Hello and welcome to today's session on endocrine, obstetrics, GI and liver, and hematology-oncology as well as surgery questions. This webcast is being recorded. The recording will be available in 24 to 48 hours in the content section of the course. Note the disclaimer stating that the content to follow is for information or educational purposes only. The session will be highly interactive with polling questions and the ability to ask questions of the faculty. When a polling question pops up, simply select your answer and click submit. If you have a question for faculty, please use the Q&A section of your toolbar. If you would like to chat with other attendees, please use the chat area. Today's faculty consists of Drs. Marie Baldessari, Luis Kaplan, Steven Pastorez, and Rahul Nanchal. None of the faculty today have anything to disclose. So without further ado, Marie, please take us away. All right, thank you, Phil. So thank you to all. I appreciate you all being here. Hopefully this session will be very instructive for you. We have a 34-year-old man with Cushing's. He's admitted to the ICU. He has altered mental status, psychosis, weakness, et cetera, tachycardia, hypertension, hyperglycemia, hyperkalemia. His ACTH level is greater than 15, cortisol greater than 75, et cetera. So it's clear that he has Cushing's. So the endocrine team recommends medical treatment to reduce his cortisol before surgery for a known adenocortical carcinoma. So they first start with oral metiropone. However, that doesn't seem to work, and he gets worse over time. He's unable to protect his airway, et cetera. So he clearly has a worsening in terms of his respiratory function as well as his neurologic function. So the question here is, which of the following is the most appropriate next intervention to rapidly, and the key here is rapidly reduce cortisol concentrations? So I think you all are supposed to indicate on the poll. And if there's an issue, oh, great. So we got a 50-50 change or distribution. So plasma exchange is really not indicated. It really doesn't decrease cortisol. Ketoconazole, although it can be given intravenously, clearly is less effective than the drugs that we've mentioned. So metiropone, etomidate, midotine. The problem is you have a patient who's really decompensating in front of you. It's a question of urgency. So as you know, in the world of critical care, when you give oral drugs such as metiropone and midotine, it takes longer. Intravenous etomidate is going to work faster. It decreases your cortisol level in a few hours. So it is the fastest. Next slide, please. It is the fastest treatment of all. So the correct answer here is intravenous etomidate. Next slide, please. Next slide. All right. So we now have a 65-year-old woman. She's hypertensive, AFib, congestive heart disease, GERD. She's admitted to the ED with hypertensive urgency. She's tachy. She has hyperhidrosis. She has a headache. And she also has a palpable abdominal mass and a blood sugar of 286. And not surprisingly, a little bit anxious. Urine metanephrines are positive. So we're clearly setting you up here for pheochromocytoma, hypertensive, tachy, hyperhidrosis, headache, elevated glucoses. And urine and or serum metanephrines positive. So her vitals are, she's tachy, irregular blood pressure. So she's hypertensive. Respiratory rate is elevated, O2 sats, 92% of 4 liters. So the question is, which of the following is the first step in management? I think this is a really great question because although we rarely see pheos, we really have to know what the treatment is here. So I think you all remember from medical school, as well as all your additional training, that you need to give alpha blockers before you do surgery. So alpha blockers are extensive, doxazosin, prazosin, phenoxybenzamine. Those are all the alpha blockers that are available to us. Now one could argue that you could give labetalol, which is both alpha and beta. But I think the take home message here is that you will never give beta blockade before alpha blockade. And the issue with labetalol is that it is more beta than alpha. So although labetalol could be a potential answer, in this case, given doxazosin or prazosin or phenoxybenzamine, you want to go with a pure alpha blocker. So before you do any surgery on this patient, at least seven days preoperatively, you want to give an alpha blocker. So why don't we give furosemide? Well, the problem with furosemide is that many of these patients have volume depleted. So resuscitating them with volume administration, particularly prior to surgery, is the right answer. So giving them furosemide and or any other diuretic is probably not the right answer. Morphine, unfortunately morphine as an opioid can actually precipitate and induce a crisis. So you probably want to stay away from the opioids. Emergent surgical intervention, well, I would argue that it's semi-emergent, somewhat elective surgical intervention, because these patients need to be treated with at least seven days preoperatively of alpha blockade. There are few patients, very few patients, if any, that require emergent surgical intervention. Next slide. Next two slides. So very wordy, but really describe to you what are the indications, contraindications for using alpha blockade and particularly not using beta blockade. All right. References are listed here. And then I will take it away to our next speaker, I believe. Great. Welcome to the surgical portion. This is an 82-year-old woman who was admitted to the hospital six days prior with limb ischemia. Let's see, can't see that. Here we go. She had a thromboembolectomy of the right common femoral artery. She's been anticoagulated with AFib and RVR. She had right lower quadrant pain that developed yesterday. She's been constipated. She is voluntary guarding and rebound in the right lower quadrant, and she is distended. She has a leukocytosis and a lactic acidosis. Her CAT scan, which you'll be able to see on the next slide, should give you a clue as to what you should do next. Your options include TPN, surgical consultation, inotropic support, empiric antibiotics, or methylnaltrexone. You can see the CAT scan here. It is illustrative, shall we say. Feel free to vote what you would do next. Okay, everyone wants to go to surgery. This is in fact the right answer. It's pretty straightforward. You do have some fairly typical findings of intestinal ischemia, including pneumatosis of the right colon. The most important feature of the pneumatosis that you see in the right lower quadrant is that it's non-dependent. So you don't need to have thick bowel wall for intestinal ischemia. You can in fact just have pneumatosis, and this is the right distribution, a classic distribution for thromboembolic disease to the intestine. All of the rest of the answers don't really address her acute change in GI habits and her white count and her lactic acidosis as opposed to intestinal resection. Great. We'll move on to the next one. 49-year-old man comes to the ED with an eight-hour history of acute onset severe epigastric pain. You should get the sense that these questions have in fact been written for surgeons, although we didn't use crayon. White count is 14,000. Other labs are essentially unremarkable. He has a use history for tobacco, amphetamines, heroin, and cocaine. He's a little bit on the hypertensive side, certainly fulfills all the criteria for the current hypertensive definition. Almost tachycardic, temperature is a little bit on the low side, but he certainly has an elevated respiratory rate. His guarding and rebound throughout the abdomen, you'll see another CAT scan. The ED physician gave him one liter of normal saline, not intentionally to induce a hypercholeric metabolic acidosis, but it's not a bad plan, and broad spectrum antibiotics. What should you do? Laparotomy, repeat CT with arterial phase and the start of anticoagulation, upper endoscopy with therapy, or the initiation of proton pump inhibition and vasopressin. Those are your options. Voting is proceeding. I feel like we should have music for these. Okay, again, we have unanimity, but I don't think that's quite the right thing to do. Let's go to the next slide, and we'll have the rationale for all this, and we'll talk about why. This is really designed to demonstrate subtle findings of free air that is above the liver. Can you go back to the CAT scan for a moment? When you look at the very apex of the patient's body habitus, you'll see skin, darker area of fat, you'll see the ribs, and then there are two areas of black density below the ribs. Both of those demonstrate free air. You should not have that kind of density above the liver. If you're thinking about the costophrenic recess, that would be much lower, and you can tell here that you're fairly well deep into the hepatic brachium because you can see the aorta. You're below the cruciate diaphragm that is visible on both the right and the left sides around the vertebral body. This is an indication for someone that has an acute abnormality of their abdominal exam to proceed with surgical intervention. All of the other options that you're presented with, you could get a repeat CT, and it might give you a better look, but you don't need more than finding free air. Endoscopy won't help you here in terms of treatment. It might be that he's perforated an ulcer, and you'll find that, but it's very difficult to fix with that, and proton pump inhibition won't change any of the free air nor the need for surgical intervention. It is different than the patient who has had pain for, let's say, 10 days. You might be thinking of that patient who comes in with just a little bit of free air, very minimally elevated white count, but they've been this way for a while. That person does benefit from an oral contrast and hand scan to ask the question, did they leak and then seal, and therefore, they no longer need an operation, but they do need perhaps proton pump inhibition and some empiric antibiotics that, if it's an upper GI tract perforation, should include an empiric antifungal for those that have gastric achlorhydria or are on proton pump inhibitors. I'm glad that we had the opportunity to discuss all of that. In which case, it's back to Marie. The harder questions as opposed to the easier ones that are made for surgeons. Let me, oh, okay, so let me, all right, oh, heaven forbid, all right, so this is a great question, and it really is inherent to what we do in the ICU. Every surgical, every neurologic patient, every patient is a medical patient, so let's talk about this patient. He's a 32-year-old, he has a TBI, comes into the ICU, et cetera, et cetera, has a seizure, he started out in AED, and in the interim, they find that his blood glucose level is 260, slightly elevated, moderately elevated, and they start insulin therapy. Based on current recommendations, what would you suggest is the appropriate course regarding insulin therapy in this patient? Blood sugar 260, TBI, not chemodynamically unstable, let's vote. All right, well, so we have a 50-50 change, 50-50 distribution. So unfortunately, those of you who voted for intensive insulin therapy is the key to improve mortality are wrong. Intensive insulin therapy is not the key to improve mortality. In fact, intensive insulin therapy in the vast majority of our patients has no change in outcome nor mortality. So I think the most important thing to remember about insulin therapy and glucose management is that too low and too high is better. So very tight control, no change in mortality, no change in outcome. And as a neurointensivist, I can tell you that very loose blood glucose control worsens neurologic outcomes. So what is the ideal blood glucose distribution? Most of us, based on our randomized control trials, would probably say somewhere between 160 to 180. So intensive insulin therapy increases the risk of hypoglycemic events. Absolutely true. Those patients who we control too tightly have hypoglycemia. However, we don't improve mortality. So A, B, C, intensive insulin therapy would not benefit this patient. And this has no relation to sepsis. And intensive glycemic control, no better than loose glycemic control in terms of morbidity and mortality. And I think we've addressed this in the first answer, that intensive insulin therapy does not change mortality. In fact, many people and authors and investigators would say it actually increases mortality. Next slide. So we have a very nice rationale here. Next slide. All right. So this is also a great question. So a 64-year-old, 63-year-old, who has, is this my question? I think so. Marie, I could do it. Yeah, I think this is your question. I only have one question. It's OK. This is an endocrine question on adrenal insufficiency. It's a 63-year-old woman with coronary artery disease, high lipids, comes in with MRSA bacteremia from a skin infection. She's lethargic, tachypneic, hypotensive, very hypotensive, tachycardic. She gets volume resuscitated. Central line is placed. She gets started on vasopressors, which quickly escalate. And six hours later, she's on near maximal dose of two vasopressors. The question for you is under which of the following situations would the administration of intravenous hydrocortisone be appropriate? Is it A, persistent shock despite adequate fluid resuscitation and vasopressors? Is it B, non-response to high-dose ACTH stimulation test? C, a random cortisol level of 10 micrograms per deciliter or a morning cortisol of 15? Or D, hypoalbuminemia with a morning free cortisol of 0.5 micrograms per deciliter. So if you could please vote. Great. So two-thirds of you got the correct answer, and that's A. So this is a patient with septic shock. And a subset of patients with septic shock do have manifestations of relative adrenal insufficiency, or what we actually now term critical illness-related corticosteroid insufficiency, or CIRSI. And these are patients who, if they have persistent shock despite adequate fluid resuscitation and requiring high-dose vasopressors, have been shown to be benefiting from the use of hydrocortisone therapy. We no longer need to do the ACTH stim test to decide if we're going to use corticosteroids. The other teaching point is that cortisol levels vary widely in critically ill patients, so getting random cortisol or morning cortisol levels can actually be not reliable. And finally, although free cortisol may be better than total cortisol, it's not readily available and can be cumbersome to do. So the correct answer here is A. IV hydrocortisone is indicated in patients with refractory septic shock who, despite adequate fluid resuscitation and use of high-dose pressures, continue to remain hypotensive. Next slide. And here's the rationale. It's somewhat long. And the reference on the next slide need to be updated because there were 2017 guidelines that came out from our group and from the Surviving Sepsis Campaign that pretty much refer to the recommendations that I just mentioned on the question. Next question. A couple of questions on hematology-oncology. This one is a 65-year-old patient with CLL, gets treated with chemotherapy. Fludarabine comes in with a hemoglobin of 11, a white count that's very high, with predominant 95% lymphocytes, consistent with CLL. Platelets of 108, creatinine of 1, BUN of 23, lactic dehydrogenase. It's very high. At start of treatment, he has massive splenomegaly consistent with his disease, widespread adenopathy. After four days, he comes in with flank pain, weakness, and nausea. And you can see the laboratory results four days after chemotherapy. His creatinine is bumped up, his BUN is high, his uric acid is 18. So that's very high. Very high LDH. Potassium is elevated. In addition to IV fluids, which of the following intervention should be initiated? Resveracase, immediate hemodialysis, immediate CBDH, urine acidification, or IV furosemide? If you could vote, please. Great, about half of you got the correct answer and that's resvericase. This patient first needs to have medical therapy given and resvericase is a recombinant form of urate oxidase and basically decreases your uric acid a lot faster, particularly in this type of patient as compared to just using allopurinol. Dialysis may eventually become necessary if there's life-threatening electrolyte abnormalities and failure of medical therapy. In which case, hemodialysis would be preferred to correct the electrolyte abnormalities over CBVH. Although urine alkalinization has been used in the past to break down uric acid, it actually is not recommended because the elevated calcium and phosphorus will actually crystallize in the setting of an alkaline pH. So that is no longer recommended. And ibufurosamide would not be effective here unless the patient has convincing signs of volume overload. The key here is to decrease the uric acid as quickly as possible and improve the tumor lysis syndrome in this patient. You can see the rationale on this slide and then the next couple of slides are the references. Final question for Emonk is a 45-year-old patient with respiratory failure undergoes a transplant, bone marrow transplant. He, three days before ICU admission, he gets dyspnea, nonproductive cough, fever, and severe mucositis. His chest x-ray shows bilateral interstitial alveolar infiltrates. His pancultured started on empiric antibiotics. He has ground glass capacities on his chest CT scan. He gets a BAL and the BAL shows progressively bloodier fluid return, but the BAL is negative for bacteria and there are no hemocedrin-laden macrophages. Which of the following syndromes is the most likely diagnosis in this patient who has respiratory failure after a bone marrow transplant? Is it engraftment syndrome, acute graft-versus-host disease, diffuse alveolar hemorrhage, or broncholitis obliterans? If you could vote, please. Great, half of you got the correct answer and that is diffuse alveolar hemorrhage. I think a little bit of the red herring here was the fact that the BAL did not show any hemocedrin-laden macrophages and that would have been certainly a big tip off. However, you don't necessarily see hemocedrin-laden macrophages right away. It takes some time for that to be seen in the BAL fluid up to 48 to 72 hours. But the patient's clinical presentation and the finding of progressively bloodier fluid return in a post-hematopoietic stem cell transplant would be consistent with diffuse alveolar hemorrhage. There will be a question for sure on a bone marrow transplant patient with a respiratory complication. So let's review that very quickly. The syndromes you need to think about are engraftment syndrome. This usually is common in the first 10 days after an auto or an allotransplant, but the features here are fever, rash, and non-cardiogenic pulmonary edema, which we don't have in this particular patient. Acute graft-versus-host disease can certainly occur, but classically it's within the first 100 days or after 100 days. And usually you have other features like skin involvement, GI involvement, and liver involvement. Bronchiolitis obliterans is a very late manifestation after allotransplant, so this would be incorrect. On all of these syndromes, the treatment is corticosteroid therapy, although macrolides can be used in patients with bronchiolitis obliterans, but corticosteroid therapy is the most common treatment modality in a lot of the respiratory complications after a bone marrow transplant. And here's the rationale and a few references that follow. Okay, I'll turn it back to Dr. Nanshal now. Thanks, Steve. This is the GI section, and the first question is a 39-year-old woman who was 29 weeks pregnant and is admitted to the hospital with vaginal bleeding and right upper quadrant pain. Within eight hours of admission, there is fetal loss due to placental abruption. And then several hours after that, she develops hypertension, tachycardia, and reports increasing right upper quadrant pain. Lab values obtained, pertinent lab values obtained at that time include slightly elevated potassium, acute kidney injury, low hemoglobin, low platelets, a very elevated LDH, and some transaminitis. CT of the abdomen obtained to evaluate the right upper quadrant was shown, and the patient was transferred to the ICU. The question is, which of the following management options is the most appropriate at this point? Choice A, transfusion of packed red blood cells and platelets. Choice B, emergent laparotomy for hemorrhage control. Choice C, right upper quadrant CT-guided drainage. Choice D, plasmapheresis with O-negative plasma. And choice C, listing the patient for emergency hepatic transplantation. Next slide shows you the image associated with the question. And please vote for the right answer. Okay, so the right answer is actually transfusion of packed red cells and platelets. Let's just go over the rationale briefly. So this is the image here shows a hepatic hematoma in the context of HELP syndrome, which usually develops in the third trimester of pregnancy, and about 30% of people can have it after delivery as well. One of the most feared complications of HELP syndrome is a hepatic hematoma, which subsequently can rupture through the capsule and shock can develop and an intrapneumatic catastrophe can develop. Most of these cases, and especially in cases where the hematoma is contained, can be managed conservatively and do not require surgical intervention. Now, if the hematoma has sort of ruptured through the capsule and there is severe shock and things of that nature, surgery may be required. Liver transplant may be required as well in rare cases if a hepatectomy was needed to control bleeding. Now, plasmapheresis has been used for HELP syndrome, but usually after 72 hours, and you would not, in this circumstance, you would not probably want to put in a drain, a percutaneous drain into the hepatic hematoma. The management, the first, as I alluded to before, the first management is conservative. It is just transfusion of FFP and, sorry, of platelets and blood, and usually things are controlled by this conservative approach. Next slide, please. That's the rationale and those are your references. All right, the next question is a 66-year-old man who was admitted to the ICU for evaluation of hematokesia. During the preceding 12 hours, there have been three large volume liquid maroon stools. He denies symptoms of peptic ulcer disease, aspirin, or NSAID drug use, ethanol use, or vomiting, including hematemesis. There is no history of diverticular disease. The blood pressure is 105 by 60, and the heart rate is 130. The gastric lavage and aspiration need clear fluid. He has a loud systolic murmur that is best heard in the aortic area. The bowel sounds are hyperactive, and there is a diffusely tender abdomen, but there are no peritoneal signs. Coagulation studies are within normal limits, and a tagged red cell scan is shown in the image which will follow. And which of the following diagnostic and therapeutic steps is the most appropriate? Choice A is obtain an angiogram. Choice B is ensure adequate volume resuscitation with crystalloid blood products as indicated, along with continued vigilant observation. Choice C is a systemic infusion of azopressin at 0.3 units per hour. And choice D is perform an upper gastrointestinal endoscopy. Please vote for the correct answer. The correct answer here actually is to obtain an angiogram. You know, the choice B says ensure adequate volume resuscitation and continued vigilant observation, which is probably not the right thing to do in someone who is actively extremisating. As you can see from the image, there is a lower gastrointestinal tract hemorrhage, which seems to have its origin in the ileocecal region. The next step would be to obtain an angiogram to correctly localize where the bleeding is, and possibly perform intervention. The other choices are wrong because, you know, obviously the person is not bleeding from the upper GI tract, so the upper gastrointestinal endoscopy wouldn't reveal anything. And the systemic infusion of vasopressin is probably, you know, not indicated right now, when you have sort of already demonstrated that the person is bleeding into the GI tract. All right, next slide. That is your reference, or that's your rationale, and those are your references. All right, so the next question is, a 38-year-old woman was admitted to the ICU for management and evaluation of massive lower gastrointestinal tract bleeding after developing orthostatic changes and a hemoglobin of 6.1. The patient had previously been in good health. Her chief concern is painless, bright red blood per rectum. She states her last menstrual period was three weeks ago, and her urine pregnancy test was negative. She denies any blood in her bowel movements or recent change in bowel habits, but she does state that she occasionally has painful hemorrhoids. The patient is on no medications, and a FlexSig was done at the outside hospital and included significant blood at 35 centimeters. The patient is currently receiving two units of packed red blood cells. The appropriate next step in her diagnostic evaluation includes, and the choices are A, mesenteric angiography, B, tagged red blood cell scan, C, endoscopic examination, if it has already not been done, and D, colonoscopy, making sure the ileocecal valve is visualized. All right. So, uh, the right answer is actually an endoscopic exam. If it's not done, uh, now that red blood cells scans and mesentric angiography are reasonable options. If there is, uh, not an easier way to diagnose, uh, the source of bleeding, uh, flex eggs in these circumstances, including retroflexion do not will sometimes miss, uh, bleeding, you know, heavily bleeding hemorrhoids and, uh, will not identify them as, uh, as well as an endoscopic example. So the correct answer is an endoscopic exam in the, in this person who has hemorrhoids, which will, and if an endoscopic and if, and it's a quick one can do it quickly. And if the endoscopic exam is negative, then the choices of a mesentric angiogram or a red blood scan, uh, would be correct. In this person, a colonoscopy is probably without a prep and an unprepped colonoscopy is probably not the, uh, right thing to do. Uh, and once, uh, you know, again, the first step is to rapidly identify the source of bleeding. And then this person who has hemorrhoids, the endoscopic exam is the right answer, right? Next, next slide. Next slide, please. All right. I think, uh, this is my last question. And, uh, the, this question is a 63 year old man who presents with a non-medical upper GI bleed. Uh, multiple AV malformations are found during endoscopy. And some, uh, uh, and there have been clips have been placed on some of them, which are off the, uh, following is the most appropriate pharmacological management following endoscopic control of bleeding. The choices are a 300 milligrams, IV bolus, and then 20 milligrams, IV continuous infusion for 24 hours. B pantoprazole, 80 milligrams, IV bolus, then eight milligrams, IV continuous infusion for 72 hours. Choice C famotidine, 40 milligrams, IV bolus, then 20 milligrams every 12 hours. So, uh, uh, slow IV push for 120 hours and D no pharmacological therapy for the first week after the bleeding episode. Uh, all right. So most of you got the answer. Two thirds of you got the answer, right? This is a pantoprazole, 80 milligrams, IV bolus, and then eight, um, milligrams an hour. Uh, high dose proton pump therapy is recommended to decrease the bleeding and, and possibly mortality, especially in people who have high risk stigmata and who have been, who have been treated with endoscopic therapies. Uh, there is no role for optotide, which is used for a very still bleeding. Uh, similarly, uh, famotidine is inferior to pantoprazole in the, uh, in, uh, uh, in the cessation of bleeding and obviously don't want to give any pharmacological therapy. Therefore the correct answer is a IV proton pump inhibitor, which is continued for 72 hours. Okay. And I think that's my last question. Uh, that's your rationale and that's your, uh, reference and I will hand it over to Marie. All right. Thank you Raul. Um, so we have a, so the next series of questions are having to do with obstetrics. As you know, obstetrical critical care is a hugely important, uh, part of critical care medicine. Uh, many of us have not been formally trained in obstetrical critical care, uh, but these patients, uh, come into our units, uh, they expect the best management, um, and you will be tested, uh, with your board examination. So the more you can learn about obstetrics, obviously, uh, the better off we will be and particularly our patients. So we have a 21 year old, she's gravital one, she's 32 weeks, uh, a little bit early. She's admitted to the ICU. She's febrile. She's tacky. Uh, not so hypertensive blood pressure, 140 over 70 fetal heart rate, one 65, not a, you know, not tremendously high, uh, one 50 to one 60 being somewhat normal. Uh, however, she has uterine fundal tenderness, uh, on examination hemoglobin is nine, seven, uh, in the world of obstetrics, that is not grossly anemic. Um, you know, she clearly is anemic, but not dramatically. So, however, white cell count is elevated. So clearly we have a elevated white cell count in pregnancy, maybe 10,000, maybe 13,000, even as high as 15,000, but 26,000, uh, cells per millimeter cubed, uh, is dramatically high. Uh, uh, fetal ultrasound is obtained, uh, nothing extraordinary. So you get this woman who is tacky, um, slightly hypertensive, um, but looks like she has an infection. What would be your first choice? All right. Please vote. All right. So most of you did the right thing. So in every world, giving antibiotics is always the right thing to do. Um, prior to surgery, prior to any other intervention, including fluids, although, uh, clearly fluid should be part of your armamentarium and intravenous antibiotics should be part of your surviving sepsis, uh, emergency delivery. A few of you have indicated that, but, you know, you really don't have evidence that this fetus is failing. And when the fetus fails, you know, that because either the fetal heart rate escalates or it decelerates. So a fetal heart rate of 165 is actually rather appropriate. So one would suggest, and one would advise that just doing an emergency cesarean delivery based on these data is not appropriate. If the patient, uh, were, uh, if they had, uh, you know, maldistribution, uh, that is, um, the fetus was malpositioned for whatever reason, it was a breach delivery. Um, then perhaps you would consider doing an emergency cesarean delivery, but in no case, in no incident here, we give you no information that this fetus is suffering. So doing an emergency cesarean delivery doesn't help the fetus. And more importantly, really doesn't help the mom. So what's most important to the mom here is giving intravenous antibiotics, as you would do with all patients in the surviving sepsis protocol, giving two units of pack cells for a hemoglobin of nine, seven, uh, similar to your patients in the non-obstetric world, two units of cells for a hemoglobin of nine, seven would not change outcome, would not change mortality. Intravenous magnesium is reserved for those patients with severe preeclampsia, moderately severe preeclampsia and eclampsia. And this patient has no evidence of any of those entities. So the correct answer here is give antibiotics as you would with any patient with sepsis. Next slide. We have the rationale here, references are on the next slide. Okay. So we take it to our next patient, 34 year old, she's gravity two, she's preeclamptic at 36 weeks. She does undergo a cesarean delivery for whatever the reason may be. Um, she is admitted to the ICU for ongoing resuscitation. And she subsequently develops acute pulmonary edema, a very common phenomenon in the patient with severe preeclampsia. So which of the pathophysiologic features of preeclampsia increase the risk of pulmonary edema? So let's see what you answer here. All right. I'm waiting for the answers, but in the interim, I'm going to go. Good. So my gosh, you all got this, this nicely done. Um, so the problem is when we look at the first one, increased circulating blood volume, you would think that any patient with pulmonary edema has increased circulating blood volume. Think of any patient we take care of in the ICU. The problem is the preeclamptic is very different than any other patient. So the preeclamptic or preeclampsia per se is a vasospastic disease. It's an endothelial dysfunction syndrome with a predilection for both the cerebral vasculature, as well as the renal vasculature. So unlike the typical normal pre, um, non-preeclamptic, that is the pregnant patient who is somewhat volume overloaded because of an increase in plasma volume and blood volume, the preeclamptic is the exact opposite than that. They have decreased circulating blood volume. So clearly the first is not correct. Decreased capillary permeability. Well, no one has pulmonary edema, I believe based on decreased capillary permeability and a preeclamptic is in line with that. They have increased capillary permeability. As I alluded to, this is an endothelial disease with dysfunction of the endothelial capillary membrane. So we have increased capillary permeability, which lends itself towards pulmonary edema. D, increased plasma oncotic pressure. So when we look at what are the phenomenon associated with preeclampsia, we see that there's a tremendous outflow of protein through the urine. So in fact, rather than an increased plasma oncotic pressure, we have decreased colloid oncotic pressure, which makes us more prone to pulmonary edema. So let's look at the number C, increased systemic vascular resistance. Well, no one would associate pregnancy with increased SVR, right? Our increased systemic vascular resistance is decreased, particularly in the second trimester because of the vasodilatory effects of progesterone. And that applies to all pregnant patients with the exception of those with hypertensive disease, and in particular, the preeclamptics. So our increase in systemic vascular resistance makes us more prone to pulmonary edema. Next slide. Next slide. This is our rationale here, our references. So next slide, we have an 18-year-old, no prenatal care. She comes in for full-term vag delivery. She's markedly hypertensive, 190 over 110. Her heart rate is 110, her respite is about 18. Urine output is noted to be a little bit on the low side, 25 mils per hour for the past five hours. So which is the most following interventions is most appropriate? All right, we're just waiting for you to all answer. Ah, y'all got it. So clearly the treatment of choice, and it's hard to argue with over a hundred years of anecdotal experience from our obstetricians, is that magnesium is really the drug of choice for many reasons. It works as an antihypertensive. It works as an anti-epileptic drug. And in fact, the most important part of intravenous magnesium is it works as an anti-epileptic. As a neuro-intensivist, I can tell you that it is rare for me to use intravenous magnesium except in my subarachnoid patients. But in the preeclamptic population, it clearly is a membrane stabilizer. So it prevents the progression of preeclampsia to eclampsia. So how is eclampsia defined? Eclampsia is defined as a severe preeclamptic with generalized tonic seizures. So magnesium is the drug of choice. Now one could argue that, you know, you should give these patients fluid. In fact, she probably does need some fluid based on my prior conversation where I said most of these patients are volume depleted. But when you have someone present with this degree of hypertension and a high risk of developing eclampsia, your first treatment should always be intravenous magnesium. We give a lot of magnesium, about two to four grams intravenously, followed by an infusion of one to two grams per hour following DTRs, following their respiratory rate, and occasionally following their magnesium levels. Intravenous furosemide, intravenous mannitol would not be considered part of our armamentarium. These patients are volume depleted, so giving them a diuretic is the wrong answer. IV enalapril could be considered. But the true, true treatment of choice is always intravenous magnesium. Oftentimes, treating them with intravenous magnesium will actually decrease the blood pressure, so there is less reliance on using antihypertensives. And I will tell you that rather than intravenous enalapril, usually intravenous hydralazine and or labetalol are the two most commonly used drugs to treat blood pressure associated with severe pre-eclampsia. Next slide. Next slide. All right. So, we have a 36-year-old. She's gravid at two. She's 39 weeks. Uncomplicated pregnancy. Hemoglobin level is a little on the lower side, 11.6. She has a platelet count of 40,000. Clearly, though, by anyone's standards, in pregnancy, you certainly can have a slightly lower platelet count, but a platelet count of 40,000 is dramatically low. And a creatinine level of 2.6, so dramatically high. Blood pressure, she's slightly hypertensive. Heart rate, 88. Respirations at 16. Urinary output less than 30 for the past three hours. So, what is your choice here? Should you start labor, do placifrescence, do an echo, do a C-section, or give her 3% saline? All right. So, so this is a complicated question because there is a spectrum of disease in pregnancy, and preeclampsia is part of that spectrum. That spectrum includes TTP. That spectrum includes HUS, hemolytic uremic syndrome. So, let's talk about both of those. So, with both TTP and HUS, you have anemia. One could argue that this hemoglobin of 11.6 is slightly low. You're clearly thrombocytopenic, and you clearly have renal insufficiency. So, what is the sinequanon of HUS versus TTP? HUS, the sinequanon is really renal insufficiency. TTP, neurologic symptoms. And nowhere do we give you in the stem that she has any type of neurologic syndromes or neurologic symptoms. Can you assume that she doesn't have preeclampsia with HELP syndrome? So, hemolytic uremia or hemolytic anemia, low platelet count, and elevated liver function test. Well, we don't actually give you all of that information. So, could it be severe preeclampsia with HELP? Could it be HUS? Could it be a variant of TTP? Probably more unlikely because we haven't told you about any neurologic symptoms. So, you're really left with HUS versus severe preeclampsia with HELP. So, what is the best thing to do here? Well, clearly, if she had documented HUS, we would, we would proceed with plasmapheresis. But on the off chance that this is severe preeclampsia with HELP, even though we haven't given you all that information, the treatment of choice is always to induce labor, always, is to get that baby delivered. Now, the good thing about both preeclampsia with HELP and HUS is that preeclampsia with HELP will always resolve after induction of labor. HUS with pregnancy may, in fact, actually resolve with labor induction. If it doesn't, then you would proceed to plasmapheresis post-delivery. So, the treatment of choice will always be induced labor first. And if you still have symptomatology, proceed with plasmapheresis on the basis that your diagnosis is HUS. Trans-thoracic echo, I think that's just a filler. C-section, I don't think our anesthesiologists nor our surgeons would be very comfortable performing a C-section with a platelet count of 40,000. Plasma expansion with 3%, once again, doesn't really have any sense here. Certainly, you want to volume resuscitate these patients, but there's no evidence that 3% is better than giving them normal saline or lactated ringers. Next slide. Next slide. All right. That does it for me. Chloe and Maurice, surgeons are not trauma surgeons. We actually don't know what platelet count means. This patient presented after drainage of an abscess and a complicated intra-abdominal infection. You can see that the patient was started on some empiric antibiotics. It was actually occurred in September. So, the intern picked all those antibiotics, vancomyopenem, and ampicillin. Day two, cultures return, identifying pan-sensitive E. coli as well as some mixed anaerobic organisms. This is a patient that is otherwise doing well and is devoid of leukocytosis. What should you do with the antibiotic regimen? There are your four choices, continue it for 10 days, discontinue antibiotics except for meropenem for 10 days, change to cefazolin and metronidazole for five days, or change to cefepime and clinda for five days. And the survey says, yep, exactly so. You're saying, but you didn't tell me four days based upon the STOP-IT trial. You can certainly pursue that as well as your patient is doing well. But here are certainly the key takeaway is a shorter, more narrow course to reduce the driving pressure for multidrug-resistant organism genesis. Next slide. Okay. 38-year-old man who was admitted. You can see there, stained multiple rib fractures and an ATV accident. He was at the recent East Coast meeting in New Haven that got shut down, but not before he got injured. He was given supportive care. Chest tube was placed for hemothorax, requires intubation at 48 hours for acute respiratory failure. The admission CAD scan shows left-sided rib fractures involving three ribs, each having two different fracture sites laterally placed. The chest radiograph, which you'll see in the next slide, will document this particular injury pattern. What should you do for this person? And you have these choices, bronchoscopy, a second chest tube, rib fracture fixation, or high-frequency oscillation. Yes, rib fracture fixation is in fact ideal for this person who has a flail chest and it shortens the duration of hospital stay as well as ventilatory needs. Bronchoscopy won't help you because it won't fix the fracture pattern and it won't stabilize the thoracic cage. The second chest tube doesn't have anything to drain, so therefore it is also not indicated. And at this point, high frequency oscillation ventilation is almost never used except outside of very specific practice paradigms, but there is no good randomized controlled trial data supporting its use in the wake of injury. Okay, moving along, 23-year-old woman comes to ED after a motor vehicle crash. She was the restrained driver, GCS is 13, airway is okay, she's breathing well, O2 saturation is well maintained, but she is both tachycardic and hypotensive. Her X-ray is unremarkable, the pelvis demonstrates minor superior and interior pubic rami fractures on the left. Her FAST is positive and is positive in the right upper quadrant and the pelvis. What should you do next? Should you proceed to CAT scan? Should you consult IR for angioembolization? Proceed to the operating room for exploratory laparotomy, perform a DPL or intubate her? What would you like to do? Everyone wants to operate. These are surgical questions. There are generally surgical answers. But there's a reason that this is correct. So FAST that is positive revealing in general intra-abdominal blood as opposed to ascites that you might find in those with cirrhosis, if you will, and portal hypertension. In the setting of injury, you must assume that it is blood. And therefore hypotension plus blood gets you some kind of intervention. If the injury was truly limited only to the pelvis and there was just blood limited to that space, you could proceed to IR and many places will do that. Some will do IR plus an exploration using a hybrid room if you have an OR that is a hybrid room. But of all the choices that you have there, the exploratory laparotomy will address not only your pelvic hemorrhage, but also any other sources of hemorrhage at the same time. DPL will not do that and neither will orotracheal intubation, which should be held until after you are in the operating room so that you do not create hypotension on the basis of impeded venous return. Next. OK, 24-year-old restrained passenger in a MBC, she loses consciousness. We're almost going to send her to Maria, but she's not pregnant. There was prolonged extrication, her airway is intact. You can see she's tachycardic, normotensive, slightly elevated respiratory rate, and an acceptably preserved O2 sat on six liters of nasal cannula. She has a forehead laceration across her scalp line, a seatbelt abrasion across her chest, and a gross deformity of her right thigh. Injuries are as follows. She has a small subarachnoid, cervical spine CT is normal. Her left CT shows a peri-aortic arch hematoma with a small luminal filling defect and a trace left hemothorax. Abdominal CT is unremarkable and she has a mid-shaft femur fracture. She's transferred to the ICU. The question is, what do you do next? Aggressive heart rate and blood pressure control, anticoagulation with unfractionated heparin by infusion, emergent thoracic aortic repair, left tube thoracostomy, or ORIF of her right femur. Okay, so this is the sole surgical question that does not have a surgical answer. So that's right. Impulse control, principally using beta-blockade, Esmolol has most commonly been levers for this. But Esmolol will generally provide some fluid for those that have had some plasma volume loss and will allow you to titrate your impulse control. Typically these patients are now managed acutely with impulse control. They may have concomitant management of non-thoracic injuries or intra-abdominal injuries that don't need open surgery. And the thoracic injury can get repaired with a stent. And if they are not suitable for stenting, they can be repaired in a delayed fashion, even up to a year later. So that is, in fact, the correct answer. Not to proceed with acute operative intervention has a very high complication and mortality rate when you proceed in that way acutely, especially in the setting of a brain injury. Next. Okay. 52-year-old man. Another motor vehicle crash. He was airlifted to a regional trauma center. He's intubated. His systolic pressure is 90. He's tachycardic, breathing at 16. Scalp laceration and open femur fracture. Fast reveals moderate free fluid in the pelvis. Laboratory studies, including a tag, are performed. The thrombolastography tracing is most consistent with which of the following bleeding disorders? Please show the trace. And there it is. The tag trace itself is in white. There are values on the bottom. This is one of the more common tag profiles that you can receive in a rapid time frame. What do you think this one shows? Hypofibrosinemia. You know, it's really close. If you look at that trace and you can look at the maximal amplitude, you can see it's three and the lysis, the LY30 is 94%. So this has a very, very truncated tracing indicating that there is hyperfibrinolysis that is occurring. This is one of the most or more common post-trauma injury profiles, so-called trauma-induced coagulopathy with hyperfibrolysis. TEG does not have anything to do with anemia, so it doesn't really manage that. It doesn't really track vitamin K deficiency. Hypofibrosinemia might have a flattened trace, but it doesn't mean that you will lose your amplitude in a very rapid fashion. And so that is the difference between answer B, the correct one, and answer C. And finally, we have a 24-year-old woman who is a, did I go backwards? I did. I think we're, did we get to the end? We did, my friend. Awesome. We're just four minutes over time. I would say four minutes on time. You guys did great. Thank you so much. I would like to thank our and to the audience for attending. Again, this recording will be available in 24 to 48 hours in the content section of the course. Please be sure to join us for our final session tomorrow, Wednesday, September 29th, from 9 a.m. to 10 a.m. Central Time. That's 9 a.m. to 10 a.m. Central Time, where we will go over infectious disease, toxicology, and neurology. So this concludes our presentation today, and thank you all so much for participating.

medical scenarios

endocrine

obstetrics

GI and liver

hematology-oncology

surgery

cortisol concentrations

pheochromocytoma management

Cushing's syndrome treatment options

adrenal insufficiency management