So an 82-year-old woman was admitted to the hospital six days ago with acute limb ischemia. She underwent thromboembolectomy of the right common femoral or femoral, depending on where you're from, and has been anticoagulated since then. She is now in the ICU with atrial fibrillation and rapid ventricular rate. Yesterday, she began to have increased right lower quadrant abdominal pain. So, okay, so they gave you all this background and now they're starting to sort of direct you as to where the question's going. She has not had a bowel movement since the previous morning. That's sort of in line with something else. She has voluntary guarding and rebound in the right lower quadrant and marked abdominal extension. So they're giving you peritonitis, right guys? So she has a very high white count. She has a nasty lactate and then they're gonna give you the CT. But you should already kind of, CT or not, be able to kind of get an idea of where they're going with this based on the history and yada yada yada. Okay, so again, it's really hard to read these. Clearly, you can see distended colon. That'll be, especially if you look on the, everywhere. One of the things they're gonna want you to comment on, have that removed. So, if you look at the sort of ascending colon, you can see in the wall, if you look really, really carefully, that there's some badness there too. But again, you don't necessarily need the CT scan to answer the question when you see it, so. Okay, so they want you to have a differential in your head and now they're gonna say, well, what are we gonna do for this? So, are we gonna give IV steak and potatoes? Are we gonna call surgery? Are we going to give inotropes? Are we going to treat with IV metronidazole and oral vancomycin? So, clearly they're saying you think the patient has C. diff. Or are we gonna give methyl notrexone? So again, the question is, do you have sort of ischemia that's, you can sit on with broad-spectrum antibiotics and TPN, meaning that they're not that symptomatic, don't have a raging white count, shock. You know, there are ways to sit on some ischemia to the gut that can slowly get better with conservative treatment. Are we in trouble? Does bowel need to come out? Is this all related to low flow to the intestines and that can be improved? You know, as long as we improve flow to the gut, is it not too late? Can you sort of fix that part? And then where's the C. diff? And I think that's where that poo question sort of came from when they're sort of telling you, not that it's impossible to have toxic megacolon from C. diff and you wouldn't have any bowel movements. All right, so why don't you go ahead and put your answers in. All right, so a little bit of a diverse sort of thing. Some people saying it's C. diff. Some people think the heart needs to be improved, that the rapid ventricular response, if it can be controlled, maybe it's no atrial kick, we're not getting sort of flow down there. Other people think that this may be ischemic gut, dead gut, and that might have been pneumatosis that was solved on the CT scan. Nope. Okay, so it's B. Gotta get someone to come in and do the next lab. So what the initial aspect was to set you up is that even though the patient's on anticoagulation, they're at risk for embolic disease. So severe, throwing a clot and all of a sudden cutting off flow to either the SMA, the celiac, or the IMA, or even further distal. So they're high risk. Physical examinations should suggest ballaschemia. The CT showed pneumatosis. Due to the patient's condition, including shock, you need to get surgery involved right away. Improved cardiac output will help us patients with peripheral fusion due to shock, but will not reverse the infarction of the intestines. So what they're trying to tell you is the patient's already sort of beyond that state. We can't sort of get to that point. Close observation is warranted in clinically stable patients with normal lactate and no evidence of peritonitis, but what they gave you was guarding, rebound, distended abdomen, lactates up, we're sort of beyond that point, and then elevated leukocytosis. Clostridium difficile, that is correct. It can cause pneumatosis, but it's sort of on the differential, but with a patient with thromboembolic disease, this should be lower on the differential diagnosis, and even if it is C. diff, they're beyond the, I mean, they didn't specifically say they were on pressors, but you're kind of beyond the point of conservative therapy. To be frank, with that kind of alias you were seeing and that stuff, I'm not even sure how we're gonna deliver the antibiotics down there. We're not gonna talk about this whole C. diff, can you bring up a loop and throw vancomycin there? We'll just get to the point that they're gonna have to go to the operating room for some sort of resection, or at least a look to see if anything has to be resected, regardless in this situation. And trying to stop opioid-induced constipation, none of you ordered that, but I mean, that's really not a good choice for this critically ill individual, so. Questions about that? Comments? All right. Let's head to the next one. 49-year-old man presents to the emergency department with an eight-hour history of acute onset severe epigastric pain. His white blood count is 14,000. Other laboratory results are normal. He admits to daily use of cigarettes, amphetamines, heroin, and cocaine. That's quite a bit. His vital signs, blood pressure 145 over 96, heart rate 97, temperature's relatively normal. Respiratory rate of 31. On physical examination, he has guarding and rebound diffusely throughout the abdomen. You'll see another CT scan. The emergency physician gave him one liter of normal saline and broad-spectrum antibiotics. So a reasonable shotgun approach when you're sort of trying to figure out what's kind of going on in someone with this sort of thing. Okay, so again, it's very hard to read these things, but clearly they want you to look for some common things that you're looking at. So you can't necessarily see any IV contrast, but you can see there's the stomach. You can see there's a lot of juice in the stomach. There's no NG tube yet, although there probably will be. You can't tell if there's an infarcted spleen, but it doesn't seem to have any issues. You can sort of look around. Again, no one necessarily seen on the scan, but you don't see any damage to the liver. You see a little bit of free fluid, and then again, it's not that easy to see or tell, but if you look up top, just above the liver, you may see something that shouldn't be there in someone that hasn't had a recent laparotomy or some sort of thing that occurred, some sort of intervention that's occurred on the belly yet. So which of the following is the most appropriate next step? So based on what you found in the physical exam, I understand the white count isn't that good, but based on the physical exam that they've shown you, because you can have stuff before peritonitis goes crazy or something like that. Should you go for an X-lab? Should you repeat the CT scan to see with arterial phase contrast to see if you have ischemia to certain organs? Will it change your management at this point or it change what you do? Upper endoscopy or endoscopy of treatment of any visualized lesions or start a PPI impressors, like a vasopressin specifically for someone who could be having an upper GI bleed or something like that. So why don't you guys go ahead and answer based on what you think is the best answer. All right, a nice mix. And again, these aren't unreasonable in some ways depending on what you think the differential is. But X-lab is what they're looking for based on the scenario that they presented to you. So the arterial phase wouldn't necessarily affect the need for this person to go to the OR who had free air. Now, it is possible to have free air and not operate on a patient. But they're not patients with peritonitis guarding a mild elevation of their, I understand most of the lab values are okay, but you still have a white count and a patient with a bad physical exam. Those are not patients you sit on with free air. But it is possible to have a divertic perf and reseal and you can kind of sit on it for a little while and you don't have to go crazy and start pulling things out. But that's not this patient. So the CT scan shows free air. Again, any time they give you a presentation of guarding and peritonitis, you don't have to go to the OR, but that should be sort of where you're looking to eliminate questions, answers, that are the best answer for the question. That's what you should start thinking. So in this case, you would want exploratory laparotomy. As they talked about it, you can have, as we mentioned, you can have non-operative management with some bowel rest and IV antibiotics. But again, that's in a perfectly stable patient who's not necessarily on immune suppression. I'm sure you've seen this in all your practices, but some of these patients on immune suppression can have a belly full of stool and you're pushing away and they don't feel anything. So they're a different population to have a different sort of clinical suspicion in. But in a regular person like this, not regular, but in a person who's not immune suppressed like this, this is, you would go off what you saw. So again, if you didn't even see it, that's probably the best answer based on the scenario. And all the other options are appropriate diagnosis, but not with a patient with free air and peritonitis on exam. Okay. Questions about that or comments? Can we look at the image again, please? Sure. Let's see if I can get the pointer to work. And I know it's frustrating because on my boards as well, I mean, it's just some of these images just don't do it, but you do your best. But that's clearly not, well, the arrow just disappeared. That's clearly not a loop of bowel. It just shouldn't be there. It's the diaphragm, it's below the diaphragm. And the patient's sort of on their back, so it's clearly a gas kind of coming up to that area. Phil, recognizing that this is not for this question, can you just remind people briefly some causes of free air that would not require a surgeon to take a patient to the operating room? Okay, so usually it's a perf tick in which the patient, and it's normally found for some other reason, and you just see free air. And those are patients, it's usually, the ones I've seen are an elderly patient, they look fine, there's no white count. They're wondering why you keep pressing on their belly. You can watch them and see what happens. And often, again, the abdomen, either with the omentum or itself, can actually help close on over those. And again, colectomies and X-laps are not benign procedures, especially in older people that may have some sort of comorbidities. So if you can sit on it, let it heal itself, give whatever antibiotics you and the pharmacist have agreed upon, that can potentially work. It is possible to have a duodenal perforation that you can sit on. It's not as common. Normally they require something, but there are some patients whose omentum may just come up on their own, and they may be very high-risk patients. So that's not a decision you would come to, I would say, as a standard of care, or do in independent thought, either as a surgeon or a medical intensivist, or an ER physicist, or any of that stuff. There may be someone who's so high-risk that you just try to see what you can kind of do, but most of them are gonna at least need a grand patch. But there are some patients where the anesthesia alone may do them in, or something like that. But I would say, again, that that would have to be this perfect patient that showed absolutely nothing else, and you're just kind of wondering what's going on. Air in the bowel can happen. You have to take a very good history, whether some, you know, it shouldn't be there long-term, but any previous laparoscopic event, any X-lap, sometimes you'd be surprised that people kind of miss when they sort of say, oh, they're free air. But if it's within at least 48 to 72 hours, sometimes it doesn't all resolve. And you'll often get the report from the anesthesiologist, not, excuse me, the radiologist, who may or may not have been given the history. So they'll call you in a panic and say, there's free air! And you kind of run over, your resident runs over, your fellow runs over, and they do this stuff. But, you know, literally, someone had been taking a look in there a couple days ago, it might have been minimal, might have just been a scope, who knows. There are, oh, there are situations with colonoscopies, where you can cause a little, maybe a little too aggressive. Some of them, again, if the patient's perfect, you might get away with it. But again, like everything else, it requires serial abdominal exams, a couple of labs, see what's going on. If they do, I guess the expression you would say is even if they fart funny, I shouldn't probably put that on the video, you gotta take them to the OR. So you don't wanna let them get to the point of shock or real peritonitis. But there are situations like that where you can specifically find other, does anyone else have any examples they wanna mention of where they might see free air that you can kinda, go ahead, please. A lot of times, ESRD patients post-dialysis will have a little bit of free air, and it's essentially when the fluid removal is done, they develop some submucosal ischemia, you volume resuscitate them, and you rarely have a surgeon that will take those patients to the OR. That's a very good point. Other questions or points? Yeah? Peg 2 placement? Sorry? Peg 2 placement? I can't hear you. Peg 2 placement? Oh yes, and that's correct, but that would go under, someone's been poking around in the last day or two, so someone's violated the abdominal cavity in some way. You could also see it with blast injury. What's that? Like blast injury. Blast injury. So you can have a Macklin effect, and you can actually have it tracked down from the mutastinum. Okay. We actually had a recent case, we ended up non-opting the patient for a completely benign exam, despite massive free air, and he was fine. Had no bowel injury. That's good to know. I don't think it'll be on your boards, but that's not, it's important to know actually, so that's. Okay, let's talk about some OBGYN. Ready. Can you hear me? Yep, there it is. All right, so our first OB case, you're terrified like I was when I saw this. We have a 21-year-old woman, gravital one para zero, at 32 weeks gestation, is emergently admitted to the ICU with uterine tenderness and malaise. Her temperature is 38.8, which is 101.9 Fahrenheit. Her heart rate is tachycardic at 125. Her blood pressure is 140 over 70, and the fetal heart rate is 165. She does have uterine-fundal tenderness on exam, but she doesn't have any discharge. Her hemoglobin is 9.7. She has a leukocytosis at 26,000. A maternal fetal ultrasound obtained before admission was normal. So the question is, given this presentation and physical exam, which of the following is the most appropriate next step? Are we going to administer IV antibiotics? Are we going to administer two units of packed red blood cells? Emergently take the patient to C-section to deliver the baby, or are we going to give IV magnesium? Magnesium, is there nothing you can't cure? So we have a febrile mother, tachycardic mother and baby, uterine tenderness. Answers in? All righty. Wonderful. So what do we think is going on? Anybody? Endometritis, almost. So this is chorioemionitis. It's a very classic presentation. It is a combination of fever, maternal, and fetal tachycardia, and fundal tenderness. It is typically an infection that's an ascending infection, typically from the vaginal flora. And essentially, IV antibiotics should work. You don't have to deliver immediately unless there are signs of trouble for either the baby or for mom. IV magnesium, though it works wonders in most things, it does not work wonders in this situation. Any idea, the antibiotics of choice for this? So if pin allergy, gentamicin and clinda. Otherwise, the initial choice is ampicillin and gentamicin. And usually, it's like a mycoplasm, but for some reason, we're still covered with ampicillin and gentamicin. All righty, any questions about that? Thank you. The next couple of questions are hemoglobin questions. For those of you taking the ABIM internal medicine exam, are usually about 5% to 6% are hemoglobin questions. So let's go over this one. 65-year-old with chronic lymphocytic leukemia is initiated on outpatient infusion pump therapy with fludarabine. At that dose, his laboratory data show hemoglobin of 11.4. White count is extremely high at 90,000 with 95% lymphocytes. Creatinine of 1, BUN 23, uric acid is 7. LDH is 597. He starts his treatment as massive spondymegaly, bulky intra-abdominal, and retroperitoneal lymphadenopathy. Four days after starting his chemotherapy, he comes in with flank pain, weakness, and nausea. And you can see his serum creatinine has now jumped to 2.4. His BUN is now elevated to 55. His uric acid has skyrocketed to 18. His LDH is now 1,800. His potassium is 5.9. In addition to IV fluids, which of the following interventions should be initiated? First of all, what's wrong with the patient? What does he have? Tumor lysis syndrome. Very good. So tumor lysis syndrome. So which of the following interventions should be initiated on this patient? Is it A, resburicase, B, hemodialysis, C, immediate CBVHD, D, urine acidification, or IV furosemide? Great, 67% of you got the correct answer, which is Rast-Burekase. So, tumor lysis syndrome is the syndrome that many patients who get cytotoxic chemotherapy for will generally develop this syndrome. It's not so much common with CLL, which is kind of like what the case was. It's more common with bulky tumors, like Burkitt's lymphoma, diffuse large vessel lymphoma. That's usually the setting when they get ARCHOV, for example, that's when they develop this constellation of abnormalities like hyperkalemia, hyperphosphatemia, hypocalcemia, very high levels of uric acid. The treatment here is focused on making sure you have adequate intravascular volume repletion, and two, you have to correct life-threatening electrode abnormalities, and then third, you have to decrease the very high uric acid levels. So, allopurinol would have been an answer here if it was a choice, but Rast-Burekase, because the patient is very, very sick with life-threatening electrolytes, you need to drop that uric acid faster, because allopurinol does not work. It lowers the uric acid, but it doesn't prevent further uric acid production, so unlike Rast-Burekase, which is basically a recombinant urate oxidase, it really works not only faster, but prevents further uric acid production. So, that is the correct answer. Urine alkalinization, not acidification, has been tried in the past to lower uric acid. The problem is that calcium and phosphate can precipitate in an alkaline pH, so it's not a good thing to be even alkalinizing the patient, which was done in the past, but we no longer do that. And then you have dialysis, whether it's hemodialysis or CBBH, these are not your immediate go-to therapies, unless medical management with IV hydration, correcting electrolytes, and correcting the uric acid, so it's not usually something that you would do, except if it's life-threatening, electrolyte abnormalities, hemodialysis would be superior to CBBHD in correcting the problem. Any comments or issues with that particular question? Okay. I'll quickly go back to the free air. It just occurred to me that, yes, if you have an upper GI perforation that you do not want to operate on, clearly, as part of your treatment algorithm, you're gonna do some sort of radiographic study to make sure that if the patient's perfect, and everyone agrees and all that, that you want to make sure that there's still no active leak along with the antibiotics and bowel rest. But again, that's not the norm for most of those patients. The only other pearl, in case they do ask it on the boards, is if you are gonna administer a Rasburi case, you have to check a G6PD level, because if the patient is G6PD deficient and you give Rasburi case, you're gonna cause hemolysis. So that might just be just a pearl to think about if you're thinking about giving, in practice, Rasburi case, you have to make sure you check a G6PD level before you do that. Okay, another hemon question. 45-year-old man comes in with respiratory failure 10 days after undergoing hematopoietic stem cell transplant for lymphoma, he has hypertension, stage two CKD. His post-transplant course is uncomplicated until three days before ICU admission, where he gets dyspnea, nonproductive cough, high fever, severe mucositis. Chest X-ray shows bilateral, interstitial, and alveolar infiltrates concentrated in the perihilar areas. His pan-cultured broad-spectrum antibiotics are started. A high-resolution CT shows bilateral ground glass opacities. A BAL is performed, which reveals progressively bloodier fluid return with each lobe examined. His BAL is negative for bacteria and there are no hemocydrin-laden macrophages. Question for you, which of the following pulmonary syndromes is the most likely diagnosis for this patient? Is it A, engraftment syndrome, B, acute GVHD, C, diffuse alveolar hemorrhage, or D, bronchiolitis obliterans? For all those medical intensivists out there, I'm sure you've seen this patient. Great, diffuse alveolar hemorrhage. Notice a little bit of that catch, you know, they said no hemocydrin-laden macrophages, which usually when you do a BAL, you get this progressively bloodier return, and then if you look under the microscope. But if it's fresh bleeding with DAH, you may not have that hemocydrin-laden macrophages. In any event, the things to know about stem cell transplant patient, they have a very nice timeline in which they develop pulmonary complications. Some very early, like engraftment syndrome, DAH, idiopathic pneumonia syndrome, and then there are those that you get much later. So that bronchiolitis obliterans, that happens kind of very late. But in the first few weeks, you have to think about engraftment syndrome. That's when the white cells start to come back, patient gets a fever, some respiratory complaints, and then has bilateral infiltrates, maybe even a rash, and usually results quickly with either high-flow nasal cannula, or maybe sometimes intubation, diuresis, capping of fluids, and steroids usually work there. In most of the respiratory failure situations in patients after stem cell transplant, usually corticosteroids is usually a treatment modality. So for this particular question, the answer was diffuse alveolar hemorrhage. Even though there were no hemocytin-laden macrophages, I think the timeline 10 days after transplant, respiratory syndrome, bilateral infiltrates, bloody return on BAL, that's pretty much pathognomonic for somebody with diffuse alveolar hemorrhage. So the correct answer is DAH in that setting. Any comments or issues? Okay. And these are just some of the other rationale for some of the other choices. And again, these will all be available to you in October. Okay. So we have an 18-year-old term woman who did not receive prenatal care. Coming to the hospital has an uneventful full-term vaginal delivery. The next day, her blood pressure is 190 over 110. Her heart rate is 110 beats per minute. Her respiratory rate is 18 breaths per minute. She is a febrile, and her urine output is noted to be 21, I mean 21, she's 25 cc's per hour for the last five hours. So, no worries. It's okay. Clinically, what is the stim pushing us towards? Just preeclampsia, or? So this is pushing us towards, and this is what I wanted to talk about a little bit, severe preeclampsia. And severe preeclampsia is defined by systolic blood pressure greater than 160 or diastolic greater than 110 on repeated blood pressures about six hours apart or sustained. You can have one of these. You can have oliguria, which she has. You can have, we don't have labs, but thrombocytopenia. You can have headaches, visual changes. Any of those in this setting, we have to worry about severe preeclampsia. So, which of the following interventions, based on that, is now most appropriate? IV Lasix, IV enaloprilat, IV mag sulfate, volume expansion, or IV mannitol? All right. All righty. So, things to note. We can go to the things. Things to note that these patients, so the correct answer is magnesium. Magnesium works, severe preeclampsia, eclampsia, go-to drug of choice. They actually are volume down, so diuresing them is actually not the way to go. So, Lasix and mannitol would not be the correct answer. And we need, giving IV enaloprilat is not going to get the adequate blood control we need to give the magnesium. So, this is a case of severe preeclampsia that needs to be treated with IV mag. And this isn't working. Oh, there it is. All righty. Oh, it's me again. A previously healthy 36-year-old gravidate two, para two woman at 39 weeks gestation with an uncomplicated pregnancy is found to have a hemoglobin of 11.6, a platelet count of 40,000, and a creatinine of 2.6. The rest of her labs are normal. Her blood pressure is 160 over 100. Her heart rate is 88. And her respiratory rate is 16 breaths per minute. Her urinary output is less than 30 cc's per hour for the past three hours. We can go to the questions. So, based on that presentation, what do we wanna do? Do we wanna begin induction of labor with oxytocin? Do we want to perform urgent plasmapheresis? Do a TTE? Do an emergency section? Or do we want to begin plasma expansion with 3% saline? Oh, okay. When I first read this, I think I was with the 60%. But then we're gonna come back. The correct answer is actually to induce labor, okay? We can go to the... So, we have a situation in which we have a triad of anemia, thermocytopenia, and renal insufficiency, which makes you think of TTP or HUS. The distinction between the two is that neurologic symptoms, which we don't really have in this situation. We do have the increase in creatinine, the decrease in urine output that suggests that she is developing HUS in this situation. It does have a high maternal and fetal mortality, so we do have to deliver. So, between the two choices, I get it. Like, you think, let's get the baby out, let's just do a C-section. And actually, the data supports, if everything else is okay, to actually do the oxytocin-induced vaginal delivery, including the idea that you're entering a surgery with a coagulopathic patient who has platelets of 40,000. So, if you can deliver vaginally, reduce the risk of hemorrhage, that would be the appropriate step. And it is, the HUS should improve after delivery. If it doesn't, then there are other things that might have to happen at that point. Questions or comments? Yes, Dr. Balk? I did not see a timeframe. If anyone else has an answer, my understanding from what I was able to look at was that if you can safely deliver vaginally, that was preferred. Obviously, if there are any deterioration, either a mom or a baby, then you would proceed. But again, it was the idea of taking a coagulopathic patient to the OR. Yes. No, but it's okay. I can hear you, though. Is MAG sufficient or what was the last part? So it is the first line of therapy. My experience has been that you do have to add additional medications, but your first line of therapy for preeclampsia is definitely initiation of magnesium. Still me. Okay. I think you kind of cut out all the others in between. No, just teasing. A 39-year-old woman who is 29 weeks pregnant is admitted to the hospital with vaginal bleeding and right upper quadrant abdominal pain. Within eight hours of admission, she suffers fetal loss due to acute and complete placental abruption. I was like, really, did we have to do fetal loss? No. Several hours later, she develops hypotension, tachycardia, and reports increased right upper quadrant pain. Her lab values at this point, she has a sodium of 130, a potassium of 5.1, a BUN of 34, a creatinine of 2.1, her leukocytes are at 11,000, her hemoglobin is 5.9, her hematocrit is 17%, her platelets are 32,000 with an INR of 1.1, a PTT of 26, her T-Billy is 1.2, her LDH is out of control, so are her ASTs and ALTs, her GGT is 40. You do a CT scan of her belly. We may be able to show that. Okay, beautiful. And you see an abnormality here. What abnormality do we see? What side of the screen is the abnormality? Say that again? Wonderful. So she has a subcapsular hematoma here around the liver. So I just want to make sure we're all seeing the same thing in the clinical setting. So we'll go to her questions. So based on the stem and the imaging, what is the next best step to manage her? Should we transfuse RBCs and platelets? Should we do an emergent laparotomy? Should we do right upper quadrant CT guided drainage? Platyporesis with O-plasma? Or should we put her on the list for a transplant? Wonderful. All righty. So at this point, most of us got it. We have a patient who has HELP syndrome that has unfortunately been complicated by a hepatic hematoma. HELP syndrome being defined as elevated liver enzymes. We saw that. They were in the 2000s, I believe. Microangiopathic hemolytic anemia, as well as thrombocytopenia. Unfortunately for her, she has this hematoma. We have to just manage it with platelets and packed red blood cells at this point. And correct me if I'm wrong. I'm not a surgeon. But you actually want to take advantage of the tamponade physiology here. So you don't want to go sticking drains in it. You don't want to go messing around with the liver in a coagulopathic patient, opening her up so she can bleed more. And then you increase your risk of infection if you stick a drain in it as well. So that's why the correct answer is just supportive therapy with platelets and hemoglobin, or platelets and packed red blood cells. Some patients do have to go to liver transplant if we can't stop the bleeding and there needs to be repair, et cetera. But that's like the really severe cases. So questions about that? Use the liver capsule to your advantage in this situation. No touchy. All right. 66-year-old man is admitted to the ICU for evaluation of hematochezia. During the preceding 12 hours, he has passed three large volume liquid maroon stools. He denies symptoms of peptic ulcer disease, aspirin, or nonsteroidal anti-inflammatory drug use, ethanol use, or antecedent vomiting, including hematemesis. He lacks a prior history of diverticulitis disease. His blood pressure is 105 over 60, and his heart rate is 130, so a little dry. Gastric lavage and aspiration yield clear fluid. He has a loud systolic murmur, best heard in the aortic area. So that's one of your hints as to where they're trying to drive you. He has hyperactive bowel sounds. I mean, that could be anything, so it's just a trick. And a diffuse tender abdomen without peritoneal signs. Coagulation studies are within normal limits, and they send him to a tagged red blood cell scan. I would say, in general, that may not be the test of choice immediately anymore for what we do with these patients, especially if they're not sort of stable. But this is what the question gives you, and your job is to answer the question that the person who wrote the question for the boards wants you to answer properly. And we don't interpret these often, so it's a, but anyway. All right, so which of the following steps is most appropriate? Go to Angio, ensure adequate volume resuscitation with crystalloid and blood products, begin a systemic infusion of vasopressin, or perform an upper gastrointestinal endoscopy. And I will say, based on what I've told you, there's the answer they want you to give, and there's what might be a reasonable response anyway. So go ahead and put your answers in. Okay, so I completely understand why people would answer that and we'll modify this for the future, but I agree, that could be a relative hypotension, we have no idea what blood pressure they have in clinic, what they are walking around, this patient could be in a form of shock. So doing your ABCs is not an incorrect answer, but clearly they're showing, not clearly, they're showing you this tag red blood cell scan with a result on it and trying to say what's next in the algorithm. I understand that we shouldn't really, maybe we shouldn't have the patient sort of in some sort of hemorrhagic issue, but it's not really the teaching point of what the question's meant to address. So you got a tag red blood scale that clearly demonstrates lower gastrointestinal tract bleeding and seems to have its origin in the ileocecal region. As a rule, most clinicians use tag red blood scales to identify sewer candidates for gastrointestinal angiography. Again, that's the question, I wouldn't say it's part of your current practice. If there's nothing evident on tag red blood cells, the angiogram is unlikely to provide any additional useful diagnostic information. Conversely, most surgeons will not operate on patients solely based on a positive tag red blood scan, which is true, because it's going to be very hard to identify once you go in there and blind resections aren't necessarily good for the patient, so you really don't have a better idea of the anatomy. Also, called gray zones are frequently false positives, even if the test is clear positive, it's not usually sufficiently accurate to specifically identify from which the bleeding emanates. Therefore, further studies such as angiography is indicated. So the question of vasopressin would be those that, again, are dying of huge upper GI bleed or even lower GI bleed to some extent, so clamped sort of the mesenteric vessels. Angiography should be obtained first. Angiodysplasia of the large bowel is often a difficult diagnosis to establish, but that's sort of something, if hopefully you can put it all together, that was sort of evolved with sort of being the murmur that you would hear is sort of related to that angiodysplasia. Okay. Can I ask a really quick, like, real-life qualifying question? When would you do TAG-RBC, then CT-ANGIO, versus bleed, just go to CT-ANGIO, see if there's something you could? Clearly shock is part of it, unless, because again, all bleeding needs to be resolved immediately, but if you don't know what you're going to take out, I mean, you just can't take out everything, although eventually on your boards they may push you to do sort of a blind resection of some sort or try to do some form of colonoscopy or scope in the OR to try and identify it. Now, that's not as easy as it sounds in someone who's not prepped, so you're still going to be in a lot of trouble. I would say, practically speaking, given the fact that a nuclear scan takes a not small – surgeons love double negatives, so we say not small amount of time rather than just saying isn't rapid, you know, or something like that – that most people go straight to CT-ANGIO or ANGIO of some sort, and I would say with the improved resolution now of what we have, you'd be surprised what they can catch. So and practically speaking, someone in the ER, I would, you know, it's sort of like if you do any thyroid questions or parathyroid questions, there are some things you can resect without doing all these tests, but the reality of the situation is the endocrinologist does them all, so it's sort of presented to you that way. Appendicitis can be diagnosed without the CT scan, but the reality is we're not in the ER necessarily, and it's not as easy as it sounds to differentiate these things, so most of these patients are going to end up having a CT scan before you go. And in this situation, practically speaking, if this person presents to the ER before involving everyone that's going on with an unclear case, a CT angiogram would not be an unreasonable thing to do in a patient who's not coding in shock to try and get a better differential to figure out what the next step is going to be. But that being said, they presented you with a nuclear scan, that's sort of the standard thing they still teach in medical school with the 0.5 versus 1 cc per hour and all that kind of stuff. All I can tell you is that nowadays the scans really are beautiful to the point, honestly now where this is unrelated, but in trauma now, we're starting to pick up all these PEs, like immediately post-op, but we don't know what they're due to, because clearly the patient didn't have all these, most of them are young individuals, like they didn't come in with all these PEs and high risks, so they're catching all these things that are related to chest injury, and we're not exactly sure what to do with them anymore, but it wasn't ever seen before because the resolution wasn't as good as it is now. So times are changing, radiology is evolving, and so will our question over time. Any other questions about that? I think that your ABCs is still a reasonable response. Okay, a 38-year-old woman is admitted to the ICU for management of massive lower gastrointestinal tract bleeding after developing orthostatic changes and anemia, so hemoglobin level of 6.1. The patient had otherwise been in good health. Her chief concern is painless bright red perectum. She states that her last menstrual period was three weeks ago, and her urinary pregnancy test was negative. She denies any blood in her bowel movements or recent change in bowel habits, but she states that she occasionally has painful hemorrhoids, so that's their first sort of chuck to you, okay? The patient is on no medications at present. Evaluation in outlying hospital included a flex sig, but again, understand there are limitations to that, not necessarily bowel prepped, and as we all like to joke, it was outside hospital, so who knows what it meant, what they saw, what the qualifications of that individual was. The exam was suboptimal, but there was blood at 35 centimeters, so the patient is currently receiving two units of PAT-GRAB blood cells. So, okay, you can make the argument that potentially they're in shock, but before you go doing crazy stuff, think about what might be a very simple, although to be honest, unless you've had an anoscopy, it's not as simple and easy as, it can be quite painful, but what is something you can do before you go, at least in the ER, under some mild sedation, assuming they're not in shock, that could be done next before running off to do all these other kind of things. So, go ahead and answer your, those are both, again, reasonable, but the teaching point was take a quick look before you start doing some of the other stuff, because, again, they gave you the history, and it is possible to have significant bleeding, not only from external hemorrhoids, but internal hemorrhoids, and it can be quite a bit, so if you can identify that first, you can eventually prevent radiation exposure, IV contrast, a whole bunch of other things. So, again, what they're trying to get at is, it could be anywhere, bright red blood per rectum suggests a patient could be bleeding anywhere from the pylorus to anus. Again, understand that 10% of bright red blood per rectum can be an upper GI bleed, but they did tell you that, at least I thought they told you, that they sort of didn't find anything in the NG tube, or anything from there above. Most people would say that you, at least, if you, before you go whisking off for colonoscopy or other kind of things, that you have to at least put an NG tube in and look from above before you run off to the other things. I would say that's actually a critical fail on anyone who's taken their surgical oral boards. So, put your NG tube in or scope before you go running off doing some of the other stuff. So, the blood per rectum indicates that the blood has been actually guessing to just a source proximal to pylorus, but mesenteric angiography tagger blood cells could be useful for localizing. These studies require a bleeding rate. Yeah, yeah, yeah, yeah. So, the correct respondents perform anoscopy, which would disclose bleeding hemorrhoids. Again, easy to say, not so easy to do, but it is inexpensive and relatively quick. Retroflexion of the flexible scope introduced per rectum is frequently not accurate. That's true. It can be difficult to visualize. And technically, you could do this without, you could fix this potentially without putting the patient under general anesthesia. Again, not as easy as it sounds, because this is sort of painful and they're in a little bit of distress, and you're already giving blood. With massive rectal bleeding, the left colon frequently fills in a retrograde fashion, accounting for the presence of the gross blood at 35 cc's in this case. So, urinal sphincter does its job, and things sort of back up. Once you've cleared the sort of lower part of the tushy, colonoscopy would be a reasonable diagnostic measure, because it provides therapeutic options if a bleeding point is identified. Now, again, your gastroenterologist may or may not do that. It can be difficult, and again, even though blood is a cathartic and hopefully cleans everything out for you, it can be really hard to identify what's going on there. So, not everyone is so enthusiastic about going in blind. In the face of normal coagulation parameters, there's no indication for the administration of FFT. So, that's, again, don't transfuse unless you have to. So, a lot of teaching points stuff. Any questions about that particular question? Yeah. Can you talk to the mic, if you don't mind, because they're recording it, and they're going to want another question. So, like in the bright red blood colorectum, so, this can happen with ischemic colitis or gut ischemia, and the other thing that you said is, you know, hemorrhoidal or some other anal bleeding. So, how significant is the portal air on the CT imaging and with elevated lactate? So, some of these patients, it's difficult to know which ones go south quickly. And so, based on my experience, patients with portal air, it doesn't matter whether it is gut ischemia or ischemic colitis, they seem to do worse. So, is it because the mucosal lining is disturbed and pathogens are getting into the system and that is causing the air, into the portal air, and how significant is that finding in the CT imaging and how seriously we need to take it? So, it's sort of a different question, is how important is portal venous air when you're sort of dealing with an acute abdomen? Now, just so you know, there are circumstances where you'll find portal venous air, and again, something that's benign. That's the exception to the rule, but there, you know, again, it's like finding free air. Don't necessarily run off for an X lap until you sort of figure out what's going on. But you're correct. It's a breakdown of tissue, lack of red blood cells, lack of oxygen leads to the death of the tissue. The death of the tissue leads to breakdowns and anaerobic, you know, other things that can generate air. You have anaerobes, facultative anaerobes, you know, no different than you might see with a clostridium, not difficile, clostridium infection where you get sort of trailing of air all the way up down a fascial plane. So it is a worse sign because it's an indicator that the death of the tissue has further progressed than you may have seen if you caught them early. So can I give you a study that, I don't remember off the top of my head if I can tell you that this percentage of patients have reached this thing and their mortality be whatever. But portal venous air on a CT scan is not a good indication, would be, definitely push you to operate than not operate in a patient that's heading in the wrong direction. It definitely happens again because the tissue is dead and the venous return is bringing the air back up. So great question. Not necessarily associated with acute GI bleeding, although it can be. But whatever is causing your bowels to not get the flow and delivery of oxygen that they need can lead to that dead tissue, peritonitis, and a bad, that thing on CT scan. I actually don't know the answer to that. A cirrhotic patient, guys? Anyone out there? How frequently do you see portal air? Not unless they've had some form of an intervention done, like, I mean, unless they've had like banding or sclerosing agents or something like that. Otherwise, if you see it, there has to be some other pathology associated with it. You have to rule out the badness first, and then you can kind of go to other things. Okay. More bleeding. A 63-year-old man presents with non-variceal upper gastrointestinal bleeding. Multiple arterial venous malformations are found during endoscopy, and the bleeding is successfully controlled with CLIPS. Which of the following is the most appropriate pharmacologic management following endoscopic control of bleeding? So it's your standard algorithm for upper GI. So you should already have like a thing in your head. If you have a memorizer, you do it all the time, but if A, then B, yada, yada. So IV actreotide, the dosing's there, but that's not really that important. You just need to, the point is, would you give IV actreotide first, IV PPI, followed by a continuous infusion for 72 hours, IV H2 blocker up to five days, or six days, or just don't do anything and see if they re-bleed, and do your second scope, assuming, or something like that. So that's the intent of the question is, what's the best intervention or non-intervention based on sort of the algorithm? So, the typical standard would be good of a high dose PPI to decrease re-bleeding and possible mortality in patients with high risk who've been treated with endoscopic therapies. There was a consensus from this in the international panel of experts, there is no evidence of effectiveness for actreotide or histamine two in these particular patients at this time. And that doesn't mean you would never give an upper GI bleed actreotide drip, but that's not the circumstance that they're giving to you, what they're giving you is what is the recommended next drug after appropriately controlling upper GI bleed with CLIPS. Okay, let's go to the next one. Your turn. All right, we have, whoa, sorry, a 34-year-old parturient, Gravida 2, parturient being actively delivering, Gravida 2, PR1 with preeclampsia at 36 weeks gestation, undergoing cesarean delivery. She is admitted to the ICU for ongoing resuscitation and soon thereafter develops acute pulmonary edema. Which of the pathophysiologic features of preeclampsia increases the risk of pulmonary edema? So, is it due to increasing circular blood volume, decreased capillary permeability, increased systemic vascular resistance, or increased plasma oncotic pressure? So the question is, you have a preeclampsia woman, what is the pathophysiology behind her now acute pulmonary edema? We have a nice play, but 50% of us got it correct. It would be the increased systemic vascular resistance. So we've talked about preeclampsia several times now, just remembering that it is defined with hypertension and the setting of proteinuria that begins after 20 weeks. There are multiple risk factors, including obesity, advanced maternal age, which is now geriatric, I was that sad, and diabetes. The cornerstones are blood pressure reduction with a multitude of things, including hydralazine, labetalol, peripartum giving MagSulfate as well. But the thing is, can we go back to the choices, please? And thank you, all righty. So again, they actually typically have decreased circulating blood volume. They have increased capillary permeability, which is why B isn't correct. And there's potentially decreased to normal oncotic pressure. So the physiology or the pathophysiology behind preeclampsia is simply increased systemic vascular resistance that yields itself to pulmonary edema. Questions? All righty. We made it through, yay. Okay.

clinical cases

acute limb ischemia

atrial fibrillation

thrombocytic syndrome

severe preeclampsia

diffuse alveolar hemorrhage

hepatic hematoma

lower gastrointestinal tract bleeding

diagnosis and management