficiently than you would with CRRT. And here are some references for you on tumor lysis syndrome. Okay, next question is a patient, a 45-year-old male admitted to the ICU with respiratory failure 10 days after undergoing a bone marrow transplant for lymphoma. He has underlying hypertension and stage 2 CKD. His post-transplant course is uncomplicated until about three days before he shows up. This is now 10 days after his transplant, and he presents with dyspnea, nonproductive cough, very high fever, and severe mucositis. He has bilateral interstitial alveolar infiltrates, mostly concentrated in the perihilar regions. He's pan-cultured. Immediate broad-spectrum antibiotics are started. A high-res CT is done, shows bilateral ground glass infiltrates. He undergoes bronchoscopy and a BAL, and the fluid comes back progressively bloodier with each lobe that's examined on the BAL. That's negative for bacteria. There are no hemocytin-laden macrophages. Which of the following pulmonary syndromes is the most likely diagnosis for this patient? Is it A, engraftment syndrome, B, acute graft-versus-host disease, C, diffuse alveolar hemorrhage, or D, bronchiolitis obliterans? If you could make your selection now. Great. Nearly 80% of you got the correct answer and that is diffuse alveolar hemorrhage. So for a patient like this who presents with acute respiratory failure, with a non-infectious etiology, there are three things you need to know. It's going to be engraftment syndrome, it's got to be idiopathic pneumonia syndrome, or diffuse alveolar hemorrhage. Engraftment syndrome is a syndrome that includes high fever, which this patient has. You do develop non-cardiogenic pulmonary edema that can show up with bilateral infiltrates, but they also have a very characteristic rash. So fever, rash, and non-cardiogenic pulmonary edema and respiratory failure is classic for engraftment syndrome. So you didn't get that rash picture in the story, so that's not the correct answer. Bronchiolitis obliterans is a very late cause of respiratory failure. You will not see that in the first two weeks in this patient. Acute graft versus host, again, is typically not associated with respiratory failure. It's usually more associated with problems with the skin, GI tract, and the liver. You didn't get that in any of the history here, so that would not be the correct answer. Diffuse alveolar hemorrhage is the correct answer, and although there was a phrase there that said there were no hemocytin-laden macrophages, that was just to trick you because you might jump and say, hey, you know, the BAL fluid did not have hemocytin-laden. Isn't that typical? But sometimes you don't get that on the BAL fluid, but when you do, of course, it's good. But I think having progressively bloodier return on the BAL fluid kind of gave this diagnosis away. So the correct answer is diffuse alveolar hemorrhage. In all of these syndromes, by the way, corticosteroids are the mainstay of treatment, so you got to keep that in mind. Rationale is rather long. You can just read that on the slides, and some very nice references as well are available for you. Okay, I'll turn it over to Dr. Cuffey. Thank you. Is this a pointer? All right. 34-year-old G2P1 with preeclampsia, 36 weeks gestation, undergoes a cesarean delivery. She is admitted to the ICU for ongoing resuscitation and soon thereafter developed acute pulmonary edema. Which of the pathophysiologic features of preeclampsia increases the risk of pulmonary edema? Is it A, increased circulating blood volume, B, decreased capillary permeability, C, increased systemic vascular resistance, or D, increased plasma oncotic pressure? Okay, a good mix but the correct answer here is C, increased systemic vascular resistance. I think we talked about this in the talk a bit more but remember some of the changes in physiology for a pregnant woman. They have a decreased capillary or increased capillary permeability and also a decrease in their plasma oncotic pressure. The other option was, oh, and their circulating blood volume is also lower, right? So in this patient probably the increase in her systemic vascular resistance is contributing to this pulmonary edema. All right, previously healthy 36 year old G2P2 woman at 39 weeks gestation with an uncomplicated pregnancy is found to have a hemoglobin of 11.6, platelets of 40,000, and a creatinine of 2.6. The rest of her laboratory values are normal. Blood pressure is 160 over 100, heart rate is 88, and respiratory rate is 16. Urinary output is less than 30 cc's per hour for the past three hours. Most appropriate next step is to A, begin induction of labor with oxytocin, B, perform urgent plasmapheresis, C, perform a TTE, D, perform cesarean delivery, or E, begin plasma expansion with 3% saline. All right, so I think most of you were thinking kind of along the lines of we need to deliver this baby, right? We're thinking that maybe she's got help syndrome. We didn't give you all of her lab counts, but she's got low platelets. We're not totally sure if she's lysing just yet, but her hemoglobin is a little bit lower, and we didn't give you her LFTs, so it's certainly within the realm of possibility. She's also quite hypertensive, and she has now renal failure, so you're also concerned that potentially this patient could have like a TTP type picture. Either way, yes, we are going to be proceeding with delivery of this patient, but we can actually get by with induction of labor with oxytocin. She's not in necessarily extremis just yet, and so we don't need to do a c-section. Okay, we have a, and I don't talk about short gut in my lecture, so I might ask you a few extra questions, but we have a 22-year-old man who undergoes resection of all but 100 centimeters of a small bowel due to mesenteric ischemia, and what I'm going to add on there is that it's connected to his colon. Paranormal nutrition is discontinued. He's been on paranormal nutrition for support, and internal nutrition is initiated, and he becomes confused, has slurred speech, but normal glycemic. The initial workup reveals a pretty significant anion gap, metabolic acidosis. So which of the following is the most likely cause of that acidosis? Is it the ketoacidosis, D-lactate, pyroglutamic acid, or selenium deficiency? And then I have to hit that there. Okay, all right, good job, 69, I guess, do I hit this here, just make it, yeah, there, so 70% of you got it right. It's delactate, and that's because the trans, so let me ask you, I'm gonna ask you a few questions to get to that. What is an actual shortcut? How many centimeters is shortcut, textbook that you'd need to know? Anybody know? Less than? Less than 200 is the textbook, but most of the time, less than 150 means you'll probably need some kind of parental supplementation of something. How much does the colon count for? Let's say he's got 100 centimeters of gut, how much does the colon give him, if we count it as extra length of small bowel? Anyone know? No, actually counts for about 50 centimeters, because remember, in your colon, you can reabsorb, but thanks for guessing, you can reabsorb short-chain fatty acids, so you can get some caloric benefit that way, and also your electrolyte reabsorption, but in this case, when you're on parental nutrition, what is that patient's remaining gut, what do you think the quality of that remaining gut lumen is right now? It's pretty flat, pretty short microvilli, because they've not been using it, so he's going to go very quickly anyway for short gut, but he's going to dump in that carbohydrate into the colon and get that delactate acidosis. How would you try to turn this patient to enteral nutrition? Last question, I promise. Anybody have an idea? Would you just stop pre-enteral and go straight to enteral? Say no. What you would want to do, right, is this patient may not get totally off parental, but you would want to keep that going until you've reestablished some of that gut flora, and you'd want to do a slow, very slow increase in enteral nutrition until you kind of got that established, and then you could give a real try of how they would tolerate enteral feeding. Okay. I could talk all day on short gut, but I won't, so let me see how I get to, how do I get next? All right. There's your rationale, references. Okay. A 35-year-old man is recovering from acute respiratory distress syndrome, and ICU day seven, he's alert, cooperative, still on the ventilator. You can see his pressure support, his in-expiratory pressure there, 400 mL spontaneous tidal volume. He's tolerating full enteral nutrition. Lab values look pretty good. Which is the following is the best next intervention to improve the outcome in this patient? Transfuse red blood cells to his desired hemoglobin of 10, institute mobility and physical therapy, supplement enteral feeding with glutamine, or infuse dexamethasatidine for nightly sleep. Okay, everybody's looking like they're getting a gold star almost. Right, we've got to get them up and moving. How many of you have a mobility program in your ICU? How many people walk people on the ventilator? All right, so that has been shown to make a huge difference in functional recovery. You learned about PICS yesterday. This is what's going to help you keep from having patients that may fall into that PICS category. Get them up and get them moving. All right. I think it doesn't like me. There's rationale. And this is not me. All right, I'm going to talk a little bit about everybody's favorite end-of-life issues. So we've got a 75-year-old man with stage 4 lung cancer, advanced emphysema, on mechanical ventilation, post-viral multilober staphylococcus pneumonia. He's got ARDS and multi-organ failure. It's on day 10 now. He's on max vent support, deep sedation, neuromuscular blockade. He's still in shock despite norepinephrine and vasopressin. We've held a family meeting. His wife and children agree that he would not have wanted to be sustained on long-term life support given his poor prognosis. And they ask that advanced life support be removed and that the remainder of his care be focused on comfort measures. Which of the following is the best approach in this end-of-life scenario? A, discontinue neuromuscular blockade, promptly remove the endotracheal tube while he is still deeply sedated to minimize delay. B, titrate down rather than abruptly discontinue the vasopressors, as sudden withdrawal of hemodynamic support may lead to undue comfort. C, administer opioids using a combination of bolus doses and infusion to treat both pain and dyspnea as life support measures are withdrawn. Or D, use judicious doses of benzodiazepines with opioids as pharmacologic agents used to treat discomfort, frequently hastened death. All right, so most of you have selected the correct answer, which is to administer opioids using a combination of bolus and infusion to treat both pain and dyspnea as life support measures are withdrawn. So the first option is incorrect as the neuromuscular blockade causes the inability to breathe and we must wait for that to have worn off before we compassionately extubate this patient. The second choice, titrate down rather than abruptly discontinue the vasopressors is incorrect because there's no discomfort associated with the discontinuation immediately of vasopressors. It's really just the removal of ventilator that can cause distress. And the last answer, it's actually correct to use judicious doses of benzodiazepines and opioids, but the incorrect part is that your goal is to hasten death. And here is the rationale along with some resources. There's no references here, but we will be talking about these in more detail in a little bit. Okay, our next patient residing in an extended care facility due to advanced dementia, COPD, and dysarthria after a remote stroke, three weeks post sigmoid colectomy and a Hartman procedure for perforated diverticulitis, complicated by pneumonia, ventilator dependent respiratory failure. Now he has multisystem organ failure and his sole surviving relative is his widowed daughter. The daughter relates that her father would not want to continue receiving medical care given the poor prognosis with multisystem organ failure, but would want to receive comfort care. Whew, we all breathe a sigh of relief, right? As a result, the daughter expects her father to die, but believes that he would find a comfortable death to be an acceptable outcome. Which of the following ethical principles best describes the daughter's interaction with the staff? So we all hope for this outcome, but now we're asked to name it technically. A, paternalism, B, substituted judgment, C, non-maleficence, D, power of attorney, E, legal moralism. All right, so we've got a slight variety in choice, which just goes to the importance of knowing the names of things. So paternalism, nobody selected that. That is where we make the decisions on behalf of the patients. The second one, substituted judgment, is the correct answer. That is where you choose on behalf of what you think the patient would want. The next answer, nonmaleficence, is technically not incorrect, but it's not the correct, not the best answer because the daughter is choosing on behalf of what she thinks her father would want. Nonmaleficence is the ethical principle of not causing harm. Power of attorney, that is not present here. Power of attorney must be signed by the patient themselves. The daughter is serving as a surrogate decision maker exercising substituted judgment. And legal moralism, I'm going to be honest, I don't know the exact definition of this phrase. Do we have it in here? It's a lot of words. All right. I think it is time to move on then.

nutrition

hematology

oncology

medical ethics

ARDS management

end-of-life care