MedAll
Communities
New

Back to Basics: Orthopaedics 101 Series - The Physiology of trauma

Share
 
 
 

Summary

This on-demand teaching session will provide a comprehensive overview of the physiology of trauma and the metabolic response to it in medical professionals. Attendees will gain an understanding of the ebb and flow response including the neurohormonal, inflammatory, hematological, and damage control orthopedic responses. The session will also provide information on prognosis, morbidity, mortality, and length of stay hospitalization. Attendees will also gain an understanding of resuscitation and nutrition and the importance of manipulating the renin angiotensin aldosterone system.
Generated by MedBot

Learning objectives

Learning Objectives: 1. Understand the two-phase response to tissue trauma, including the neurohormonal response, inflammatory response and hematological response. 2. Describe the homeostatic mechanisms that the body uses in the ebb and flow phases to restore the body to its pre-injury state. 3. Explain the physiological response to trauma in terms of pain, vasoconstriction, heart rate, renin-angiotensin-aldosterone system amino acid and carbohydrate metabolism, etc. 4. Outline the clinical implications of understanding the metabolic response to trauma, such as choosing the best timing for surgery, predicting prognoses and predicting morbidity/mortality. 5. Discuss how the metabolic response to trauma can be managed, including the use of metabolic therapies and monitoring.
Generated by MedBot

Related content

Similar communities

View all

Similar events and on demand videos

Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

Feedback for money to distribute. No, he's gone. Never mind. We'll work it out. OK, fine. So there's only a small group of us here. So please do dive in if you've got any questions. I don't know if um I don't think I'm able to see your comments in the chat. So if you just shout out if you've got any questions or want to interrupt or if something doesn't make sense, um Just dive in because otherwise I don't know if I'm leaving anyone behind or if it's something that you already know. Um So I'm currently an ST four registrar at called just a hospital. Um I'm on my knee rotation at the minute. Um So today I'm gonna be talking about the physiology of trauma or the metabolic response to trauma. Um Can everybody see my slides before I carry on? Can someone shut down? Yes, we can. That's great. Fine. Ok. So like I said, I'm going to keep this fairly brief um cause I know it's eight o'clock at night and physiology at this time of night is not what most people want to be doing. I'm gonna go over why it's relevant and what it is. Um We'll obviously talk about the ebb and flow response and then we'll break it down into your neurohormonal response, inflammatory response, hematological response. And then a brief chat about damage control orthopedics and the injury severity score. So a little bit of clinical relevance and relief at the end. Ok. So the metabolic response to trauma, um we're looking at systemic and local physiological responses and changes and the whole point is basically to restore the body to the preinjury state. So your body is working as hard as it can to undo everything that's been done through trauma. Um However, this response can sometimes cause harmful side effects and that could be at an end organ that's distant from the site of injury. Um And the reason that we study it is because there are metabolic therapies that we can use to manipulate the recovery. There are markers that we can use to dictate the timing of surgery. And I'll come to that at the end. Um And it also helps us with prognosis, um understanding morbidity, mortality, um length of stay hospitalization, that kind of thing. So, um I always hated dry science and lectures. So I like to know why, why it's relevant. So first we'll talk about ebb and flow. You've probably heard about this before, particularly if you've already done your exams. Um So it was Cuthbert's paper 42 and the long and short of it is, um, you initially when you have a traumatic event or an injury, the body's response can be split up into two main phases, the ebb phase and the flow phase. So everything slows down and then everything speeds up essentially. So, within the 1st 12 to 24 hours, we have our ebb phase and this is a hypometabolic response um after the initial injury. And um you can see from my little box of notes that I've written there. So we have a lower basal metabolic rate, lower oxygen consumption, there was a drop in body temperature and reduced enzyme activity. Um Then after that 1st 24 hours, the body goes into a flow phase and this can last days to weeks. Um we can split this late phase up. Um And you see the opposite effect of all of these things. Um And when people say what's the body's response to stress or trauma, this is usually what they're talking about this model. So I thought I'd first go into more detail about the early phase. Um Shout out because there's not that many of you. So if you wanna just shout out, can anybody think of any kind of physiological responses that you'd see in the ed phase if this is something you're familiar with? So when everything slows down, anybody does, do they get issues with sort of gi tract motility ileus? Um Yes, yeah. So um that's true. You can get ileus. Um I've not mentioned it specifically in my talk, but there is a brain gut axis which can um be affected if you have a traumatic brain injury. Um it can affect how the gut functions um through the enteric plexus and you can get translocation of bacteria, everything slows down and it can um later on cause a massive inflammatory response. So, yeah, good. Anything else? What about more straightforward stuff? What happens to your sugar, fat and protein? Do you get ketosis at this stage or is that later ketosis? Uh probably a little bit later on. But before that just your initial what goes up? What goes down anybody? Oh OK. So um so sorry, here we go. It was just a delay on my computer there. So the neuroendocrine response to tissue trauma and hypervolemia hemorrhage according to the kind of ebb and flow model. So, like I said before, you have a drop in your body temperature, um there's a drop in cardiac output and as a result, you have poor perfusion particularly to your musculoskeletal tissue and your abdominal organs. Um And you'll be familiar with this from your kind of initial kind of fight or flight response, right? Um Reduced renal perfusion and low urine output and you'll have all seen this with your trauma patients um or an A&E on the wards. Um You know, you put in a catheter to monitor and nothing's coming out. Um You know, you have a look at the first set of floods and they've got an AK I um and this is a result of sodium and water retention. Again, we'll go into more detail. Um when we talk about the neurohormonal response hyperglycemia, so you get a rise in your blood sugar. Um And we'll talk about that in more detail later. Um And you have reduced energy expenditure initially. So your body is trying to reduce the amount of energy it's burning and conserve energy. And you initially, you start to get a little bit of protein breakdown. Um And this is important when you're thinking later on about resuscitation and nutrition. So late phase, everything is tends to the opposite way. So you're thinking now that you've your post resuscitation, you've seen and done your primary survey and obviously seb's gone into that in detail, the patients now on ICU, they're probably swollen from all their water retention, but they're stable. Um So now what we see in the late phase, they've got a raised core temperature. So usually you go to see them on ICU um for those of you that will review ICU patients, maybe if you're in TN O, you go visit your major trauma patients, they've got a bounding pulse, they've got pink puffies, peripheries, they're warm to touch even though they're maybe tubed um raised cardiac output. So the heart's working harder. Now, um we've said pinkies peripheries and massive diuresis. So that catheter that we inserted down in um in research, they now have massive um diuresis and and urine production. Um and then we see hyperglycemia and gluconeogenesis. So now your body is trying to keep up um generate more carbohydrate, but generate more sugar um to um to manage this increase in um energy expenditure. Um You also find that you get insulin resistance, so your sex hormone function, insulin drops, which again results in kind of worsening hyperglycemia. Um as we've said, increased energy expenditure and then you get massive breakdown of your protein. So I think within the first three weeks, you can lose 20% 1/5 of your kind of protein deposits in your body, which is massive. Um And then we also get increased growth hormone and prolactin um production as well, which can contribute to your um insulin resistance. Ok? Um And yeah, and decreased um th TSH and gonadotropin. So your thyroid stimulating hormone. Ok. So any questions about that so far, it's hopefully all, quite clear. Um I can't see you all the charts. So like I say, shout out um in between these sections if you want to clarify anything. So we'll talk about the neurohormonal response, which I think is quite important. So it's probably at the crux of, of um a lot of the changes that we've just discussed. So you, you know, you're familiar with ebb and flow. Now, now we're gonna look into the nitty gritty. So the neurohormone response is triggered by pain So you have um injury. Um So the site where the trauma has happened, stimulates your A and C pain fibers. So you have afferent signals through your pain fibers up to the thalamus essentially. But for those of you that are interested, the exam answer is your ventral posterior nucleus of the thalamus. Um And this then sends signals to your hypothalamus. Um And you have this integrated response from your hypothalamus. And from there, the response can be split into two sides. So on the left, you can see there's the sympatho adrenal axis, on the right is your classic HP axis. Um And hopefully, these are things you'll have come across in medical school. So really a lot of this is just gonna be a reminder of what you already know. Um but applying it in the context of trauma. So hopefully, it's not too um not too monotonous for an evening session. So if we look at the left, your sympathoadrenal axis, and as we've said, it starts at the hypothalamus, so you've had your afferent pain signals. A and C fibers stimulates the thalamus, the hypothalamus. Um And as a result, you have nerve impulses that travel down through the spinal cord through your sympathetic pathways. So, remember, you have kind of pre and post ganglionic pathways. You'll have a ganglion that's close to your end effector organ via your splanchnic nerve splanchnic meaning entrails. I'm sure you'll all remember from the Latin. Um And this directly can stimulate the adrenal medulla. And as you know, the medulla is responsible for screening your catecholamines. So, adrenaline, noradrenaline and dopamine. Um and we'll review this again shortly. Then on the right, you can see the H pa axis. So, against pain, thalamus, hypothalamus and you know this one already. So your corticotropin releasing hormone is released from the hypothalamus and then your ach from your um pituitary gland. And then this causes the release of glucocorticoids and mineralocorticoid from your adrenal cortex. So that should feel nice and easy. So, sympathoadrenal medullary axis. So that's the image that you saw on the left. So this is neurological and sympathetic stimulation of hormone release. So, as we've said, adrenal medulla is your secretor of catecholamines. Um And we know this causes um restriction of your um uh sorry, noradrenaline vaso constriction, but you overall adrenaline produces your fight or flight response. So, arterial constriction in your skin, muscle, gut and kidney um coronary and pulmonary heart rate, um increase in increase in contractility of your cardiac muscle and again, dropping insulin that's driving your blood sugar up, um activate system. Again, that's something you should be familiar with from med school. Um And then the kind of sweating, fear, alertness, impending, doing that kind of thing. Um I thought I'd briefly just remind you of the renin angiotensin aldosterone system cos obviously, this all links together and when you're thinking about your um resuscitation of your patients um in recess and then later in ICU pre and you know, perioperatively, these are the things that you're going to be manipulating. So, renin secreted from your juxtaglomerular apparatus in your kidneys. Um This causes the conversion of angiotensinogen which is made in the liver to angiotensin. One, obviously, one is converted to two by ace, which is secreted in the lungs. Your angiotensin converting enzyme and angiotensin two works twofold, firstly causing vasoconstriction again, working alongside your catecholamines. Um and then also stimulates the secretion of um sorry, activation of aldosterone at your um which works on the distal convoluted tubule to resorb sodium um and potassium and therefore also water. Um And there's a little note about here about vasopressin. So, ADH will also work to um cause sodium and water retention. Um But that's obviously through your collecting duct at the very end of the Nephron. Um So, again, that contributes to your water retention in your sick swollen bounding patient. Um On ICU H BA access, um we've already gone through this. Um And hopefully, it should be all ha for you. So I won't say it again. Um and just to reiterate. So, secretion of the adrenal cortex of mine mil mineralocorticoids, um mainly aldosterone, which is part of your ras system. And we've just discussed that and glucocorticoids. So, um the role of cortisol is production. So production of sugar, gluconeogenesis, breakdown of glycogen protein and vat. So, glycogenolysis, proteolysis, lipolysis, and then suppression. So, suppression of inflammation of. Um so you can see how this axis will contribute towards that phase of your e and flow model. And of no, as I mentioned earlier, the pituitary gland is also secreting prolactin and GH which is worsening your insulin resistance. Um And then I just, I found this image and I thought it was a really nice summary um of the neurohormonal axis. So on the left, you can see the spinal cord, the injury, um stimulating your afferent nociceptive pathways. Um You know, if you want to screenshot this, if you find this useful, you can um in the middle are your effector organs that are going to secrete your hormones which are in this blue column in the middle. Um And then on the right are the changes that we've discussed um already. OK. Um Oh, and I also liked this table. I thought this was quite useful. So depending on how you learn, I thought, you know, pictures are useful. Some people like lists, some people like tables. Um Again, you can screenshot this if you like. But um I thought this table was useful. Um When I was revising, I just had a list in my mind of which hormones go up and which ones go down. Most things go up. Um You know, sex hormones, insulin, thyroid hormone goes down, but your adrenaline stress hormones, water retaining hormones, all go up. Ok. All right. Any questions about the neurohormonal response, feel free to jump in if anything wasn't clear, hopefully, most of it was quite straightforward. So we'll move on to inflammatory response. So, um I just thought I'd remind you this again. This is medical school level, but um I don't know how often you all look at physiology. So it doesn't hurt to remind you. So this is the local response to wound healing and it's relevant because obviously in trauma, if you've got a polytrauma, like the one that um seb was describing the degree of tissue injury and therefore local inflammation, which can trigger a systemic response is gonna be much greater. Um And that's the problem. So this is your wound healing pathway. So it begins with hemostasis, um your local platelet response and then triggering of the clotting cascade, followed by inflammation which is driven by your local neutrophils and tissue macrophage response. Um and then proliferation remodeling, but we won't go into that for now. So your local response um as we've said, clotting complement cascade, um cascades are activated. Um but in terms of the local inflammation, it's mainly your neutrophils and your macrophages that are responsible for secreting all the things that can cause this massive systemic response later. So, um cytokines, histamine oxygen free radicals or ros they're sometimes noted as um nitric oxide, Arachidonic acid derivatives, um prostaglandins and prostacyclin, um and particularly cytokines are important for mediating the systemic response to trauma. So you have your local tissue injury, this activates your leukocytes as we've seen. And the main cytokines that are involved are il one il six, which is probably the most important and TNF alpha. Um So if you were to remember any cytokines, those would be the big three to remember. Um And the problem is there are receptors all over the body um for these cytokines and that's why you have a systemic response. And I've split the systemic response into these four main categories. So there's an increase in your basal metabolic rate and your temperature, the liver is working hard at gluconeogenesis. So, again, driving your sugar up um and also production and release of your acute phase proteins, then stimulation of your leucocytes. So you get mass stimulation of your leucocytes and obviously, there's a whole um kind of immune mediated response thinking about the innate and adaptive um immune response. But I'm not gonna go into immunology in much depth today. Um your HP axis which we've discussed at length and then proteolysis. So again, that profound protein breakdown breakdown, approximately 20% in the first couple of weeks, um massive protein loss. So that's something that again, you're gonna be thinking about in terms of um nutrition so that these people survive ICU before they step down to the ward hematological response. So I'm not gonna spend too long on this because I'm sure almost definitely none of us are hematologists. Um But unfortunately, for exams, you know both entry level and uh exit exams for FRCS, you just have to know the crossing code. Um So I thought I'd mention briefly, I like this diagram um because it's simple and maybe a bit easier to remember than some of the other nonsense diagrams that you see. So intrinsic pathway and extrinsic pathway. Again, this is something you've all have been through. Intrinsic is your endothelial factor stimulates 1211 9 with the health of 810, which is the common pathway. Extrinsic is your tissue factor. So, um seven is activated from external injury. Um Tissue factor then activates 10 and your common pathway is 10 and two. So, prothrombin is then converted to thrombin and then one is fibrin. So you get crosslinking um which leads to clot formation. Um and that's relevant. I'll talk about that in a second. Um The other thing you know, headline hematological thing that you'll need to know is the triad of death. I'm not sure if subs already mentioned this. But again, I'm sure a lot of you all have come across this already. So, hyperthermia which decreases your coagulation, which leads to coagulopathy. You have an increase in lactic acid in the bloodstream as a result, which causes acidosis and as a result, your cardiac muscle can't function as well. You have decreased performance of the heart and obviously, your systemic circulation is less because your heart's not functioning as well, which causes a further drop in body temperature and the spiral continues until you die unless we intervene. Um And this is relevant to you because obviously you want to be thinking about your management of major hemorrhage. So when you're in A&E or when you're managing that major trauma, if you rotate through your major trauma center, um you know, you're gonna be thinking about activating the major hemorrhage protocol early. You can always step it down later, but activate it early. Um Where I worked. The last major trauma center I worked in was in Nottingham and we had pack one and PAK two. This is the guidance for Norwich. It looks pretty similar to me. Um So you're gonna be thinking about replacement of blood intervening early with blood rather than um crystalloid fluid. If you can, if you know that there's massive hemorrhaging, you've done your ATL S ABC assessment already. So, you know that there's gonna be loss of blood. Um You've done your F scan, et cetera. Um And has anybody used this or seen this before? Does anybody know what this is? So, is like a really fast um coagulation. Well, it looks at your clotting clotting factors or the ability to get. Yeah, exactly. So I think this is for me, this is a good reason to have some idea of what's going on with the clotting cascade. Um So none of us are hematologists. But um if you've not seen this before, rotational thromboelastometry, um it used to be called thromboelastography. So you might see Roeg or ROM. Um These machines can do rapid assessments and tell you which clotting factors the patients low on. So you're gonna be doing your major hemorrhage resuscitation pack one pack two, whatever it is, your trust does. But you can also with your later stages of um blood replacement and resuscitation, have a look at where you're um missing clotting factors and think about replacing those. So that's something to look out for. If you go to a, if you've changed, over, look out for this machine, um you know, find out how to test and who to speak to. Um you know, if you want to talk about um think about replacing your patient's clotting factors. So I think that's one good reason to have a rough idea of what's going on um with coagulopathy. And the other thing I thought I would mention. So, obviously, in trauma, there's another thing that we see is disseminated, intravascular coagulation. Um So we all know D IC but again, I just thought I'd remind you, I really liked this image. Um It quite simply divides the pathogenesis into two parts. So if we look at the left, you have activation of your intraocular coagulation cascade. And we've already just seen and been reminded of what those um stages are and this results in massive platelet consumption, um massive coagulation factor consumption and fibrinolysis and this is what you're going to see in your blood. So drop in platelets rise in your PT and A PTT. And remember they kind of represent the two halves of the initial uh initial clotting cascade intrinsic and extrinsic and a rise in your D dimer. And with the, with the slide did not change as we are still looking at. Are you? Oh Yeah. Uh What about now? Um I can't, I can't really see, it still says rot on that. Can everybody else see the next slide or for us? Pathogenesis? I see. OK. Sure. My mistake. Probably. Sorry. All right. OK. I'm sorry. Um I don't know if you want, I can wait a second if you want to log out and log back in. Do you want to do that or should I carry on? What browser are you on? Cos there's a known problem with metal with one of them. I don't know if it's chrome or you should go on to Chrome. Yes, it's fine now. Perfect. Oh Good. OK. Fine. So you've got massive consumption. So you get massive um clotting and then when you've run out of platelets, you've run out of coagulation factors and you're getting breakdown of your clots, you then get massive uncontrolled bleeding, impaired coagulation and bleeding and the patient will just bleed and bleed and bleed to death. Um The other problem you can see on the other half of the chart is endothelial damage. So you can get microvascular thrombosis. Um So you're throwing off clots, as we said in the early stage. Um and this can obviously cause stroke M I um ischemia, failure of your end organs, important end organs which are already under duress. So hopefully, that's quite clear. But I just like this chart cos I've never seen it put so simply before um you know, to summarize D IC. So hopefully that's useful for you too. OK. Damage control orthopedics. This is probably the more um the funding. So um the two hip hypothesis, has anybody heard of this before? Seen it? Is this all old ha for everyone? Is this new for anybody? Uh Yeah, new for me. Is it OK, fine. Um So the two hypothesis is the idea that um the initial trauma that the patient goes through um often a severe insult like the patient that you were discussing with sub. So patients jumped off a building or over on, you know, off an overpass onto the concrete below has been run over by a car and so on. So they have this initial severe insult as a result, your immune response um and neuroinflammatory response has been primed. So you have this massive inflammatory response mediated by your neurohormonal response, um you know, mediated um by your cytokine response um by local tissue injury, hemostasis, you have a hematological response, et cetera. Now you want to go and take that patient to surgery. So, you know, they've got an open fracture that needs fixing. Um You know, maybe they've got some sort of vascular injury, abdominal injury that needs operating. The problem with us taking them to surgery is that is a second insult. And what can happen is when you have a second insult, you have a exaggerated host response. So because your immune system is primed, you then have an even bigger inflammatory response. And the end result of this can be acute respiratory distress, distress syndrome, multiorgan failure, um or mods multiorgan dysfunction syndrome. And that can lead to death. So the first hit is the injury or the trauma. The second hit is the surgery. Um And this is really important because now that we understand this, um and now that we have a better understanding of the metabolic response to trauma, it's really important that we um you know, manipulate our knowledge of these pathways so that we can work out the best time for surgery because you want to get them operated on soon enough that they're not gonna die of an infection from their open fracture, but they're not gonna, you know, bleed to death um from their femur fracture and you know, they need to have a nail and their femur fracture, um for pain management and for recovery and stop them bleeding. Um but you don't want to take them to surgery so soon that they just die on the table or die in ICU the next day. So, damage control orthopedics this is the concept that you do your initial resuscitation. So you're down in recess and you sort them out or um I don't know if I think you mentioned right turn recess where they're so unwell, you know, you take them to theater but you do your initial resuscitation. Um and then you're gonna be monitoring their lactate. I think ATL S teaches that oh ao principles of um fracture fixation course um teaches that you monitor the lactate and as long as it's less than 2.5 it's safe to go to theater. Um There's a lot, there's many more things that you can monitor. So that's one important marker that we look at. Um and the phrase that we use alongside damage control orthopedics is span scan and plan. Does anybody know what that means? Scanning external fixator, scan them and then plan your operation? Yeah, exactly. So, you know, the, you want to deal, you need to get them to ICU otherwise they're gonna die. But what you wanna do, you don't wanna be doing a long, you know, three hour fixation of the pong fracture. Um you know, with plastics involvement and skin coverage and whatever else you need to get that bone out to length, um You need to make sure the soft tissues are safe that there's no neurovascular impairment distally. You know, vascular will get in and do their thing and make sure that there's blood flow to the um distal end of the limb and then you get them back to ICU. Um, you can do act scan for the parts that need fixing and then you can plan a controlled definitive operation later, but there's lots of different things. So I think it was, um, Pete Jis. Um, he's a professor of trauma and orthopedics in Leeds. Um, he's a giant. He's written loads of papers about this and I think he came up with the con concept of damage control orthopedics or he's contributed to the theory. Um So there are all these different things that we can look at. These are markers of um patients that will not be stable enough. It's not safe to return to theater. And if they have that second hit, they're more likely to die. Um So I'll talk about the injury severity score next, but essentially you can calculate this score. Um And if you have a score of more than 20 thoracic trauma or a score of more than 40 um multiple injuries including Abdo Pelvis and you have hemorrhagic hypovolemic shock. Um admission platelets of less than 95 admission body temperature of less than 32 mean pulmonary arterial pressure of 24 pa O2 of less than 200. And do you remember I mentioned IL six. So that's probably um one of the most useful cytokines that we can monitor. Um So a score of more than 600. These are patients that are probably not yet fit for theater. Ok, for definitive fixation. Um, so we can use these to help time our surgery. And I think there's been papers that show, um using some of these markers like IL six and returned to theater within 2 to 4 days, there was much higher mortality than those that returned at 5 to 8. Um So it's interesting. So the injury severity school finally. Um So this is a school we used to assess trauma severity. Is anybody familiar with this school? Because if you all know it, then I won't go into such details. I've only heard it mentioned in sort of, as you said, sort of calculating where someone should really be dealt with rather than its ins and outs really? Yeah. Ok. So, I mean for you guys that are in A&E this can be useful for you in terms of, you know, you receive a patient that um you know, turns out to be a polytrauma patient and you think mm maybe they should be managed elsewhere and if there's consternation, you can use the score to argue your case. Um And as I said, this is the school. Well, one of the few schools, there's a few trauma schools um but it correlates with morbidity or I've misspelled that mortality and hospital stay. So the length of time you spend after the trauma. So it's a range from 3 to 75. Um and in A&E like I say you're gonna calculate this score and a score of more than 15 is classified as a major trauma. And it would be, you know, good objective measure to say, I think this patient needs to go to Cambridge. So it assesses nine body parts, um which I've listed there, head, face, neck, thorax, um abdomen, spine, upper limbs, lower limbs, and then they've got another section that says external slash other and then you mark them um injury in, in terms of severity. So if any of you have got MD CALC, the app, um you can look this score up and play around with it and calculate injury severity score and they score them as a minor moderate serious, severe, critical and maximal, which is untreatable on arrival. Um There are definitions for each of these, what's categorized as serious versus severe. So you can look that up. I think all fib has a really nice summary and then to calculate the score, it's a squared plus B squared plus C squared. So almost like Pythagoras theorem but not quite. Um So you take the sum of the squares for the three most severely injured body parts. So you know, if the most injured body part is head thorax and lower limb, then you would take those three scores. Um and then you would square that and add that together and that will give you your score out of 75 more than 15 as a major trauma. And at which point you want to think about involving your major trauma center, you're gonna be thinking about calling itu early, you're gonna be involving your seniors. Um I'm not sure where you will work, but um when I worked at Queens Medical Center, we categorized trauma calls into green amber and red, red was all the consultants had to be downstairs in A&E everybody had to be out of bed. Um pa wouldn't intervene straight away. Um OK. So this was just a summary of all the different things. Again, you can screenshot this if it's useful to you, but it's just a little summary of all the different um responses that your body has. Um you know, in response to trauma. Um There's a lot of references if it interests you. Um and that's it. So I think I finished a little early but I didn't want to go on too long because it's quite a dry topic. Um So any questions about any of that? Was that all very obvious or was it useful? Is there anything else you'd rather discuss? Anybody? Was that all revision? And it's very obvious. Was there some new stuff in the? Mhm. Pretty useful. Lots of basics. That's pretty good. Yeah, lots of basics. But I think really that's the, you know, that's mainly what you need to know. Um You can obviously go into, you can look at, you know, N A PDH oxidase and you can look at all the biochemical pathways. But I thought that would be a bit heavy for an hour long session. Yeah. Um, yeah, but it's just taking what you already know and applying it in the context of trauma and then using it to work out. Ok. Practically. What do I need to be monitoring when I'm down in A&E what blood tests am I gonna request? You know, do they have a ROM machine? Because I need to think about replacing my clotting factors. Um You know, I'm seeing them in A&E, you know, why do they look pink? And they're diaries now compared to how I saw them in research when I know their hemoglobins dropped. So it's really just applying it in that context because obviously it's a little bit different compared to seeing um you know, perhaps your septic patient um or other unwell patients from a medical point of view. Yeah. Cool. Any questions? What are your thoughts on uh early appropriate care by Valia? Uh uh Do you, do you follow that as well at uh I mean, in east east of England, I'm new to east of England. I don't really know. Uh Oh, ok. I've heard of that. Tell me, tell me what early appropriate care is. Uh It's, I think it's a coin. It was Coval, isn't it Heather Valia? Uh basically to look at various parameters to decide if we can do part of the surgeries and fix the major long bones if required, if the patient can take, the physiology can take it and then stage it appropriately. Something like that. Ok. Yeah. Um, I mean, I think there's reasonably strict criteria as to what should, and shouldn't go to the trauma centers. So I think for the most part we shouldn't, and don't see, um, major poly traumas. But, I mean, II was last in West Sus. I've only been at Colchester for about a month. Um, when I was in West Suffolk, sometimes you'd have patients coming in from the countryside and they're not stable enough to transfer to Adam Brooks and we would be closer and, you know, they fall off a 40 ft deer stalking tower and be in spinal shock and have open fractures and stuff. So sometimes there's been situations where we've had to deal with. Um, you know, some cases where Adam Brooks has been totally full. It's the middle of winter, they've got a couple of injuries that could be managed in house and then get transferred over. But I think on the whole that shouldn't happen. Um, because of the criteria that we have in this region for who should go to the trauma centers. Um, you know, because the outcomes are better, you know, when patients are managed when patients with multiple system injury, um, are managed in major trauma centers, the outcomes are better. Yeah. Do you normally get the CT trauma scan? Uh, the trauma series CT scan called, just to calculate the is and then call the trauma coordinator to show them to no Adam Brooks normally or how do you guys go about in a and yeah, so we have the, we have the trauma network. Um And obviously if it's clear from an ed perspective that the, you know, you've calculate, you've done the CT trauma, you've calculated to the ISS, obviously, orthopedics will attend, um, in a trauma capacity. But if it looks like they need to be transferred straight over, they can be networked, the trauma network takes over and the referral is done through the trauma network and they should be transferred kind of automatically. So we shouldn't from an orthopedic point of view have to get involved much. Really. Ok. If it's clear they need to go over. Ok. Sure. Thank you. Yeah, sure. Thank you. Nice. Anybody else? I'm sure that's enough for everyone for tonight. Um Fine, I'll let you all go then if nobody has any other questions. Thank you for attending. Thanks with you. Thank you. See you buh-bye. Take care. Bye. Thanks. Yeah, you're welcome.