For this particular Q&A session, we're going to deal with questions, surgical questions, solid organ transplant, GI, environmental, and blood emergencies. We're graced today by expert faculty, two of whom are former Society of Critical Care of Medicine past presidents, Heather Lee Bailey, the first emergency medicine intensivist president of the society, and Lou Kaplan from UPenn, also former president of SCCM, and of course we have Nicole Siparsky from Rush and Rajat Kapoor from Indiana Health Pulmonary Critical Care. So we'll start off with the first question, and I'll have Dr. Kaplan come to the stage. How many people here are surgeons? Great. This may be in block lettering for you. It makes it easier for me. First patient, 54-year-old man with alcoholic cirrhosis and hep C is in the MICU with acute hepatoencephalopathy. We're all happy he's in the MICU, not the SICU. He has anisarco. You can see the labs there, his INR is 1.5, bilirubin is 2, creatinine is 1.2. He gets a contrast CT to rule out PE. It's negative. While he's being evaluated by the transplant team, an echo shows substantial tricuspid regurgitation. You've now seen a lot of echoes in different lectures, so you should be familiar with that. And significantly reduced tricuspid annular plain systolic excursion, which I will not say three times quickly. No other abnormalities are identified. Without further optimization, this patient has an increased liver transplant perioperative mortality due to each of the following, hepatopulmonary syndrome, acute PE, intraoperative hemorrhage, acute perioperative stroke, or portopulmonary hypertension. I have to tell them to scan the QR code. You should know now. Scan the QR code. You'll find things in your phone. Will this let me know when everyone's voted? This is great. We've got a mix of answers. Okay. If you were in the portopulmonary hypertension group, you have the correct answer. This patient is, in fact, an excellent candidate for a liver transplant. Echo is routine. All the pre-transplant patients get that. We do manage a lot of the pre-transplant patients in the SICU, even though we'd like them to be in the MICU. And this one finding, portopulmonary hypertension, is very strongly associated with perioperative mortality risk. And in particular, that risk is uniquely tied to elevated pulmonary pressures that are transmitted across the right side and then increase the venous pressure for the transplanted organ. This drives bleeding and poor graft failure and creates a number of issues so that the therapy that you really want is to reduce your PA pressure and decrease your pulmonary vascular resistance. Which way you do that is not as relevant as whether you do that. The other answers that were there, acute P, he doesn't have that. I'm just going to go back for a second here. Perioperative hemorrhage is not driven by any of those particular findings, because remember during this, you generally bypass the liver, so you are on a support system and you have cannulae, and so you can control that quite nicely. There is no tie to perioperative stroke from an increase in your pulmonary vascular resistance and pulmonary pressures. So portopulmonary hypertension is, in fact, the best answer for this particular question. Questions about that? We're all good. Okay. Lots of fun references. 24-year-old woman, restrained passenger in a high-speed crash. She is one that experiences a loss of consciousness. Takes a long time to extricate her. On primary survey, airway is intact, equal breath sounds. You can see her vital signs listed there. Does not require a substantial amount of O2, but it's not exactly a normal SpO2 either. Forehead laceration expected, seat belt abrasion and bruise across her chest. She was restrained. She has a deformed right mid-thigh. Her brain CT shows minimal subarachnoid hemorrhage. Cervical spine CT is normal. Chest CT shows a periortic hematoma with a luminal filling defect and a small left hemothorax. Internal CT has a grade three liver laceration. There's a blush. And there's a grade two splenic laceration with a very small amount of pelvic blood. She has a mid-shaft right femur fracture. What should we do next as the next best step in management? Heart rate and blood pressure control, therapeutic anticoagulation with unfractionated heparin, emergency thoracic aortic repair, placement of a left tube thoracostomy, or urgent repair of her right femur. You are now all experts at getting all of these questions on your phone, and you can now vote. Great. Those of you who said heart rate and blood pressure control, you are correct. The imperative here is to make sure that the aortic injury does not progress. The control of so-called DPDT, change in pressure over change in time, is your acute goal. It is tempting to immediately repair the aortic injury. In fact, if you're a surgeon, this can be lots of fun. A lot of this, well, at least for you, maybe not so much for the patient. A lot of this is now done endovascularly, and when you look at patients who undergo emergent operative repair, open or using an endovascular approach, if you can wait, stabilize other injuries, femur fracture, solid organ injuries, they do much better. Their anesthetic risk is less. Their perioperative mortality is less. All of their outcomes are improved. And so that's why that initial control of heart rate and blood pressure, commonly using Esmolol, despite its fluid load, makes the most sense. Anticoagulation with a hepatic and splenic injury generally results in more bleeding, which is, that can drive you to the operating room. And if you are looking for RVUs, that is one way to do it. Tube thoracoscopy for minimal hemothorax is not necessary. If it was a combined hemo and pneumothorax, and they're on a ventilator, then you have to worry about the pneumothorax progression. And urgent right femur fracture repair, if it's isolated femur fractures, those get driven very quickly to the OR, because if that's their only injury, there's an outcome in performance metric that is enhanced. But not in the complex constellation of concomitant solid organ injuries and a thoracic aortic injury. Yes? What about the luminal filling defect? There's a little clot there. So with a lot of blunt aortic injury, you will have a wall hematoma. You'll have some intimal disruption. And when your intima is disrupted, it is a very thrombogenic surface. It's the same reason that if you look after patients that have had balloon angioplasties of, let's say, their iliac or their superficial femoral artery, they always get some kind of anti-platelet agent so that that intima that has been fractured by the balloon, whether it's drug-coated or not, is less likely to result in clotting. You may be familiar with this from carotid endarterectomy, where we literally rip it all out, and they get filled with white clot syndrome. It's all platelets. So for the same kind of reason, I'm glad you asked. Other questions? Great. And this constantly gets looked at. When should we take care of patients? The last big series was in 2021. 52-year-old male driver, also in a motor vehicle crash, airlifted to your regional trauma center. He arrives intubated, a little hypotensive, tachycardic, breathing at 16 with an obvious scalp laceration. So he's breathing with the ventilator. It's set at 16. And he also has an open femur fracture. He has an extended fast that shows moderate free fluid in the pelvis. Laboratory studies, including at Teg, are performed. This is yours, isn't it? It is. Why are you letting me talk? It's a seniority. Oh, dear Lord. You take care of this. I enjoy your voice. All right. Now you have issues. Okay. Where were you at? Labs and Teg? Teg. Okay. Lab studies, including Teg, are performed. It's a seniority. Oh, dear Lord. You take care of this. I enjoy your voice. All right. Now you have issues. Okay. Where were you at? Teg. Okay. Lab studies, including Teg, are performed. The Teg tracing shown is most consistent with which of the following disorders? I'm going to show it to you, and then I'm going to flip back to the slide. So here's the Teg tracing. I'll give you a second to look at that. It's a beautiful Teg tracing. Isn't it? Remember that in your mind. And then we're going to flip back. So which of the following bleeding disorders is evident from the Teg? Is it acute posthemorrhagic anemia, hyperfibrinolysis, hypofibrinogenemia, or a vitamin K deficiency? Okay, it looks like just about everyone has voted. So the correct answer is hyperfibrinolysis. Going back to the tag, and we're going to talk about this more in a minute, but fibrinolysis occurs after the platelet plug and the clot have formed. And if it happens excessively, the taper of the tag will be very steep and rapid, and that is suggestive of hyperfibrinolysis. 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. Several hours later, she develops hypotension, tachycardia, and reports increased right upper quadrant pain. Tabs at the time include a sodium of 130, potassium of 5.1, BUN 34, creatinine 2, leukocytes 11K, hemoglobin 5.9, hematocrit 17, platelets 32K, INR 1.1, PTT 26, T-Billy 1.2, LDH 20,000, AST 2,300, ALT 2,100, and GGT 40. A CT scan of the abdomen obtained to evaluate the right upper quadrant pain is shown in the next slide, which I will show you in a moment. The patient is transferred to the intensive care unit. Which of the following options is most appropriate? I'm going to show you the slide and then come back to the answer. Here is the single image that you're going to base your plan on. All right. Go back to the question now. So which of the following management options is appropriate? Transfused red blood cells and platelets, emergent laparotomy for hemorrhage, right upper quadrant CT guided drainage, plasmapheresis with O negative plasma, and listing the patient for an emergency liver transplant. Okay, so looks like pretty much everyone has voted. So the majority wins. The answer is transfusion of red cells and platelets. So keep in mind that this patient had a perihepatic hematoma, which was the gray crescent around the liver on the CT image. It is evidence of HELP, or hemolysis elevated liver function and low platelet syndrome, which is typically characterized by elevated LFTs, a hemolytic anemia, and thrombocytopenia. So it's a common condition in the third trimester of pregnancy. It can affect women even after they deliver, and it's important to keep this syndrome in mind. Typically the treatment is supportive, and often expeditious delivery is appropriate. I think that's it for me. Is this the next person? Yeah, this is me. Again, you can enjoy my voice. 24-year-old woman who has asthma presents to the ED with cough, wheezing, and dyspnea. Inhaled albuterol, IV magnesium, and IV steroids don't seem to work for her. She develops hypoxemic and hypercarbic respiratory distress. She's intubated. She's placed on invasive mechanical ventilation. She's sedated using propofol and some fentanyl. She goes to the ICU. She goes to your ICU. Although she's dyssynchronous, she is neuromuscularly blocked with a bolus and then an infusion. Of course, the nurses are following your protocol, and they place electrodes over the ulnar nerve at the wrist, and they get four out of four twitches. They're all of equal strength, the first to the fourth. So-called train-of-force stimulation says she's neurologically intact before she gets her cystatric urine. She's still a little dyssynchronous, and therefore the infusion gets turned up. And now she has a train-of-force of zero over four. Which of the following recommendations is the most appropriate to evaluate the degree of neuromuscular blockade? Changing the electrode placement location, increasing the current from 60 to 80, assessing the post-titanic count, getting a new stimulator device, this one must not be working properly, or reversing the electrode polarity. Notice that this is a different question than the one that you're usually asked, which is the nurse says, what would you like me to do with the drip? All right. So this is important. If you thought that you should change the electrode placement, that's not going to be the right answer. Who's an anesthesiologist in the room? We got one. It's amazing. Okay. So the rest of you who got this correct, you should go into anesthesia. So if you change the electrode placement, it says, I didn't really believe what I had when the electrodes were in the place in the first place. That's not the right answer. You've done something that's changed the patient's ability to respond to the electrical impulse. It also means that changing the nerve stimulator also isn't the right thing. There is no value in reversing the polarity, and if you don't get a response at 60, there's no reason to go to 80. The post-titanic count is something that most of us don't do a whole lot with. When you think about a patient that has no twitches, and they previously had four twitches, you have no idea how completely blocked they are. So you can give what is known as a titanic stimulus, and that is listed here, 60 milliamps at 1 hertz for 3 seconds after a 60 milliamp, 50 hertz pulse delivered for 5 seconds. So it's a two-step process, and you see how many contractions you get after you have had titanic stimulation. That way you can say they are profoundly blocked, and the number of twitches you get correlates with the amount of receptors that are saturated. Now does this functionally make a difference for you? No, because you're turning the drip down anyway. But the assessment of how deeply blocked they are, and the determination of whether you should reverse any of that blockade with an agent, is aided by understanding what the post-titanic count happens to be. Because if you have all your receptors saturated, maybe some reversal is appropriate. Lots of reviews of these things, because this is an area that we don't spend a lot of time talking about, and we don't spend a lot of time assessing. Let's see. Here we go. Something that is much more familiar. 38-year-old man admitted to the ICU with multiple rib fractures in an ATV crash. He was, of course, driving down the middle of the streets of West Philadelphia, where ATVs are, of course, illegal. A left chest tube is placed for an enlarged hemothorax 24 hours after admission, and then he requires intubation 24 hours after that. He has what you would expect, hypoxemic and hypercarbic respiratory failure. This external CAT scan shows multiple left-sided rib fractures. Three of his ribs have two different lateral fracture sites, and they're all adjacent to one another. I will show you his chest x-ray in a moment, and you'll be asked to decide what the best management happens to be. Here's his chest film. As you can see, he's intubated, he has a central line. One side is more impacted than the others, and he has a bunch of rib fractures on the left. As you can see, if you look right up in here, they don't have a good pointer, the rib contour is somewhat discontinuous. Anybody have had rib fractures before besides me? Yeah? Do you have discon... Are you lumpy bumpy after the rib fractures? A little bit? Yeah. So, this guy is lumpy bumpy. Let's go back. You can either bronchoscopically evaluate him. You can place a second chest tube. Send him to the OR for acute rib fracture fixation, or you can start with inhaled nitric oxide therapy. Let's see what you'd like to do. Great, if you guessed acute rib fracture fixation, that is the correct answer for this kind of patient. This is a classic patient that demonstrates a flail chest. Three ribs, all in a row, two different floating segments. And therefore, when you inhale, chest wall should go out. Those segments that are free-floating go in, so-called paradoxic motion of the flail segment. Beneath of that is a contused lung. The degree to which you can stabilize the thoracic cage also helps you to re-recruit the injured lung. It substantially decreases pain, especially if you combine this with, let's say, liposomal bupivacaine, known as Expirel. That lasts for several days. Or you do what is very common now, which is cryoablation of the subcostal nerves. And therefore, they stay pain-free for months. You don't need a second chest tube, because you didn't have a space-occupying lesion there. Inhaled nitric oxide, which has not been demonstrated, I think, to change the outcome for any condition, but it does change your pharmacy's budget. And you might like your PO2 a little bit better. It doesn't really need to happen here. And you could bronchium, and that's reasonable to do, but it's not the best thing to do, because it will not change the contusion. It will not stabilize the flail segment. This used to be very, very controversial. But in fact, it is not controversial at all at this point. And you can see by some of these references, two from 2023, one from 2022, this is a significantly investigated topic. Questions? Comments? Think rib fracture fixation is nuts? It's fun to do. There's lots of new bioengineered products in this space. Everything used to be titanium. Now we have others that are increasingly flexible and will move with you instead of being rigid. And you get to use fun little drills. Okay. And now this is not me. Though I know you'd like to run a marathon. Oh, yeah. I need a CAT scan first. And new knees. And new knees. This is a 55-year-old male who is unfit, decides to run a half marathon on a hot Saturday afternoon. At mile 7, he collapses and is brought into the emergency department. Upon arrival, his skin is hot and sweaty. His temperature is 40.6 degrees S, or 105 Fahrenheit. He's tachycardic at 140 in sinus. His blood pressure is 90 over 60. Fluid resuscitation is initiated, as well as cooling procedures. A catheter is placed, and reddish-brown urine returns. Your analysis results show a large amount of blood, but an absence of red blood cells. Which of the following is the most likely cause of the reddish-brown urine? Renal infarction, malignant hyperthermia, acute cardiac failure, or rhabdomyolysis? 100%. I got the easy question. Almost. I was all excited. But in reality, what this patient has, he's got heat stroke, right? It's important to remember, in this rationale, they said hot and sweaty skin, and many may be thinking, oh, I thought heat stroke was hot and dry skin. Well, there's two types of heat stroke. There's classic, which is non-exertional, which not today, per se, since we're having a rainy day here, but how most of the country is in 100-degree weather. That is the temperature that you're going to get these classic, non-exertional heat strokes, hot and dry skin. Exertional heat stroke, in general, they're going to be sweaty. They're exerting themselves. First key thing here is to identify that it is heat stroke. The second is that red-brown urine with the no red cells, but positive blood. That is what we see with rhabdo. I think we've more or less covered all of this. Malignant hyperthermia, this individual didn't get an anesthetic prior to running, as best as we know. It's not the presentation for renal infarction. Heart failure is also his vital signs go along more with dehydration and his exertion. This is a relatively easy question. I think that's the only one that I have. Does anyone have any questions on this? There are several references. There is also a New England Journal article on both rhabdo, and there's another one on heat stroke. CCM just published a CDR on heat stroke earlier this year, and there will be a heat stroke guideline coming out sometime next year as well. Any questions on either heat stroke or? Excellent. We'll talk about environmental later today. All right. A 45-year-old woman who was a restrained passenger during a head-on motor vehicle accident was extricated in a prolonged fashion. The car had significant front-end damage with intrusion into the passenger compartment. In the emergency room, the patient was hemodynamically stable with bilateral tibia and fibula fractures, abrasions from the seat belt across her abdomen, and a transverse fracture through the posterior elements of the L1 vertebra. She was admitted to the ICU for pain control and splinting of bilateral lower extremities. In the evening, she developed increasing tachycardia and abdominal pain, progressing to peritonitis. Her hemoglobin levels remained unchanged. Which of the following is the most likely diagnosis of her delayed onset peritonitis given the known injury pattern? Is it esophageal rupture, iliac artery or vein injury, pancreatic injury, or splenic laceration? Oh, that's a good one. Oh, we've got some controversy here. Interesting. OK. So the correct answer is a pancreatic injury. Let's go back to the question stem. So what in this question stem screams out pancreatic injury to you? Chance fracture. So the L1 vertebral fracture is a classic injury that's associated with a severe energy transfer. And so when you see that injury, you'll often see other really serious injuries, including intraabdominal injury, which would be the pancreas, and also usually pretty significant orthopedic injuries. Very good. Why is esophageal rupture not the answer? That's just not a thing we see too much in trauma unless you have a profound blow to the chest that's really isolated. Generally speaking, people get pulmonary contusions, cardiac contusions. But the actual esophagus itself doesn't just suddenly explode. In terms of the iliac artery and vein, those you may see with pelvic fractures. But I think isolated vessel injuries in the absence of a pelvic fracture are a little less likely. Splenic laceration would certainly cause pain. And if allowed to bleed for a long time, that blood would be irritating to the peritoneum. But that would probably be a person who would not be hemodynamically stable. So last question for this session. A 63-year-old man presents with a non-vericeal upper gastrointestinal bleeding. Multiple AV 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? Options. Octreotide 300 milligrams IV bolus, then 20 milligrams per hour IV continuous infusions for 24 hours. Pantoprazole 80 milligrams IV bolus, then 8 milligrams per hour IV continuous infusion for 72 hours. Femotidine 40 milligram IV bolus, then 20 milligrams every 12 hours. No IV push for 120 hours. No pharmacologic therapy for the first week after the bleeding episode. Majority of the people have the right answer. It's pantoprazole 80 mg followed by 8 mg per hour. Any stomach-based or upper GI bleeding, post-endoscopy, the benefit of pantoprazole is it reduces the risk of re-bleeding and also reduces the risk of re-intervention need. Most of the time, it's beneficial in a peptic ulcer disease, but it has also shown benefit in non-ulcer, non-variceal AV malformation-based bleedings. And there's no evidence of effectiveness of octreotide or famotidine in this situation. So thank you.

critical care

surgical issues

transplants

GI emergencies

pulmonary hypertension

Thromboelastography

perioperative risks