Multiprofessional Critical Care Review: Adult 2024 (MCCRCA24ON)-Board Questions: Infectious Diseases, Surgical Trauma, Liver, and Gastrointestinal

Board Questions: Infectious Diseases, Surgical Trauma, Liver, and Gastrointestinal

Video Transcription

So, we'll start with the first question. The first part of the question-answer session is more related with liver GI trauma and acute surgery.  So, an adult patient presents to the intensive care unit after exploratory leprosy for open drainage of an abscess associated with complicated intra-abdominal infection.  Vancomycin and meropenem are started as empiric therapy. On post-operative day two, culture yields E. coli, susceptible to all cephalosporins tested,  including cefazolin and mixed anaerobic organisms. The patient is stable and afebrile. There is no leukocytosis. Which of the following is the most appropriate  antimicrobial regimen? We can use our poles.  We continue the current triple antibiotics for 10 days. Discontinue antibiotics except meropenem for 10 days.  Change antibiotics to cefazolin and metronidazole for four days. Or change antibiotics to cefepime and clendamycin for five days.  And this is where the Jeopardy music comes on.  I think I go press next and that should give us the answers, right. So the main focus of this question was two. One is de-escalation of antibiotics, the antibiotic stewardship.  And the other part is the new recommendations in terms of changing the duration of antibiotics. So the antibiotic therapy should be de-escalated based on the culture results.  This is an E. coli which is pan-sensitive. We can always de-escalate it down to cefazolin. But we also group multiple anaerobic organisms. For anaerobic organisms,  we have metronidazole and clendamycin. Anytime you have an intra-abdominal source, clendamycin does not have a good sensitivity to bacteroides.  And that's why you can actually go to metronidazole.  The STOP-IT trial has recommended reduction  in the duration of antibiotics. The old recommendations of 10 days and 14 days is now de-escalated down to four to seven days depending on the etiology or the source of infection.  And just by a show of hands, how many people in their own practice would have started Venk and Meropenem on this patient?  Okay, so it's still up for debate and obviously there are guidelines. But in someone who's not immune suppressed specifically or has a reason, I wouldn't say overkill,  but when we do our antibiotic stewardship, there are other methods that can be considered acceptable. So depending on your hospital biogram, microbiogram,  some would consider in the appropriate patient Ceftrax and Flagyl's acceptable. You could do some other form of combination. But you may not specifically need MRSA coverage  or extended basal lactamase-resistant kind of coverage to start in a patient like this. So I'm not preaching, and you have to do, but I am gonna preach about antibiotic stewardship.  That is the job of every intensivist to sort of make that work. And as a joke on rounds, there's no magic antibiotic we're gonna find on a thermo vent down in the ocean somewhere.  It's really up to us to keep what we have going and basically as Raj was saying, less use and not using at all is the only way  we're gonna be able to maintain our antibiotics in our ICU. It was actually one of the ways I was able to convince one of the surgeons that kept wanting to do  broad spectrum for six weeks. I would show them that we had nothing left to kill their pneumonias with, and they sort of understand that the sort of problem  that they were sort of creating in our ICU for them, and it's in their own best interest for their patients.  Any discussions, any questions? Yeah, questions? Go ahead, please. Quick question. I believe a couple of weeks before I had a patient in my ICU, the patient was immunosuppressed,  which was a patient had underlying autoimmune disease process, and patient was in a very high dose steroid, and patient had acute ischemic bowel,  which had a X lab and removal of part of the colon, and the patient had end ileostomy after that. Now, our ID physician want to continue the antibiotic  for 14 days, and the main reasoning they are giving  that patient is immunosuppressed, that's the reason they want to continue, even though there's no leucocytosis and no fever,  we can scan the patient a couple of times to prove the patient doesn't have any intra-abdominal or any abscess or any fluid collection.  I was advocating to stop the antibiotic after seven days or six days, but they wanted to continue for 14 days. But is there any strong evidence to continue for immunosuppression?  Unfortunately, no, and that's an area, and I'll let Raj, of course, back up. We don't have very good data in the transplant or immunosuppressed population. We really need it.  Hopefully, you all can help contribute to that by publishing in journals about what you found. But it does, being immunosuppressed does change  the gut microflora, MRSA and pseudomonas may show up, but which football scorer, whether it's seven or 14 days, the data really isn't out there. Like you, I read the literature.  So, yes, I do what's right for the patient, but it's hard to do antibiotic stewardship in that, and you just have to collaborate until better data comes out. Raj, thoughts?  So, at least within our center, our practice, our trauma surgeons are on the other extreme. They minimize antibiotics to no more than 48 hours sometimes,  which makes us uncomfortable.  But based on the trauma literature, and we have some trauma critical care fellows here,  it essentially states that if you do not see contamination, if the only thing you see is ischemic injury without a leakage or without a contamination,  you would stop at 48 hours after the surgery. In an immunosuppressed patient, you would expect that some of them are on preemptive suppressive medications,  depending on their level of immunosuppression.  But going up to 14 days does not have any evidence of preventing. It essentially goes back to when we would give azithromycin for COPD, or so you would use  some of the other antibiotics for suppression. It just promotes more and more resistance, and the other part we also need to remember  is immunosuppressed patients are at the highest risk of C. difficile infection, so the longer you give them antibiotics, the higher is the risk of C. difficile,  and C. difficile in an immunosuppressed patient is fatal for the most part, so.  Other questions or comments?  All right, next question then. We have a 55-year-old man is admitted to the ICU with septic shock secondary to viral pneumonia. He is on mechanical ventilation.  His medical history is remarkable for chronic lower back pain and type 2 diabetes mellitus. Home medications are tramadol and metformin.  Which of the following statements is true regarding the use of stress ulcer prophylaxis? So A, nosocomial pneumonia risk does not increase with SUP.  B, proton pump inhibitors are more likely to reduce mortality than H2 receptor antagonists. C, SUP is associated with clostridium difficile diarrhea.  And D, the surviving sepsis guidelines do not include a recommendation for the use of SUP. So please type in your answers.  All right, Raj, if you want to advance. Yeah, we'll get to 10, yeah.  All right, most of you picked C. And if you want to go to the correct answer. Yeah, so C is the correct answer.  So stress ulcer prophylaxis is recommended primarily to prevent GI bleed because of mucosal ischemia that can happen in stress situations.  I'll go through the other. One of the biggest caveats of using stress ulcer prophylaxis  is you get rid of the acid content in the stomach. And once you do that, you are increasing the flora that can grow in the stomach.  And also increasing the risk for C. difficile diarrhea. Proton pump inhibitors is mostly from a clinical standpoint become the go-to medication for patients  who are considered to be high risk for GI bleed. There is no evidence that proton pump inhibitors prevent GI bleeds better than histamine receptor blockers.  The other part, there is significant evidence that stress ulcer prophylaxis does increase the risk of C. difficile diarrhea. It's more predominant in immunosuppressed patients,  but definitely has been shown in other populations.  Surviving substance guidelines do definitely recommend  a stress ulcer prophylaxis to be used for patients who are on the vent for more than 48 hours. Intracranial injuries, burn patients.  And I think the same thing about HCAPs or VAPs,  stress ulcer prophylaxis is known to increase the incidence of VAPs or HCAPs. Still, to prevent VAPs or HCAPs, it's not recommended to stop stress ulcer prophylaxis.  Phil. Yeah, so again, I think Sandy, as our president, would also say as a pharmacist, if you don't need the drug, please get rid of it. So polypharmacy is always suboptimal.  There's always something negative to a drug that a patient doesn't need. It's not clear to me how long versus resuscitation anymore  on ventilation you really should be on sort of these things, but I know in the burn and TBI population because of Cushing's and Kirling's ulcers, it may be a different amount.  But until again, better data comes out, just do your best to try and get them off. Some pharmacists would say when they're fully fed, some would say this, some would say that.  Some say seven days after a mechanical ventilation, but I haven't seen great data on any of those to date, but I do try to get them off,  especially if they weren't on it when they came in. Raj, any comments on that? No, I mean, if they're not on home PPI or H2 receptors, we tend to stop them pretty much.  If they can stay extubated for 48 hours,  we go ahead and stop those.  Questions, comments?  All righty.  Previously healthy 46-year-old man presents to the emergency department with a three-day history of confusion and headache.  Temperature of 39.4, heart rate of 110, respiratory rate of 15, and a blood pressure of 150 over 80. He's lethargic and mumbling, but his cranial nerves are intact,  and he can move all four extremities with full strength. He then has a generalized stonic-clonic seizure lasting three minutes. His head CT shows supple hypodensities  and bilateral temporal lobes. Lumbar puncture reveals a WBC of 33, a lymphocyte predominant, RBC is 97, protein of 102, and glucose of 90, with a serum glucose of 120.  So why don't we stop at this point? Can you go back, Raj? Anyone have a differential at this point and sort of what you're thinking?  Could you talk into the mic?  Is it not? Herpes.  Anyone else thinking anything besides viral at this point? Bacterial, is there anything that's sort of pointing out here that may sort of  point you in that direction as a board question? Is there any sort of hints or anything there?  Oh, try talking to, I'm sorry, just talk into the mic so everyone can hear.  The hypodensities on the CT scan with herpes.  Okay, Raj, you wanna go ahead? Yeah, so this one is, I mean, I think multiple parts to it, and I'll go through each line. And just trying to make the case down,  I think we can look at the lumbar puncture and just the first line, and your presumptive diagnosis is definitely herpes.  But a previously healthy 46-year-old with a three-day history of confusion and headache. So it's a subacute course over three days, definitely febrile, but not a very significantly  septic patient, heart tachycardic, but respiratory rate and blood pressure is okay. Lethargic, essentially altered mentation, but not a focal deficit.  Generalized tonic-clonic seizures, which is consistent with potentially encephalitis,  or meningoencephalitis. And CT with bilateral temporal lobes, which is, as everyone picked it up correctly, is herpes, does tend to go to temporal lobes in terms of findings.  And the lumbar puncture, a little bit of inflammation with WBC of 33, lymphocyte predominant, and a glucose of 90, and there's a reason they put it out as a serum of 120.  If the serum level was much higher than that, then you look at a different,  that glucose of 90 then is not normal.  Early treatment with which of the following medications is most likely to improve mortality?  So, you want to take the disc? Sure, so let's, it is acyclovir, as we were talking about, sort of a viral infection.  So, based on the cell count presentation, this patient most likely has herpes simplex virus one, encephalitis, so most of you are sort of on the right page.  This is the most common cause of sporadic encephalitis in the United States, and typically presents with fever and acute neurologic deficits over several days, as Raj was saying.  And a high percentage of these patients will end up having seizures. Temporal lobe abnormalities are common on imaging, most obviously on MRI.  CSF will show the lymphocytic pleocytosis, which was one of the hints in the question, and elevated erythrocytes in protein. Glucose is normally normal.  Acyclovir, an antiviral, has been shown to improve mortality, as well as functional outcome when instituted early for HSV, herpes simplex encephalitis.  So, like all sepsis, early treatment. Steroids are not routinely recommended for herpes simplex encephalitis, and there's no evidence to improve mortality.  Aspirin, again, is sort of trying to distract you as a treatment for a subacute infarct, because they're sort of showing you different things that may make you go in that direction.  Ceftraxone would be a reasonable to begin while awaiting the gram-state results, but the rest of the clinical picture does not fit with bacterial meningitis.  Amphotericin B would be for fungal meningitis, and again, as we discussed, that would be specific to a low-glucose and immunocompromised patient.  Raj, would you necessarily start with ceftraxone if you suspected bacterial meningitis, or do you think there are other drugs that may be optimal?  So, if this patient is seen for the first time in the ER,  knowing the history that we know, then yes, I would start with the, at least within our organization at IU, based off the antibiogram.  He's 46, so definitely does not need ampicillin, but we would start with ceftraxone, vancomycin, and acyclovir. And actually, we would start with dexamethasone.  And I know, I think a couple of people picked dexamethasone as the answer.  It is not shown to improve mortality, but it is indicated in patients with pneumococcal meningitis, which is still,  I don't remember the exact statistics, but I think it's probably still one of the most common  forms of meningitis that we would see. So, first line, yes, I would start with the whole regimen, but once you get the results back from the LP, and your WBC count is only 33,  with the rest of the results the way they look, quickly de-escalate down to acyclovir.  And just remember, as a board question, there can obviously be some red herrings, but they really try to focus on what the person's really trying to pull out of you.  And so in this question, they're trying to get you to sort of understand, this is herpes meningitis, and that would be sort of the best answer in this situation.  Questions, comments?  Okay.  Let's do a little trauma. A 38-year-old man is admitted to the ICU after sustaining multiple rib fractures in an all-terrain vehicle accident.  So this is quite common where I come from in Florida. He is given supportive care, a chest tube is placed for hemothorax on the day after admission,  but he requires intubation 48 hours after admission for respiratory failure. His CT scan on admission shows multiple left-sided rib fractures with three ribs  having two different fracture sites laterally. Chest radiograph is shown below. Raj, if you could advance that. Now, I know on the boards it's always hard to see the image,  but normally, if you're lucky and you can actually get to see it, that's fine. But I think there were some hints already in the question where they're trying to push you with this.  So what kind of chest would you say this may be if they talked about multiple fractures on the same? Anyone have a differential sort of what's going on?  So it might be, this person may have a flail chest, they may have issues breathing, they may be a difficult wean off the vent. So that's really where they're kind of trying  to push you a little bit with this. So, which of the following is the most helpful course of action in this patient's subsequent management?  So as we please choose, as you're saying, bronchoscopy, that would be if you're trying to pull something out or if you were worried about pneumonia.  Placement of the second chest tube, that would be if potentially you had a retained hemothorax or a pneumothorax or something that wasn't working.  Left rib fracture fixation, that would be, again, if you felt that the patient's fractures were impeding them from breathing appropriately  and being able to be liberated from the ventilator. And high frequency oscillator ventilation, that, well, we can discuss that in a minute. So go ahead and pick your answer.  All right, let's see what we got.  Okay, wonderful. So let's, most of you picked the rib fracture fixation. Let's go to the answer. So the patient has a flail chest with significant underlying pulmonary contusion  and respiratory failure. Several case control studies indicate that he would be expected to benefit from early rib fracture fixation, which is now recommended treatment guideline.  Neither bronchoscopy nor placement of second chest tube would measurably improve his work of breathing. High frequency ventilation has not been shown  to improve mortality circumstances and likely to be beneficial in a patient who is being adequately oxygenated with ventilator management. Now, if you're to ask me which patients  meet criteria for rib fixation, there is a lot of publications and a lot of differing opinions. And as the trauma surgeon over here and the burn surgeon trauma surgeon can tell you,  it's quite, it's being debated a lot in the trauma literature. What I would say is each hospital or group typically comes up with their own algorithm. And based on the literature,  we'll kind of use that to make the decision. Most of these involve getting some sort of 3D reconstruction. It's not without risk. Nothing's without risk.  So everyone doesn't necessarily get it. But there are specific patient populations that we're still working on trying to identify that could benefit from this, do better,  get off the vent faster, et cetera.  A question or comment? No, sorry. Questions, comments on the?  All right, why don't we move to the next one, right?  A 45-year-old woman was a restrained passenger during a head-on motor vehicle accident. Extrication was prolonged. So that's sort of your first hint.  The car had significant front-end damage with intrusion into the passenger compartment. In the emergency department, the patient was found to be hemodynamically stable  with bilateral tibia and fibula fractures, abrasions on the head, abrasions from the seatbelt across her abdomen, so a seatbelt sign,  and a transverse fracture through the posterior elements of L1 vertebrae. So again, big hit to the tummy, went all the way through the back. So a lot of force, right?  She was admitted to the ICU for pain control and splinting of bilateral lower extremities. In the evening, she developed increasing tachycardia,  abdominal pain, progressing to peritonitis. Her hemoglobin levels remained unchanged. So before we even go to the answers,  is this patient in hemorrhagic shock?  Right, so they're telling you that there. So she's developed peritonitis. So anyone want to comment on what causes delayed peritonitis in a patient with a seatbelt sign?  That's sort of the main intent of the question.  Yeah, could you speak into the microphone?  Yes, and what else? So right here, guys, you took a big whack, and it actually was so big that it actually fractured a vertebrae. What else lies just around the duodenum  that can also sort of have a problem?  The pancreas, very good. So these things don't typically show up when the person arrives. You know, if you have a perforated duodenum or pancreas hit, it's not like gross stools  going everywhere. So this is one of the reasons people with these things have to be admitted and have serial belly exams and stuff. It's sort of a delayed presentation  that can occur over the next 12 to 24 hours. You won't necessarily even see specific labs that can tell you right away that this has occurred in the patient.  So why don't we go to, I know I'm sort of trumping some of the questions, but we can still sort of go through this. So pick your answer.  Esophageal rupture, which has its own issues. Iliac artery or vein injury. I mean, again, we would expect hemorrhagic shock. Pancreatic injury or splenic laceration.  Outstanding, well done. All right, so let's go to the answer.  So again, you have to have a high element of suspicion given where the fractures are. The type of fracture isn't important, but it's sort of explaining why you could have  such a large amount of force to your mid-abdomen.  With seat belts, it's become a little less common with lap belts, but in the old days, it was just the one across your belly. And although it's uncommon,  you have to have sort of a high level of suspicion. So again, you have not only did the force go against it, it was compressed against the vertebrae behind it.  And again, if you send someone home immediately with some of these signs, they may end up bouncing back in your ER or heaven forbid that they actually end up  dying at home from sepsis or other types of inflammation. And in the initial phase, as I said, CT scans are gonna miss this because it's not easy to see.  It's not a fracture, it's not bleeding, it's not sort of torn right in half or anything like that that you're gonna obviously see. And enteral contrast isn't always the norm,  nor will it necessarily show a leak at this point for you to see on the CT. So again, it's setting up a standard scenario where they sort of want you to get that answer  for what you have.  Let's see if there's any more rationale. Okay, so questions, comments?  Trauma in general? Okay. I was just gonna add that if with even more delay, you can see bowel ischemia from bucket handle devascularization of bowel also. So even further out.  What's that? Even a little further out. So like next day kind of thing. Yes, yes. So even further out.  And normally you get repeat labs.  Nothing's as good as serial abdominal exams, but that's what you have to sort of have an eye index of suspicion.  Okay, another trauma question. So, and again, look for the hints as they sort of show them here to you, because that's sort of usually what the board question's doing.  23-year-old woman, MVC, Glasgow coma scales 13. So do we have to intubate yet?  No, okay, good. Airways intact, respiratory rate 16, oxygen saturation is 98, but heart rate is 132,  and blood pressure is 7647. So I'm not gonna ask you what type or grade of shock, but are we in some sort of shock?  Yes, okay.  Her chest radiograph is negative for acute injury. Pelvis has minor superior and inferior pubic rami fractures. You have a FAST that is positive,  revealing free intra-abdominal fluid, both in the right upper quadrant and the pelvis. So who here feels comfortable doing FAST?  Okay.  The FAST in trauma, what's one of its core tenets if you do it and someone's hypotensive  in a trauma patient and you see fluid? What's the basic concept of that?  Do you need a CT scan? Do you need to do this? Do you need to, no? But what sort of, on your, even your general surgery boards, what do they tell you to do?  Into the microphone if you don't mind, sorry.  The tachycardia hypotension, positive FAST equals OR. Correct. So that's one of the main benefits of being able to do a FAST. You don't have to whisk them off the CT,  take the risk, all these sort of things. It allows you to make that clinical decision. And abdominal bleeding is one of the key aspects of all ATLS and trauma resuscitation.  Stop the bleeding first. That's your key. No matter what else is going on,  no matter what you may see is a dissection in the aorta and in the head, you'll have to do them simultaneously because you won't be able to fix the other issues  unless you acutely stop the bleeding. And you will resuscitate them in parallel to getting them to the operating room. This person requires immediate treatment.  So that's sort of the main thing they're bringing out in the question. So let's go to the next.  Does anyone here want by raise of hands still do DPO?  Okay.  It's sort of being replaced. It's also because of a lack of skill sets, it takes a long time to do so it can delay patient care.  Now, don't be tricked again by E.  You could make an argument, oh sure, this patient's in an electric shock. Maybe I gotta tube them first, ABCs. But again, it's like the other one that Raj was discussing.  It's not, yes, you might give dexamethasone in the ER, but it's not really what the question's trying to pull out of you. It's sort of a core tenet of critical care.  So let's see, hopefully you guys, 100%. Oh yeah, love it. All right, so let's go to the explanation.  I think I've kind of already, let's talk about why the other ones are wrong. CT scans of the chest, abdomen, pelvis, or DPL would only delay definitive care.  Angioembolism, again, we've already identified it's not the pelvis that's specifically bleeding. And if it was, you would still be required to the OR  because you may have to do multiple things. So people now do pelvic packing, other sort of things. Or if you are lucky enough to have a hybrid OR, you may do the exploratory lap  and then have someone come and angioembolize. But if you don't stop the liver or spleen bleeding at that point, the patient will exsanguinate.  So yes, you may do multiple things at once, but the key tenet of the question is that you go to the OR.  Sure, they should be all tricky and intubated,  but whether you do that downstairs or you're able to give them a whole blood or whatever your current ERs,  whatever you have available in terms of blood products as you're whisking them up and allow the anesthesia to intubate or the ER attending, it just depends.  But again, the point of the question is positive fast plus hypotension or shock equals exploratory laparotomy.  All right, Raj, why don't you go?  Okay, great.  So 24-year-old woman was a restrained passenger in a high-speed head-on motor vehicle accident during which she lost consciousness. Extrication time was prolonged.  On primary survey, her airway is intact, breathing, breath sounds are equal, and vital signs are heart rate of 116, blood pressure 126 over 80, respiratory rate of 20,  and oxygen saturations are 98% on six liters. She has a laceration on her forehead extending across the scalp line, an abrasion from the seat belt across her chest,  and a gross deformity of her right thigh. A brain CT scan shows small subarachnoid hemorrhage. Her cervical spine is normal. CT chest shows a periaortic hematoma  with a small filling defect and a trace left hemothorax. An abdominal CT shows no solid organ or hollow viscous injury. Plane radiograph of the right femur  shows a mid-shaft femur fracture. She is transferred to the ICU.  Which of the following is the most appropriate next step in the management?  Aggressive heart rate and blood pressure control, anticoagulation with heparin infusion, emergent thoracic aortic repair, left tube thoracostomy,  or open reduction and internal fixation of the right femur.  Nice mix. So this is, I'm gonna go back to the question. So 24 year old restrained passenger in a high-speed head-on  motor vehicle accident where she loses consciousness. So that  severe trauma like essentially what a lot of trauma centers called in as a trauma one. Extrication time is prolonged. Primary survey, her airway is intact. So  as Phil said ABC airways intact, breathing's fine. We're coming to the circulation pressure is fine.  She has a laceration across her forehead extending across the scalp line and an abrasion from a seat belt across her  chest and a gross deformity in the right thigh. So we are dealing with three main  traumas. One is in the head with the traumatic subarachnoid.  Second is the peri-aortic bleed with the possible small, shouldn't say possible, with left hemothorax. So there's a concern for aortic injury and a  rupture. And the third is a femur mid-shaft injury.  The when you look at these three, so subarachnoid, a small traumatic subarachnoid is  if the patient is neurologically intact, proceeds with an IR angio in  distant, in recent future. It's not done in an urgent basis. It's done in a recent future.  The second part is when you're looking at a peri-aortic injury and a filling defect with a small leak. This needs an  emergent thoracic aortic repair, but not all centers have that capability. So for the patient to be moved to a center that has that capability,  prior to that you have to have an aggressive heart rate and blood pressure control in this situation.  Works essentially in the same way that you would deal with dissection or  impending rupture of a thoracic aortic aneurysm.  Your heart rate needs to be less than 70, some places would say 100, or a blood pressure definitely less than 110.  Definitely not anticoagulating this patient. Emergent thoracic aortic repair,  it's emergent in the sense you need to identify a site that can do it, move the patient, but before that you would get the blood pressure and heart rate control.  Left tube thoracostomy, you would not want to do that until you've recovered the, you've taken care of the aorta and then  open reduction and internal fixation of right femur would be all the way in the end.  So do you want to? Sure, so what's, of course you never want the patient to be too hypotensive, but what's more important to  maintain systolic blood pressure first or to stop the heart rate?  Heart rate, yes, sheer stress. So if you increase the blood pressure against a really rapidly squeezing heart,  you're gonna either tear a dissection or anything open further and you could potentially make it worse.  And as Raj was saying, even if you have the capability of either doing a stent or an open repair, you got to get them to the IC,  I mean to the OR and you have to have the surgeon be able to come to the bedside and do this procedure or  interventional radiologist, I guess depending on your  facility. We use Esmolol, of course, because it's the shortest acting and of course if someone's in hemorrhagic shock or some form of shock,  you want to be able to turn it off really fast or titrate it as well as you can. But you still have to maintain a blood pressure. Now, this isn't necessarily specific to this,  but normally your blood pressure shouldn't be normalized. You just want enough to get the brain and the kidney perfused. If you actually look at the sort of casualty  stuff in the military, whether it's the Israeli Defense Force, the British, the Americans, they often have something called permissive hypotension.  That's not just specific to this, that's for other things as well, leg injuries, you name it.  But you'll totally, this is a guesstimate, but a systolic blood pressure somewhere in the range of 90, just enough to maintain perfusion.  You can do something like that for about two hours before the risk-benefit ratio changes.  So again, you're doing your ATLS, you're doing this, you want to sort of maintain just enough, but not enough to sort of worsen what you have. It's not true in an aortic injury,  but some people say popping, you don't want to pop the clot, whether that's a leg injury or something. But again in this case,  start with decreasing the shear stress and then make sure you have enough  blood pressure to maintain perfusion to the head and the other organs in the body.  And if you don't have,  you know, if you're not going straight to the art, clearly this patient needs immediate admission to the ICU and sort of aggressive treatment.  I think, yep, that's the description.  Any questions? I saw some people writing some stuff down, comments on that.  Okay, how are we doing for time, guys?  We're doing well? Okay, let's keep going, Ron.  52-year-old male driver in the motor vehicle accident is airlifted to a regional trauma center.  He arrives into bayonet with systolic blood pressure of 90, heart rate of 118, respiratory rate of 16, and an obvious scalp laceration and open femur fracture.  Extended focused abdominal sonography and trauma. So again, you're doing the chest, the heart, everything, basically. Reveals moderate pre-fluid in the pelvis.  Laboratory studies including thromboelastography are performed. All right, now this is what it shows. Now, I don't have a good answer  specifically except that if you don't, if you do tech reads, you might want to just work on memorizing it.  A lot of us are very spoiled because we get an answer back and the computer just tells us the number and what product to give. So not everyone is necessarily an expert in this.  The anesthesiologists are because they normally get them as the case is going along and they don't get those results right away.  And they have to sort of interpret it as they're going along. But you can sort of see the angle here as it kind of goes up. Now,  I've got two slides to be put in. Go ahead to the next one. Oop, go back.  Well, they were there.  Well, okay, let's just start with this because  it's okay if you get this wrong. Hopefully the slides are in the next two parts. So, did that tech tracing  demonstrate acute post hemorrhagic anemia, be hyperfibrolysis,  hypofibrogenemia, or a vitamin K deficiency?  Now, of course, I mean, let's be frank.  Probably these are not going to be your best answer, right? That's not really what they're trying to pull out of the question and it doesn't really have anything to do with the  severe trauma patient, typically. I mean, sure, but that's not really what they're looking for. They didn't give you a history of other stuff like that. Okay, go ahead and pick one.  Okay, we have a nice mix here. Hopefully we have the  images on the next one. There we go. All right, so  these are available everywhere. This is just one example. Having a basic understanding of your R, alpha, angle, K, and MA time gives you sort of a better idea.  It sort of says here at the bottom. So, R measures the time of formation of the fibrin strand polymers. K is the speed at which the clot forms.  Alpha, the slope drawn from R to K.  So, you can kind of see that as it was sort of drawn there. And the MA is the strength of the clot. So, if we go to the next one.  Sorry, it's a little, but again, we can get this to you guys. Sorry, it's not as clear as it should be, but it sort of explains sort of the difference between your R angle,  excuse me, your R level, or time, your alpha angle, your MA,  and your lie. And then here's some examples kind of here of what's sort of occurring. So, Raj, we can kind of go back to that.  Before we do that, sorry, go back to that thing right there. So, you can see that an  alpha angle sort of a certain amount of degrees integrates a low fibrin level, and  I think that's sort of one of the sort of intents of the question right there. So,  also, if you have a lie 30 greater than 3%, it's primary fibrinolysis. So, those are the kind of things you would be looking for  in that sort of question. So, why don't you go to the next one? So, TAG, it measures whole blood coagulation.  TAG has gained acceptance for the evaluation of trauma-related coagulation defects to guide treatment.  The accompanying TAG tracing with the elevated percentage of clots as it dissipated at 30 minutes, so lie 30, so greater than 3%, is most consistent with hyperfibrinolysis.  The tracing does not correlate with hemoglobin level. Thus, acute anemia is best monitored. Anemia is best monitored by CBC. So, in general, we don't use TAG to measure hematocrit.  It's really meant to sort of determining lack of or appropriate clotting strength or even hyper clotting. The standard TAG does not measure vitamin K deficiency.  Fibrin levels influence the K time in the alpha angle. K time is the time it takes to achieve a certain level of clot strength.  Alpha angle is the angle  slope between R and K that measures the speed at which fibrin buildup and cross-linking takes place. Hence, the rate of clot formation and  thrombin burst. Now,  I know there'll be a lot of questions on this. Again, my advice for this particular one, like some of the drugs that you have to memorize before your boards, is just to go through  some of these different, just repeat, look at the R,  re-understand the MA and the K. Go through it a couple times in your head and once you get an understanding of that,  get a better idea of at least what each defect would kind of be, the core defects, and how to sort of deal with those.  And that should kind of help. I would say in real practice, again,  the companies have made it quite easy for us to use this tool. And they usually have something online that sort of allows us to sort of...  Raj, you want to comment on this at all?  I just use it... I just use a real crude way just for my own  memory, and I wrote it down for that reason.  So, if you look at the terms R, K, MA, G, and  lysis 30. So, R is called the react time or the reaction time.  It's the reaction time for the fibrinogen to start kicking in and start forming the clot. So, if your reaction time is low, that means...  Or your reaction time is really long. If it's low, it's great. If it's really long, that means you've got lack of fibrinogen,  you've got lack of all the factors, because your fibrinogen is not even initiating the development. So, in that situation, you give...  Essentially, you would give FFPs, you would give whole blood if you can, because you need all kind of markers.  The next is the K time. And your K time is called the kinetic time. So, you've got the initial clot form,  but now you need to figure out how fast the clot can form. And if your K time is prolonged,  you're looking again at the fibrinogen or the platelets. So, if that is abnormal, you would give  cryo or platelets.  The angle, there's not a good way of  figuring out how to approach that, but it's how quickly  the clot is forming. The next one is the maximum amplitude, the MA.  And the maximum amplitude is a...  It basically is strength of the clot.  Depends again on the platelet number and platelet function. If that is abnormal, you're looking at giving platelets. G, try to remember it with the word gravity. Gravity is strong.  So, G essentially signifies the strength of the clot. And if strength of the clot is abnormal, you are looking at,  again, the entire coagulation cascade. Because there's problem at multiple different levels and your clot is not strong. The last one is lysis 30,  which essentially means, how quickly is your body getting rid of the clot that is formed?  And which is what was abnormal in this situation, in this patient, which is a sign of hyperfibrinolysis.  And your goal is, at that point, to give them more, I think it's cryo at that point.  Yep, sorry.  So, yeah, so, Raj, you wanna go down a couple?  Back? Yeah, where they show the example. So, unfortunately, again, unless you do this all the time, it can be tricky. So, the best way to learn this is to have them run  and then interpret them and check sort of the CB2. Because, again, like Raj was saying, it's not obvious for all of them. And some of it, it's just, I would say, for your boards,  if you don't do them all the time and you're not comfortable with them, I would find some sort of review method like this and basically at least memorize one key aspect.  You know how you do with your AV, XY descent, those kind of things. If you can't remember everything off the top of your head, you still need to understand it.  So, there's sometimes that there's certain key aspects that you're looking for, for certain types of things that you see in valvular disease. I would say the same with this.  So, again, here's some specific examples. I think, as Raj was sort of saying, if you go back, sorry, if you go back to, it's hard to see.  You see that teeny little blip? That's basically, the line's sort of a distraction.  So, that's sort of your prime example, using sort of the lie 30 that he was talking about, where it comes back immediately for hyperfibrinolysis. And then, if we go to the next.  Yeah, it says, like, lie 30 is 94%. Should be wrong. Yes. And again, this is, you can't do this for your boards, but again, the companies, whether it's Rotem  or Hemonics or whatever, doesn't matter.  They give you these levels, and then, again, I'm not saying do this, you need to understand it, but they'll normally tell you exactly, if the number is this, give blank.  If the number's that, give blank. So, it can make it very easy to get lazy with it, and just not be able to remember everything you see, in terms of the drawings and figures.  But, I would say, have a basic understanding, and if it's not clicking in your head, because you don't do it all the time, I would say anesthesiologists, again,  are usually the best at this, because they have to do it all the time in the OR, when they're dealing with patients who are bleeding,  and they're trying to figure out what blood products. And if you don't go into the details of this, if you see that the ACT is normal,  and you go into the actual options, definitely, we're not looking for anemia with TEG. Hyperfibrinolysis, if we don't know how to interpret that, if your ACT is normal,  you do not have hyperfibrinogenemia, because if you have low fibrinogen, your ACT will get increased. Vitamin K deficiency, this is just not the right clinical picture,  to identify a vitamin K deficiency. So, in addition to the TEG, if we do just use the elimination part, ACT, PT, PTT, which all of us can remember easily,  you can easily just use that, and identify the answer here.  All right, let's go to the...  And then, real fast, go back, you could...  Again, as Raj pointed out, it's the live 30, that's really sort of the thing that you're trying to memorize for that, so.  Okay. Again, how are we doing on time? Okay, all right, let's go to the next one.  54-year-old man with a history of alcohol dependence and IV drug abuse is admitted with jaundice and a three-day history of fever. He has a temperature of 38.7, so he's febrile.  Pulse rate of 105 and a blood pressure of 130 over 85. Examination reveals tenderness in the right upper quadrant and enlarged liver, ascites, and uptundation.  So, okay, you're already getting your differentials in your head, you're starting to think, okay, what's causing this person's liver failure and insufficiency?  Results of the liver function tests are as follows, and this is something you should sort of pay attention to. AST 130, ALT 70, bilirubin, 28 milligrams per deciliter.  INR is 1.9, so that's not surprising. It's not functioning appropriately. Abdominal ultrasonography with Doppler study shows ascites and hepatomegaly,  but blood flow in the major hepatic veins and inferior vecina is normal. So, can anyone just say off the top of their head, what that excludes for this form of liver failure?  So, you have normal veins, go ahead, speak. Correct, so you're already sort of getting an idea from the question. Okay, it's not that form of liver failure,  so we're gonna take a look at what they're gonna give you for selection, go ahead.  So, you have A, non-alcoholic steatohepatitis. B, acute hepatitis B infection. C, acute hepatic failure from acetaminophen overdose. And D, acute alcoholic hepatitis alone.  So, go back, now, I guess it depends on...  Okay, nevermind, keep going.  Forward, answer your question.  All right, so let's see what you got.  All right, so B, or alcoholic hepatitis based on the history, so let's go.  So, we've got a nice mix of B and D.  A real crude way of figuring out acute hepatitis is viral hepatitis.  Clinically, you can, if you identify it real early in the course, you can have your LFTs or your ALTs and ASTs and the hundreds, but for the most part, by the time these patients  seek clinical care, your transaminitis is much higher than 130 and 70.  Hepatomegaly, fever, those are signs for hepatitis.  They've already given in the history that this patient has a history of alcohol dependence, so non-alcoholic steatohepatitis is definitely low on the differential.  One of the other things also is the AST to ALT ratio in non-alcoholic steatohepatitis is generally less than one. In this case, the ratio is more than one,  so that would go more with the diagnosis of acute alcoholic hepatitis alone. No history is given for acetaminophen overdose in the question, so definitely C would not be the answer.  So, as we discussed, the pattern of AST to ALT ratio greater than one argues against non-alcoholic steatohepatitis and acute hepatitis B,  but it's consistent with acute alcoholic hepatitis. The pattern and the degree of elevation of transaminases is not consistent with acetaminophen overdose.  Demographics, clinical picture, and the normal blood flows in the Doppler's argue against Baccieri syndrome.  So, questions?  Yeah.  No.  Yeah, go ahead.  It's fine. Can we get up?  Oh, okay, thank you. So, my question was just, do you normally see that degree of elevation in viral hepatitis of the T. bilirubin as well, or just,  because I normally just get it alcoholic? So, I don't think I have the slide for that, but the transaminases, the bilirubin, and the INR,  in a liver injury, they follow the dome patterns, but they kind of have a progressive approach. So, the first thing that you always see is a real significant transaminitis.  Generally would kick in within the first couple of days.  Your bilirubin elevation follows that, is generally would lag by at least three to four days. By the time you would already see the transaminases peak,  your bilirubin is then starting to creep up, and your bilirubin will continue to increase by the time alkaline phosphatase, and your ALT and AST would already be coming down.  And the last thing to follow is generally the INR. So, your bilirubin may not be elevated initially, but depending on the severity of liver injury, bilirubin will go up.  I don't think so. I'm not sure. John, any quick comments on that? Okay. Steve? Okay.  I don't think so. You would lie that.  Okay.  54-year-old man with alcoholic cirrhosis and hepatitis C is in the medical ICU with acute hepatic encephalopathy. His laboratory results show an INR of 1.5,  a total bilirubin of two, and a creatinine level of 1.2. He has substantial peripheral edema. A contrast CT scan of the pulmonary arteries showed no filling defects.  In the process of evaluating him for liver transplant, an echocardiogram shows substantial tricuspid regurgitation and significantly reduced  tricuspid and annular plane systolic excursion. There are no left ventricular or other valvular abnormalities noted on the echocardiogram.  Without further optimization, this patient has an increased intraoperative mortality from liver transplantation due to which of the following?  Hepatopulmonary syndrome, pulmonary embolism, hemorrhage, cerebrovascular accident, or portopulmonary hypertension.  So you have a good mix between the two most common options here, hepatopulmonary syndrome and protopulmonary hypertension. So if we were to go back to the question,  on the question, they're essentially discussing this as advanced end-stage liver disease as a patient who's getting worked up for transplant.  In the question, they do not comment on a patient being hypoxic or hypoxia with exertion, dyspnea, but they do comment on peripheral edema  and then a very good echocardiographic finding without really giving away the diagnosis of this patient having pulmonary hypertension because of substantial tricuspid regurgitation  and reduced tricuspid systolic excursion.  The answer here is protopulmonary hypertension.  The advanced liver disease essentially interacts  with lungs in two forms. One is the hepatopulmonary syndrome, which is a marker where the hypothesis is patients can develop micro AV malformations  and essentially develop shunting causing hypoxia, which is more consistent with platypnea.  And then the protopulmonary hypertension,  based on my understanding, I don't think there is a defined pathogenesis yet. There are several hypotheses of why this happens, but what we do know is once patients develop this,  if these patients go for liver transplant without optimizing pH treatment, they have a very high risk for mortality. So these patients have to be placed  on pulmonary arterial hypertension treatment before they proceed with liver transplant. Phil, anything you want to add? No, I think it's a wonderful summary.  And again, you can sort of rule out at least some of these in advance. I mean, things like pulmonary embolism, none of you picked, but that's sort of the norm  and sort of what do you think of patients are gonna die intraoperatively from a liver transplant.  Any questions, comments on?  Essentially defines the same discussion.  Okay, so how much time do we have left, if any?

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Rajat Kapoor, MBA, MD; Philip A. Efron, MD, FACS, FCCM

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