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Ok. Um So the talk today is um on general cases which will explore how to approach and treat um some neurological neurosurgical emergencies. Um We apologize for the disruption over the last few weeks. Um And we hope that most of you can still make it today. Um Just a quick reminder to fill out the post feedback form. We'll put it in the chat and we'll put up a QR code at the end of the talk. Um Again, these will, we'll use these to distribute the certificates at the end of the course. So make sure that when you're filling out the feedback forms to keep the same name as you did previously, um If you have any questions, feel free to ask them in the chat. Um And I'd like to welcome uh Rose Elton, a ST five neurosurgery registrar in the London Deanery. Thank you for coming today and I'll let you take over. Oh, thanks guys. Um So I'm probably just gonna turn my camera off briefly, so I'm not um staring myself for the next hour. Um But um, yeah, I'm Rose, I'm a neuro registrar working in London. Um And I've been asked to do some neurosurgery cases today. Um, I've picked two cases. Um, one is considerably longer than the rest of them. Um, I think I've picked, I won't give a surprise way too much. I think it's already been shown on social media. Um, but, um, we'll focus mainly on one case, I think for about three quarters of the time and then we'll do a quick one at the end. Um, because it's cases rather than lectures like you've had for some of the other ones, a bit of interaction would be great. Um I'll open the chat so I can see that. But if you want to kind of shout out answers, I'm also um I'm also happy with that or, or pop them in the chat. Um But it'd be nice just to have a little bit of interaction um as it's more like a case based discussion um rather than, than like a formal lecture like I said. Um So let's start with the first case. Um So case one, this is actually a patient. I um I saw at work a couple of weeks ago. So this is the exact near enough the exact history I had um from, from her at work. Um So we've got a 59 year old lady who came in with family, um who about four o'clock that day had had an acute onset severe frontal headache. Um Family said they heard her kind of suddenly say kind of, you know, come and come and help me and then she briefly lost consciousness before recovering to Jesus 15 and, and complained of this headache. Um, she felt very sick and actually had a couple of episodes of vomiting, um, but didn't have any focal neurological deficit. So no limb weakness, no cranial nerve deficit. Um, in terms of relevant history, she was hypertensive, um, taking, I think one or two medications. Um, and she smoked five cigarettes every day and she said that her mom had died from some sort of brain bleed. She wasn't sure what, um, when she was in her seventies. Um, so based on this, I don't know if anyone good game away. Um, I don't know if anyone has any thoughts about what the most likely diagnosis is based on this history or what some differential diagnoses could be and what investigation you would do as a, as a junior doctor seeing her. Of course, someone said brain aneurysm stroke, good xy, good hemorrhage, good. So all really good answers. So I think basically based on the answers people are given, giving. Um, we're thinking of vascular cause and, and this is very much when you think of someone having an acute headache and then with, you know, with the loss of consciousness nausea, you're thinking something vascular of the neurosurgical pathologies, you know, when we're thinking tumors or, you know, you know, other, other things like that tend to have a more insidious onset. Um whereas for, for a sudden acute onset, severe headache, we're thinking vascular. Um So she said brain aneurysm which typically causes a subretinal hemorrhage, a stroke, pituitary um apoplexy which is AAA bleed into usually a pituitary tumor. Um And, and someone said subin hemorrhage. So, yeah, we're thinking a bleed. Um So this was her, her CT head she had. So the first investigation we would do typically for this sort of patient was a CT head and I was actually called once the CT had already been done, which was, which is excellent. Um So again, I don't know if anyone in the chat wants to say what they can see. Um These are two separate, this is the same patient. Um One's obviously lower down and one's slightly higher up. Um So I don't know if anyone wants to comment on what they can see on this CT. Yeah, good. Someone said blood in um basal systems, a star sign, hyperten spaces in systems, blood in the systems. Perfect. And what do people think about with the one on the right? Um Because obviously that's a little bit higher up than the basal cys. Any thoughts on the one on the right? Someone's put ac a good in. Probably. Exactly. Yeah, good. So this patient, as you can see on the left, she's clearly got blood in the basal systems and the Subhi noid spaces and someone said star signs. Yes. So we call this a star or a STLL sign. Um So you can see, I I don't know if you can see my mouse mo um moving on the screen, but you can see this star pattern um which is is typical of blood throughout the basal systems. Um And the one on the right, as you can, as somebody correctly said, you can see this intraparenchymal hemorrhage. Um And as someone again, very correctly said this is in a sort of ac or anterior cerebral artery territory, which is, which is excellent. So this is a classic subarachnoid hemorrhage. Um And important to note that when we say um subarachnoid hemorrhage, we do, we do differentiate between spontaneous and traumatic um traumatic subarachnoid hemorrhage. You see um in the subarachnoid spaces in the ci kind of the cortical. So, so kind of where I'm moving my mouse, you might see subin hemorrhage here in the cortical. So side, whereas this subarachnoid hemorrhage in the basal systems is a spontaneous subarachnoid hemorrhage from a vascular abnormality until proven otherwise. Um And, and for her, obviously, there was no trauma in her history. Um But this is, this is not a traumatic sub hemorrhage, this is a spontaneous vascular subarachnoid hemorrhage. Um You um so now that we've established you had a sub reid hemorrhage. The first of our classification systems we're going to talk about. So this is something that we use pretty much for every sub noid hemorrhage um patient that we see it's a way of communicating to your consultant or senior or colleague um about the clinical status of the patient. Um And it's, it's an easy descriptor. So we would say a patient is WFNS 12345 depending on their clinical status. Um WFNS is the World Federation of neurosurgical Societies and they came up with this classification system. Um They have actually made a modified version which is slightly different, but for the most part, most people use the, the original. Um So this is, this is the original. So, um for anyone who's G CS 15 and someone said, do you recommend between WFNS or Hunt and Hes? So the hump and hes is another um classification scheme we use on the um the clinical status of the patient. What I found is that it's very dependent geographically. Um So I recently went to a course um with lots and lots of European neurosurgical trainees who all use the Hunt and classification. But, but I've worked at several neurosurgical centers in the UK and in the UK, it's, I think it's pretty universal that we would use the WFNS. But it is worth noting that there is also the hump and classification as someone has mentioned. Um But, but like I say in the UK, this is pretty universal. Um So some GS 15, they WFNS one. if they're 13 or 14, the only difference between WF and S two and three is whether they have a limb deficit or not. Um And then four is G 12 to 7 with or without limb deficit. And similarly, WF MS five is, is a GT S less than seven with or without a deficit. Um So our lady, she's on arrival, she's GS S 15 with no deficit. So she'd be a WFNS one. So that's how I would communicate this to my consultant. Then the um the second classification system that we, we use again when describing um the patient and, and the scan to our consultant is the fissure classification. And this is um specifically relating to the CT head and it describes the extent of blood on the CT head. Um It's useful one because it's, if a consultant is not in front of a computer, right from the off, it kind of gives them an indicator of how let's say severe, the CT head looks. Um but clinically, the reason it's, it's used and, and the um the original research that was done on this is that the extent of blood load um on the CT scan based on the fissure classification is directly relatable to the risk of vasospasm. And we'll talk about vasospasm a little bit later on. Um But that is the only thing that the fissure classification tells you, to be honest, it's the risk of the patient developing vasospasm. Um And this is the, this is the paper here. If anyone wants to have a look at it, look at it afterwards um by Fisher. Um So this is the official classification. Again, there's an original under modified. Um We still, for the most part use the original fissure classification which you can see on the left. Um So fissure one is no retinoid hemorrhage. Um which you might say, how, how can you diagnose it? This is typically people who have a very good history for subarachnoid hemorrhage and then may have it diagnosed um based on a lumbar puncture. So it would have a, a normal CT scan, but a lumbar puncture would be performed and there'd be the blood in the in the CSF which would confirm subarach. Um Two, a fissure two is diffuse subretinal hemorrhage, less than one millimeter thick. Three is thick. So more than one millimeter thick and four is thin, but with clots or either clots in the parenchyma or clots in the ventricle. So, intraventricular hemorrhage and like I say, for the most part, we still use the original fissure. The reason the modified fissure was done, which you can see on the right was that people found the original fissure a bit confusing because rather than it being the higher fissure, you had the highest risk of vasospasm. You had, it was actually shown that fissure threes had the highest risk of vasospasm. So 37%. So you can, as you can see on the picture on the left. Um So that's why the modified fissure was made because people just thought this was too confusing. So, in the modified fissure um which you can see on the right. So one is thin, two is thin with clots, three is thick and four is thick with clots. And that um has a direct um relationship with the higher risk of vasospasm with the higher fissure score you have. Um But as I said, for the most part, most of our, our um um our communication we have at the moment still would use the original original fissure Fisher scale. Um So our patient would have a fissure three on the old scale because she has got diffuse thick, subarachnoid, definitely more than one millimeter thick and she has also got localized clots. Um So she would be fissure three and she'd be the highest risk of vasospasm based on that. So, obviously, we, we're thinking that she has got an aneurysm somewhere. So this is her original CT. Um Obviously, we're slightly limited by not being able to have um um not a, not a video of her CT, but I'm just wondering if anyone based on this CT is able to see an abnormality. I've tried to um get the best cuts I can, but I'm just wondering if anyone can see an abnormality on this CT, probably best seen on the um the sagittal in the middle and the axial on the right. No. OK. So if we look at, if you look at the one on the left, so we can see with the CT A. So the CT angiogram, so standard CTCCT scan with, with con contrast injected to the um veins, this is essentially used to illuminate all of the blood vessels in the brain. You can see on the left, the main vessels we can see are the two M CS. Um So if you can see my arrowhead two MC A S coming off here and then the sagittal in the middle, we can see the AC A coming off here and then the axial on the right, we can see this abnormality here in the center. And you can see it also on the one in the middle, you can see this abnormality here. So this patient has an aneurysm of the anterior communicating artery cause we can see here. AC A is coming off here and we can see here, come here. And uh like I said, it's very hard without um without having the full um full scan, but the A ones would be coming here. I and the A twos would be coming up here. So this would be an anterior communicating artery aneurysm. And as someone correctly said, we could kind of have possibly predicted that based on the clot she had on the original um original CT scan. So quite often with these patients, they'll have a higher distribution of blood in a particular territory. And you can often guess or, or I should say predict in advance where the aneurysm is likely to be. So this patient has an anterior communicating artery aneurysm, which you can see here. So you've seen this, I've seen this patient in the A&E I've had that history. I've had that CT scan. I've had that CTA. So I can see she's got a retinoid hemorrhage with an Acom aneurysm as a junior doctor. What management plan would you instigate immediately there and there in the recess department? BP. Management? Good. Any other thoughts prevent vasospasm? Cool. Like I say, we'll talk a bit more about vasospasm. OK. So in terms of an initial oh, senior input. Good. Yes, absolutely. Tell your consultant that, that this person's here, you probably wouldn't need senior input in the immediate phase in terms of immediate management. But you'd absolutely let your consultant know that this patient was here. Um Someone said surgical intervention. So again, as a junior, that's probably not something you're going to do immediately. But that's, that is again something we'll talk about in a, in a second. So in terms of what I would put in place immediately there and then is something that is often referred to as the SUBAC protocol. Um I know some centers hate this phrase, but it's um uh it's, it's quite accepted phrase that people use. Um So the patient must be accepted at a specialist neurosurgery units. There's been lots and lots and lots of evidence that these patients have to be in a neurosurgery unit. They're best managed there. They need to rec receive treatment there. So, if they're in a DG, they'd have to be referred to your local tertiary neurosurgical center um until the aneurysm is treated, which again, we'll talk about in a bit. The patient should be on bed rest. Um You need to have a urinary catheter with strict fluid monitoring, which we'll talk a bit more about in a second while that's important. And then you want to start several medications. Um So for every retinoid hemorrhage, aneurysm or subin hemorrhage, you need to start niMODipine, um which we'll talk about, you should give them analgesia because their headaches are severe and can be severe for days. Going into weeks. You give them laxatives because you don't want any straining, um which could push their BP up and you give them antibiotics cause they also often feel very sick. Um Someone very great A BP management. So we try and keep the BP as normal as possible. Um The caveat to that being the, the most important thing is to not have big fluctuations. So, if there's somebody who is very hypertensive, normally, you don't want to bring their BP down too rapidly because a change in BP can um affect the aneurysm. So you try and keep it as normal as possible. But the main thing is to, to bring it down slowly um tranexamic acid, there are studies now which show that giving tranexamic acid in the 1st 24 hours um can be helpful. Um That's not accepted or I say accept, but it's not used at all neurosurgical centers. Um The place where I currently work, it's not routine. Um but I know lots of places it is and there is evidence that tranexamic acid um can be helpful. And then at the bottom, I put this Triple H therapy because a lot of people have probably heard about this. Um The Triple H therapy um essentially refers to management of preventing vasospasm. Like I say, we'll talk to that about that again in a second. But, but this Triple H therapy is essentially ensuring people are well filled. Um So give them lots of IV fluids um as part of that, they often become very hemo diluted and then the last one hypertense them. Um So you'll see that that's kind of in direct opposition to the normotension I've just mentioned. And like I say this, this triple H is normally once the aneurysm has been treated. Um and it's a a vasospasm preventive uh preventative measure, but you wouldn't hypertense them um before the aneurysm has been treated, but you'll often see people talk about this Triple H therapy. So this is the paper looking at niMODipine. So some of you might know this already. It's a nice thing to read. So niMODipine trial is called the brat trial, it a trial done in Britain. And it's the um uh essentially niMODipine is the only medication and the only uh preventative uh intervention that's been shown to, to stop or to reduce the risk of vasospasm. Um So this was a um a randomized control trial done. And like I say, in Britain, um and they, they proved that people had niMODipine compared to um compared to placebo had a lower risk of vasospasm. So this is the, this is the paper looking at at niMODipine, which some of you might be interested in reading. Ok. So same day as the patients presented. So about 56 hours later, um we called saying that she says, says her headaches suddenly got much, much, much worse. Um We go and see her and she's a little bit more confused, not, not really orientated to where she is and she's a bit more sleepy than she was before. And we noticed that her BP is not very well controlled at all. It's going up and down all over the place. Um What do we think might have happened to this patient or what, what could be going on? It was been given. So, yeah, the patient was given a dose of amLODIPine price. This event, hydrocephalus, good edema, vasospasm, rebleed. Good, good, good. So, in the 1st 24 hours, um and uh the, and, and pre securing the most common causes of deterioration are rebleeding and, and hydrocephalus. So this is the patient ct scan. So you can see compared to the one previously. And hopefully, you can see there's a lot of blood in the ventricles now, which wasn't there previously, that frontal hematoma is bigger. Um Whereas the ventricles were, I mean, again, hard to see on this, this image, whereas the ventricles were a reasonably normal size before you can see these, these um occipital horns are quite plump and that'll be because of the blood within the ventricles. So, this patient has essentially had a rebleed. So, if a patient in the 1st 24 40 hours prior to securing of the aneurysm, complains of a severe headache, a sudden acute onset headache. Again, your automatic thought is that she's had another vascular event. So you're thinking rebleed and if they start to become drowsy or confused or, or not quite themselves, you're thinking hydrocephalus, um you can have hydrocephalus without a rebleed. So, um hydrocephalus often develops in people with sub retinoid hemorrhage because you get impaired absorption of CS F. Um So you can have that in the absence of a rebleed, but, but especially in the situation of rebleed and in this case where the ventricles are now filled with blood, um There's, there's gonna be a definite uh impairment of absorption of CS F. Um So now that we've got this scan, the patient's drowsy confused. What treatment do they need immediately to treat this? This, the, the findings on this scan, someone said EVD and shunt because I think, I think, um be things. So the lines we're going on is that she needs something, you know, some people could argue, you need to treat the aneurysm. But the lifethreatening issue at the moment is the hydrocephalus. Um, so completely right. We need to have um CSF diversion. Um Shunt is something you consider lace down the line because lots of people just need temporary CS um diversion. Um But she definitely needs to have CSF diversion because she's got hydrocephalus. Um So she's had rebleeding, IVH and hydrocephalus. So, um in terms of CS F diversion, there's two commonly used methods. Um By far, the most commonly used method in sub hemorrhage is an EVD which stands for an external ventricular drain. Um But you can also um use a lumbar drain depending on what the scan looks like. Um So just I a couple of pictures here. So one on the left is an external ventricular drain. So as as it says, it's a drain that's inserted, very small burr hole goes through the brain parenchyma into the um frontal horn of one of the lateral ventricles. And then it has an externalized tube which is tunneled out of the skin um in the head. Um and is attached to an externalized drainage bag which sits on a drip stand next to the patient. And this just bypasses um all of that intraventricular hemorrhage and treats the hydrocephalus. Um On the right, you can see a lumbar drain. So that's exactly the same thing. But instead of draining from the top, you drain from the bottom. Um, the caveat to a lumbar drain being that if a patient has lots and lots of intraventricular hemorrhage, then obviously, a lumbar drain may not be successful because the CS F may not physically be able to bypass um, all of that hemorrhages in the ventricle. Um So a lumbar drain is more commonly used. Um uh if patients have got head hydrocepha without um significant um IVH. Um So does drainage rate matter in this case or is that something you can't control? Um So for both of these, you can control the amount of fluid that's drained. Um You have a um on the, on each of the drainage bags, you essentially have um essentially a controlled manometer where you can drain either based on um centimeters of water or millimeters of mercury. Um And you, with these things, you can either do a pressure dependent drainage or a volume dependent drainage. So you can either say I want to drain 10 mils every hour um and adjust um the, the drainage on that basis, but we tend to not do that in sub retinoid hemorrhage and we tend to leave it at a certain um pressure or height. So, for example, a commonly used height we would say is 15 centimeters of water, which means that when the pressure in the fluid in the ventricles or, or in the, and from the lumbar drain exceeds 15 centimeters of water it'll drain. Um, and, um, we know that, you know, 15 centimeters of water is a, is a reasonably normal pressure for most of us. So, in these patients with the Hydrocephalus, it will certainly exceed that and it will, and the fluid will drain on that basis. Um, like I say, for her, she would certainly have an VD because of the amount of blood in her ventricles. And I've just popped on the bottom right there. So, brain books a London based Neurosurgical charity and they do lots of nice videos on youtube and they've actually done a live surgical video of an external ventricul drain being inserted. Um And it's a really nice video for anyone who wants to see um, what this actually is. So, um I'd recommend having a watch of that. I'm not uh not sponsored by them, but it's a very good, uh, it's a very good teaching resource. So, yeah, so she certainly needs an EVD. So once she's had the EVD inserted, obviously, the next most important thing is thinking about how we're gonna look at the aneurysm in more detail and, and how we're gonna treat the aneurysm. Does anyone know how we would look at an aneurysm in even more detail than the CT angiogram? We've already got lovely. Someone's put DS A. So, exactly. So, DS A oh A DS A is a digital subtraction angiography. Um It's a type of um uh fluoroscopy and DS A has two benefits. It can either be used as a diagnostic tool to look at an aneurysm a little bit better purely as an imaging technique or we can use it to treat the aneurysm. And this is where I'm sure most of you will have heard about coiling and in order to coil an aneurysm, we have to use a DS A. So DS A is done by the Interventional neuroradiologist. Um in the uh angiography suite, it can be done under either local or general anesthetic depending on whether you're just looking at the blood vessels or, or trying to treat an aneurysm. And um you have access either via the I uh either via the groin, um via the femoral artery or via the wrist, via the radial artery and you thread a little metal guide wire up through the vessels similarly to if you were putting in like a cardiac stent or, you know, doing a A PC I for A for an M I. So you thread a guide wire up through the arteries to the brain. Um and then you inject your, your contrast dye and everything illuminates um in order to see the vessels clearly and the reason it's called a digital subtraction angiography, they do a scan before the contrast has been injected and afterwards, and then they subtract one image from the other so that all the bone and associated um you know, kind of bone teeth, everything you don't want to see is taken away and all you're left with is the vessels because they are um brightly illuminated with contrast. Um And this picture on the left here is kind of a standard step uh set up for what you'd um uh what we see in Angio Suite. Um This is what an Angio uh uh A DS A typically looks like. So you can see compared to the CT A, it's got much, much um better images and you can see here, we've got um uh a few different, few different views depending on which vessel you want to look at um as part of your angiogram. So the dye can either be injected into one of the common carotids. The catheter can be passed a bit further up and you can choose to inject it into your external carotid or your internal carotids or if you want to look at the posterior circulation, um then you um inject your dye into the vertebrals. And so you can see some examples of that here. So they're labeled. So I won't, won't um won't actually say what they are. But you can see, for example, on the left hand side, far left, this is a common carotid um injection because you can see here, some of the external carotid um branches are illuminated here, but you can see here, the internal carotid is really lovely illuminated. And here you can see the middle cerebral artery nicely illuminated here. So this is a a common carotid injection. Whereas the one in the middle, you can see the structure looks very different. And um hopefully, most of you who know your um arterial anatomy can see immediately that this looks um very different and and it's nice and easy to pick up the basilar artery in the middle. So hopefully, most of you recognize the basilar here and your two PC A S splitting at the end of the basilar. So we know that this is looking at the posterior circulation and this is a left vertebral artery injection. So you can see here your left vertebral artery here. You've got branches coming off here. So this is probably your pica probably your ICA here and your superior cerebellar here. Um So the three main branches of the basilar uh of the vertebra going into the basilar basilar artery here and then finishes into your two PC A S and then on the far left, um you can see this is a left IC A injection. So you can see again, middle cerebral coming off here, you can see your two anterior cerebral and in the center there's that Acom aneurysm we were looking for. Um So this shows shows really nicely the target um target that we're looking for. Then we can look at these pictures in slightly more detail and the radiologist can make some nice pictures from it. Um So you can see, oh, sorry, I'm just trying to move this text box. Um So you can see on the left, this is just a magnified um view of what we've seen. So again, IC A MC A two AC A s and A come in the middle and the one below it again is also your IC A but instead of being uh a coronal or frontal view, this is a side on Sagittal view. So you can see IC A coming up here, your AC A is curving back here and you can probably just about see your Acom in the middle there. And then this picture here shows nicely the Acom aneurysm sitting here in the center. So as I mentioned, once you've done the DS A and seen the nice pictures, you can then try and coil it. Um So using the same guide wire that you've used to inject. The contrast, you can pass thin um coils up it. Um And these small coil metal coils fill the aneurysm, um they stop flow blood flow blood through the aneurysm, the aneurysm thromboses and is no longer a risk of bleeding. So that's essentially how a coiling of an aneurysm works. Um Sometimes that's not possible and in this patient's case, the neck of the aneurysm. So this bit here, the base of it was too wide. So whenever a coil was passed up here, it just slipped back down again in that situation. Um We're forced to, to try and another option to treat it. So that was when a patient would be offered a surgical clipping, which this patient was. So in terms of clipping an aneurysm, here's some photos these are taken from the internet, obviously rather than this patient. So this is a standard oh, criteria for call versus clipping. Good question. So, um again, there was a big trial done called the I A trial, um which was um a Multicenter International trial looking at um ruptured aneurysms and it was a direct comparator between coiling and clipping in terms of efficacy of treating aneurysms and the safety. And um following that trial, it showed that the um efficacy and well the efficacy was comparable and that um treating aneurysms by coiling was considerably safer in terms of adverse outcomes. So people either with a poor functional outcome or, or dying. So nowadays, pretty much all aneurysms if possible will be coiled and that will every, every patient will have a DS A to look at it and pretty much every aneurysm they will attempt to coil. So they, the interventional neuroradiologist have first refusal. Um and if they are unable to or it looks technically challenging or as we said, a wide neck, um then then we will clip um the only um uh kind of alternative to that is if a patient has a very large parenchymal hemorrhage. This is typically with the middle cerebral artery aneurysms. And if that person has such a big um intraparenchymal hemorrhage, that they need to have an operation anyway to take that hemorrhage out, then we would obviously kick the aneurysm at the same time. Um But like I say, for the most part, first refusal goes to the IRS, they will try to coil first and if they're unable to coil, then we will clip it. Um So on the left here, this is the standard positioning. Um for a clipping, we'll do a standard pterional craniotomy, which some of you might have heard of. Um So craniotomy located over the teron um uh sh you can see is this region here and this green bit here is uh what is the kind of hole we would make? So that's the standard pterional um craniotomy, that green shape there. And here you can see a nice aneurysm um looking up at us and this picture here, you can see the tip across it. And on the far right, you can see what a standard aneurysm clip looks like. Um So this patient went for clipping because they weren't able to coil and this is what her scan looked like afterwards. So you can see here. Um You can see the hole in the bone where we had to make a burr hole. You can see on this one here again where we went through and you can see this metal artifact in the center is um is the k we paste across our aneurysm. So she's all right on the water a couple of days. Um Her external ventricular drain is working well. Um But on day five, despite still being GSS 15, she says she suddenly can't move her leg and she can't lift her leg at all off of the bed. Um Any thoughts on what might have happened to her? Good. Someone said vasospasm, we've talked about vasospasm so much. We all knew it would cause it. So someone said rebleed so good. So, um, once we've clipped um, that scan, we did, I just showed you a second ago, we'd always do a CT scan afterwards and we can tell on that whether the aneurysm has been definitively treated. Um, you're completely right. She may well have, if we'd have looked at that scan and said, actually the clip's not completely over it. There's a small bit of aneurysm we've left and she completely could have had AAA rebleed. Um But we were happy with her scan that the clip was completely off across the aneurysm and there was, there was no aneurysm left to bleed, but that's a very good thought. Um So, no, so, so, um, new isolated weakness, um is, is, is often consistent with vasospasm as, as someone correctly said. Um So any idea what investigation we should do to confirm whether she's, well, whether it's likely she's got vasospasm or not. So you, yeah, absolutely. So, again, it's not very commonly used in the UK. There's lots of face in the UK that don't use transcranial Doppler. Um But you, yeah, you absolutely can use transcranial Doppler. Um, in terms of something slightly slim, simpler, um, most places would start off with doing uh another CT head and a CT angiogram, um which is what we did for her. Um So, so we've talked about vasospasm a lot without yet really explaining what it is. Um as the name suggests, it's spasming or, or narrowing of the intracerebral arteries. And this is one of the major complications um associated with um aneurysm, subin noid hemorrhage along with the rebleeding and hydrocephaly. You've already mentioned um This most commonly peaks around day 4 to 7. Um And as you've mentioned already, the only intervention that's been proven based on randomized control trials um to, to try and prevent or reduce this is is niMODipine. Um And the problem with vasospasm is if you have the arteries in your brain narrowing or spasming, obviously, that reduces blood flow to a certain part of the brain. And if blood flow is sufficiently reduced, it can cause ischemia. And um if that ischemia persists, then obviously, you can get an established infarction. So people often present with, as I said, limb weakness because it's, it's essentially similar to a ti a or a stroke. They have reduced blood flow to a certain part of the body. Um and, and they, they present with a limb deficit. So this patient having new leg weakness would be very consistent with her having vasospasm. And as you mentioned earlier, with this Triple H therapy, in order to try and prevent this or treat this, we have to try and um increase the caliber of those vessels and stop the spasm. So we do this by giving them lots and lots of fluid so that the um the vessels are, are, are filled with blood. Um We hypertense them because if we push force the BP, force the BP through, um then it opens up the the intracranial arteries and then if needs be, we can do a uh an angioplasty. So what we would normally do with these patients, we'd normally admit them to the intensive care unit for a few days and try and get their BP sometimes as high as 100 and 80 or 200 systolic. Um and often to try and get a BP that high simple fluids is not sufficient and they need um vasopressors. So, medications such as metaraminol or noradrenaline, um in order to achieve blood pressures this high. So, so all of these patients pretty much will go to the intensive care unit to have this treatment. Um If two or three days worth of hypertensive therapy with, with vasopressor doesn't work, then again, we'd talk to our colleagues in interventional neuroradiology who again would do another um digital subtraction angiography. And during that, they can either inject niMODipine directly into the arteries um with the guide wire or they can do a mechanical angioplasty. So they can place something such as a small metal stent to physically keep the blood vessels open. Um So that's how we, how, how we treat vasospasm. So this is our patient scan. So you can see here this was her one of her early post post-surgery um scans. So you can see as we saw clip placed here. Um uh The only reason you can't see this middle cerebral, I think is actually just the um the slice we're looking at, but you can see middle cerebral here and you can see ac here. Whereas if you look at this one afterwards, you can see how thready the A CS are here. Um And that would fit because vasospasm typically affects the territory where, where the um the aneurysm and the bleed is um the mechanisms of vasospasm are not very well understood. But in the most simplistic terms, we know that having a very heavy blood load in the brain is extremely irritant to blood vessels. So they hate having fresh blood around them. Um So when there's a very and that's why our fissure score, you know, the the higher the blood load, the more likely you are to have vasospasm. When there's very heavy blood load, the blood vessels get very irritated and then they enter this spasm and like I say, you can see that nicely on this um on this scan where this ac A you can see really well here is, is, is thready and almost nonexistent on this right hand side. And what this causes is something like this. So you can see here this um she's now got a a right sided ac infarction. So even with hypertensive therapy and, and, and all our little measures, she unfortunately has irreversible ischemia in that region. So we've treated her spasm as best we can. We've treated her hydrocephalus. Unfortunately, our patient is very, very unlucky. And whilst this has all been going on, obviously, these patients have blood tests every day to keep a close eye on them. And suddenly you notice this. So you can see that as the days have gone on. You can see this was literally only only a couple of weeks ago as the days have been going on. She's suddenly developed hyponatremia. So this is this is her sodium there. Um What does anyone know about sodium and subarachnoid hemorrhage? What can, what can happen with people with sodium and subarachnoid hemorrhage? Any thoughts? Ok. So, so people with separate hemorrhage get lots and lots of or as I said, there are lots of sodium problems with, with people with sub hemorrhage. We've got yes, good. Someone's for si DH Fantastic. Anyone know the other one you tend to get with, with seid hemorrhage. The other type of sodium problem, we've got about 10, 15 or D I. Good. We've got about cerebral salt. Uh CS W so, CS W if anyone doesn't know is cerebral salt wasting good. So they are, those, those three are essentially the three sodium problems you get with, with, with brain problems. Um And we, like I, I was saying, we've got about 10 or 15 subarachnoid hemorrhages on our ward at the moment. And nearly every single one of them has had a problem with hyponatremia. So it's very, very, very common. So I'll just put this a little bit here. So um somebody did mention D ID I is diabetes insipidus. Um I must admit diabetes insipidus is not that common in subretinal hemorrhage. It's, it's normally and as you can see. So, so diabetes inhibits I've included it here because diabetes insipidus is normally a hypernatremia. Um But I've included it here because I think it's good to think of these three sodium abnormality causing conditions together because they can be a bit confusing. Um But like I said, so D I diabetes insipidus is, is less common in subretinal hemorrhage and it, and it's that typically causes hypernatremia. Um But it's good to think of these three together because they, like I say you get all three in, in, in different brain problems. Um So with Subhi noid hemorrhage, it's normally SDH so syndrome of inappropriate antidiuretic hormone or cerebral salt wasting and both of those cause hyponatremia and they, they have almost the completely opposite treatment. Um So it's, it's good to try and differentiate from them. Um So si DH as the name suggests, so you get inappropriate release of antidiuretic hormone. Um So that means you're um essentially retaining fluid because you're not diarrheas. So you can see at the bottom you get very high volume status, you might be edematous. You, you, like I say, you're retaining fluid. And the reason that causes low sodium is because your blood is very, very dilute. Um So you can see here you get a low serum osmolality. So that's um kind of the, the concentration of salt in your blood, which is very low because you're holding on to so much water. Um As a result of that, you normally get quite high urinary sodium because you're trying to, you pee out sodium to try and make water follow it. Um So you get a high urinary sodium but you tend to have quite a low urine output, as you said, because you're holding on to water. So this is the, this is the um uh kind of set of abnormalities you get in SI A DH and um we'll talk about the treatment in a second. Whereas um cerebral salt wasting, which is um the other type of sodium abnormality which um which causes hyponatremia in cerebral salt wasting. The primary problem is that you pee out too much salt. So, even though in s ADH, you end up peeing out a lot of salt, that's not the primary mechanism. That's a, that's a um a compensatory mechanism to you holding onto too much fluid in cerebral salt wasting. The primary problem is that you pee out too much salt. Um because of that, you um pee out a lot of water to try and balance that, um that salt you're peeing out. So that's why it's very different to SI DH because you have a high urine output versus a low urine output. And you tend to be um have a very low volume status. So you'll be very dehydrated versus SI DH where you're holding on to all your water. So the easiest way I say the easiest way, but one of the key ways to differentiate between these two is to look at the volume status of the patient, look at how much they're peeing. Um And, and whether they're dehydrated or whether they, they, they seem fluid overloaded. Um And for all these patients, we would send a serum osmolality, urine, osmolality and urinary sodium. Once we see that the sodium goes off. And like I said, just to mention D I um not typically seen in sub aid hemorrhage though we have got a patient at the moment who has got very bad dia D I is a diabetes insipidus. Um So, whereas si A DH is, you've got too much antidiuretic hormone, diabetes, insipidus is where you don't have enough antidiuretic hormone. Um, and this is more common in pituitary problems. So this is more, um, people who've got pituitary adenomas or have had pituitary surgery. Um, so because you don't have enough of this antidiuretic hormone, you pee out loads and loads and loads. Um, so people have huge volumes of urine, very dilute urine and because that their, their, um, their blood becomes hugely concentrated with salt, which is why they're usually hypernatremic. Um And these are people who say they can't stop peeing and they're extremely thirsty. Um But like I say, this is typically more in pituitary abnormalities, but it's, it's worth including this in the spectrum of sodium disorders because we do see all three in, in neurosurgical problems. Um And the reason I said this is important is because the treatment is quite different. So for S ADH, I put fluid restriction there, um the treatment for S A DH is fluid restriction. We've just said that they're holding onto too much fluid, they're edematous, they're not peeing enough. You have to be a little bit cautious in subretinal hemorrhage. Um As I've just mentioned, the risk of vasospasm is high and I've just said that to treat vasospasm, they've had to be very well hydrated. Um You know, hypovolemic hemo diluted. So we have to be a little bit careful. Um So we, we do this kind of in conjunction with our endocrine colleagues because in an ideal world world, people who have SDH for other medical problemss, you would food restrict them. So we can, we try and do a little bit of fluid restriction with caution and they need hypertonic saline and salt tablets. Whereas with cerebral salt wasting, we've just said that they're often pee out large volumes to follow the salt that they're peeing. So these people need lots of supplementary fluids and they may also have hypotonic saline and salt tablets. So, so slightly different treatments. Um because for S ADH, you definitely don't want to over hydrate them. Um But like I say, the problem with S ADH is that fluid restriction can be a bit risky in Subhi hemorrhage because of because of the risk of vasospasm. Um That's actually my last slide about case one. So before we move on to case two, we'll just summarize. So we had a lady who was presented with an acute subarachnoid hemorrhage from an anterior communicating artery aneurysm. She had the initial protocol initiated. However, despite that, she suffered a rebleed early on because of the rebleed, she got intraventricular hemorrhage and hydrocephalus needing a drain which is common. She then developed uh she then, so then she was treated, she had a failed coiling. So she underwent surgical clipping. She then developed vasospasm and had to have hypertensive treatment. She then developed um hyponatremia must admit I can't remember if she was SDH or cerebral salt wasting but she required treatment for, for hyponatremia and sub hemorrhage. Um and this is, I mean, not all patients have every one of those complications but, but most patients will have at least one or two of those complications. So that's not a, not an uncommon pattern. And these are all the complications or the serious complications you can have with sub retinoid hemorrhage. So, hydrocephalus, rebleeding, um spasm and sodium abnormalities um before we move on, I don't know if anyone's got any quick questions about anything subarachnoid hemorrhage related. Anything about the case? That didn't make sense? Cool. I think everyone's happy. So, like I said, the, the last one is literally, it's sort of 15 minutes just a, a quick one to finish off because I think it's about your hemorrhages. It was um is a very chunky topic. But for something a little bit different, we're gonna do a little bit of spine. Um I think everyone gets focused on cranial stuff. So we'll do a little bit of spine for those interesting spines. This is our second case. Um So again, this is a um I think a history of someone we saw recently. So this is a, a 34 year old guy um who for the last six months has had lower back pain and some leg pain in his right leg. However, the last two weeks, instead of just having sciatica in one leg, he's had sciatica in both his legs and for the last 24 hours. He feels as though he can't completely empty his bladder. He's having to go multiple times, um, because he goes to the toilet and, and, and feels that he can go again a short while later. And this morning he had, um, an episode where he went to the bathroom and a short time while later had some incontinence. Um, he's normally fit and well, um, with no significant past medical history. Um So what are, what are thoughts going through people's mind at the moment? What's, what are we worried about? So, someone's put ce s so called quina syndrome. Good. So obviously, the next stage for him would be to examine him. So he's as expected, Jesus 15, he's got antalgic gates who he's clearly in pain when he walks. Um We do a straight leg test on both sides. So a patient lies flat on the bed and we ask them to lift their legs straight in the air and he can't do that past 15 degrees on either side, which is abnormal. So once he gets to 15 degrees, he complains of severe shooting pain down the back of each leg. He doesn't have any deficit. So he's not got any weakness anywhere in the legs. Um And we do a apr examination on him. He's got normal anal tone and normal perianal sensation and we do a bladder scan. So we ask him to pass urine as much as he can and then we do an ultrasound scan of the bladder and he's got 230 mils left in his bladder. Does this change our thoughts? What do we think? What do we think is going on with this patient? And what investigation would we do? Will we do for him? Good. Someone said an MRI Spine. Anyone do anything other than an MRI spine, Dre? Because we, we've done the DRE already. So that was the normal anal tone, normal perianal sensation, but good Dre is very important. So, Dr a digital rectal examination or, or apr depending on your terminology. So hopefully, so hopefully everyone, everyone can see the most the thing we're most worried about here is cord quina syndrome. And in terms of spine, there's few red flag emergency pathologies, Corder Aquinas syndrome being one on a similar vein, metastatic spinal cord compression. And I think the only other one would be kind of a uh a serious spinal cord injury. They the kind of serious, I mean probably possibly a few others, you know, maybe spinal abscess, but but these are cords by far are bread and butter in terms of spine emergencies. Um So what is Cordner Syndrome? So it's good to have in your mind a very strict set of criteria um in order to, to diagnose or or to to say query cord quina syndrome, they should have back or leg pain. Um the leg pain can be in one leg, it can be in both legs. It may be only back pain, it may be only leg pain. And then in addition, they should have either a problem in bladder or bowel function. Um, would say we often say now any problems in bladder or bowel function cause, um, as you'll see in a second, there are different stages of cord quina syndrome. And people often say, you know, I've got urinary hesitancy, I've got urgency. II, I feel like I can't empty my bladder. So we we now say any, any evidence of, of bladder or bowel dysfunction, um sad, sad or genital sensory disturbance. Um And then the bottom one is, is a, is a severe uh progressive neurological deficit. So this is, this is the criteria for cord quina syndrome. And, and the reason I say this is I, I actually had a referral only about, I don't know, two days ago where I was referred to someone with new bladder and bowel dysfunction. Um but they had no back pain, no leg pain. They were refers to query cord require syndrome and, and, and it doesn't technically meet the criteria. So this is this is your criteria for cord require syndrome. Um And the reason I say any urinary symptom is important is that we, we do need to know that there are different stages or different. Um uh that Cordner syndrome is a, is a progressive problem and that we want to try and catch people before they develop complete Cordner syndrome. So, the first step in developing Cordner syndrome is bilateral ridiculous or bilateral leg pain. Um And I'll show you a diagram shortly about why people get bilateral leg pain before the urinary symptoms start. But so suspected in the first age is when people go from having an isolated unilateral leg pain to bilateral leg pain, incomplete is when they start to get any of these kind of vague bladder symptoms I talked about. So, um they say when they pass urine, they, they, they can't, they have the sensation of needing to go, but then when they go, they can't feel the flow. Um they say they're actually not having the desire to, to go to the toilet much at all. So they, they, you know, they, they in their head, they know they know they should go and try and pee. Um but they're not having the, the, you know, they're not getting the signals from the brain to go and pee. Um or like I say, they, they feel that they're going more often um or that they're having to push very hard to pee. So that would be an incomplete Qu Quina syndrome. Once you've gone past that stage, you go to the retention stage, which is what our patient sounds like he's possibly in. So when the nerves going to the bladder have reached a stage of compression, that um uh they now will no longer able to have the, the signal that it needs to empty. Um So, in that, um at that stage, you get neurogenic retention, so you no longer have the trigger to pass urine. So you retain it. And that's when you get incontinence because uh the con incontinence you get with qui is essentially an overflow incontinence. It's, you're not getting the, the, the parasympathetic signals to go to the bathroom. So your, your bladder fills up, fills up, fills up and then ultimately, it overflows. Um So that's why you start getting incontinence and then complete quina syndrome, which is the stage we never want to get to is where they have complete loss of, of parasympathetic sacral outflow. And that's when in addition to um the urinary retention with incontinence, they get um complete loss of anal tone, um complete loss of bladder bowel function, they get the, the sudden anesthesia or genital numbness. And that's when like I say, all of the sacral parasympathetic outflow has been damaged has, has been compressed. Um So we're trying to get patients in this either suspected incomplete or retention stage to prevent complete cord quina syndrome because, because complete Chord Aquinas syndrome is essentially, um you know, depending how long it's been left, it, it's essentially an irreversible state of loss of bladder or bowel function, um which obviously for patients and it's often young patients, um you know, is a, is devastating for their, you know, kind of you know, emotional mental wellbeing, if they, if you know, if you're a 34 year old with um complete bladder and bowel incontinence. Um So, like I said, we're trying to get them at these early stages. So this patient must have an MRI lumbar spine. Um We usually just start with the lumbar spine. Um uh Obviously, you can get problems further up the spine, which, which can cause bladder and bowel problems. But we're talking about Cordner syndrome. So compression of the quad, so compression of the, the lumbar sacral nerve roots. Um So we get an MRI lumbar spine in the first instance, how soon should this patient have an MRI? Anyone got any thoughts on on how soon we should do this in an ideal world asap good within 48 hours. So, I mean, so the, so the old, the old rule, you should just say uh as, as, as someone said is, is, is, is an emergency, MRI. So as soon as possible, if, if they're showing the symptoms of Corwin syndrome, do it as soon as possible. The problem is is that a lot of these patients obviously present to small district general hospitals and, and most of these don't have MRI uh scans overnight um in order to rule out Corrine syndrome and, and as part of the national guidelines, we have to say that every hospital in the country has access to an MRI 24 7, but often that access doesn't mean or it doesn't have to mean within their own hospital. It can mean referring to a local hospital who, who, um, there's a set up to provide an MRI. So we say in an ideal world emergency ASAP, but obviously if someone's at a neighboring hospital, they then need to be transferred to um, the bigger hospital that will do an MRI. Um, as I'm sure everyone knows there's something like, you know, many, many, many hour ambulance waits at the moment. So um it it can be really tough. Um But, but the the technical answer is as soon as possible. Um And actually you guys are getting the the brand new brand new guidelines. These were only released about I think a week ago. So these are the brand new um g so getting it right first time called Quina guidelines. Um And if you see here outlined in red, they've said that the current recommended standard is is within four hours. Um which to most people probably sounds like quite a long time. But if you know, if a patient is referred to me at one o'clock in the morning, um you know, they uh getting patient transport from a neighboring district general hospital, which in itself may be an hour away and then getting an emergency ambulance given the current status can be very hard. And then once they get to your hospital, you have to request it, you have to have the Mr radiographer come in overnight because they don't stay at a hospital overnight, they're at home and they get called and there's an emergency. So this four hours is very, very tricky. But this is like I say, this is the new gold standard and um I'd say everyone who's interested in your surgery, Google this because like I said, this is the brand new guidelines as of I think I got something about a week ago. So four hours is the current recommendation. Um This may be very basic for some of you. But I think a lot of people get very used to looking at CT heads. A lot of you may not have looked at many spine, MRI. S. So just this is just what a normal spine, MRI should look, it would look like. So, um when looking at a spine, MRI for pathology in pretty much every situation, we look at A T two first because obviously on T two, it shows up the, the CS F nice and brightly and white. So it's the easiest one to see most, most pathologies. And if we're considering cord quina syndrome, which is most commonly from a herniated disc, then T two is absolutely what you'd look at first. And we typically look at the sagittal and the axial, this is one normal sagittal um MRI would look like. So you can see here we've got the um the vertebral bodies outlined. Um we can see normal discs here, we can see the CS F in wide and you can see these um black um lumbar sacral nerve roots passing down. And if we look at the axial view of what a normal spine, MRI would look like. Again, we can see here um vertebral body or disc here um uh pars. So bony pars lamina and spinous process white CS F in the middle. And all these little black dots are the nerve roots of the quad qunu. And you can see that the black dots at the edge here, this is the foreman where the nerve roots exit, exit the the spinal canal. So these little black nerve roots will be exiting or traversing here. So you can see here one nerve root here is exiting and this one is passing down to exit the next level. But all of these black dots and nerve roots. Um So if we look at our patients, um well, before we look at our patients, MRI scan, like I said, this is, this is what we're looking at. So, um most commonly in lung pa in young patients, the the cause of corner syndrome is, is a disc herniation. Um in young patients, we have very soft discs. Um So as I'm sure you all know, you have your disc annulus um um with the, the soft um nucleus PPOs in the center. Um and, and what happens is through strain or wear or, you know, heavy lifting this soft um PPOs in the center can protrude out. And as you can see in this picture on the on the right, our patient probably had this um middle picture initially. So they had a little bit of protrusion of disc which irritated this nerve root, which is why they got unilateral leg pain. And the reason I mentioned earlier why bilateral leg pain is is a red flag is that if you're getting bilateral leg pain, it means that this disc protrusion has protruded centrally enough to get both this nerve root on this side and this nerve root on this side, which means it's very close to the quina. That's why um unilateral leg pain even though can still cause chona is less of a worry. It means the disc is probably to the side rather than in the center. So the central disc prolapses with bilateral leg pain are the real worry for quadra quer because it means it's right in the middle and it's very close to the to the, to the quad nerve roots. Um So this is the situation that we're that we're worried about in this patient. And this is just a sagittal view of that disc protruding and irritating a nerve root as it's as it's passing down. So this is what our our patient's MRI scan. So this axial is through this level here. Um I'll leave my arrow there. So I don't know if anyone um fancies saying what what they can see considering we've just seen what a normal MRI scan should look like. Good. Someone's put L4 disc protrusion, any other, any other um uh takers. So John's completely right. So remember if we count, so we're down the bottom so we'll count from the bottom up. So you've got L5 here, L4 here. So we can see between L4 and L5, you can already see this disc looks a little bit abnormal here. Whereas the other ones are all nice um sort of rectangular blocks. You can see that it's a little bit abnormal. And whereas at every other level, you can see lots of CS F um behind the virtual body and in front of the, the cord nerve roots here, you can see this dark bit here and this dark bit here. So you can see how tight it is there. So you can see a disc protrusion. And if you're looking at the axial again, it's not very helpful because I can't see the levels above and below. But I promise you this is a T two image. So there should be bright white CS F in this space here and it's all black, which means there's disc occupying the whole of the middle of that canal. Um And you can just about see probably a tiny bit of white there. The nerve roots are probably squished in there. So we can see that this is a very large L4 5 disc protrusion. So what should we do? This patients presented with bilateral leg pain, urinary symptoms. They've got 230 mils in their bladder which um we tend to say above 200 is definitely abnormal. Um sort of between 100 and 200. It's possibly abnormal, but above 200 is definitely abnormal. Um and they've got that 45 disc protrusion on their MRI scan. So, what should we do for them? Cool. Someone said laminectomy, Diskectomy 45 decompressive laminectomy. Lovely. So hope hopefully everyone agrees. We need to do something to take the pressure off. Um You know, the pre there's pressure on the the nerve roots. This patient has got Corder Quina syndrome, not complete, but they have got Corder Quina syndrome with urinary retention. So they need emergency surgery um to prevent them getting into that complete stage. So someone's put laminectomy and discectomy, someone's put decompressive laminectomy. There's kind of um uh a couple of different operations. Um So, so you can either they're kind of, you can do bits of one bits of both. Um So a laminectomy just refers to taking the laminar off. Um You can see on this picture on the left. So this is the spinous process. This is one lamina, this is the other lamina. So you can either do a hemilaminectomy which means take one lamina off, you can do a full laminectomy and take all of the back off. So the, the the spine is process and both lamina go or you can do it or you can do a discectomy. And what if someone's got Quina syndrome, what most people would do it very, what most people would do is they would do either a full laminectomy or a hemilaminectomy, which you can see in the right hand picture. This is a hemilaminectomy and then they would go around the spinal canal and do a discectomy. Um It would be unusual with, with a big disc protrusion to do a laminectomy only. Um But you can, but like I say, the variation would be as to whether someone does like this one on the right where they just remove a little bit of lamina to get to the disc or the one on the left where they would do a full laminectomy. And like I said, they would normally go for the nerve, go, go for the go for the disc again in that situation. Um But that, but so that's kind of what um the kind of the schools of thought are, but most people would do a laminectomy or hemilaminectomy with a microdiscectomy. Let's just pretend he presented with a slightly different history. Um This is the last bit. So I know we're going slightly over time. It's just so he had a slightly different history. So same patient. So again, six months of lower back pain and right leg sciatica again for two weeks he's had bilateral sciatica, um, no bladder or bowel symptoms. But for the last 24 hours, he feels as though he's been dragging his right foot and can't lift it up properly again. He's fit and well with no significant past medical history. Would your approach change? What are we thinking for this patient? Would, he's got no bladder or bowel symptoms. His pr examination is normal. His post void bladder scan is normal. Um But he's saying he can't lift his right foot up. Does that change our management? So someone could be a peripheral nerve problem? Any other thoughts? Can you get weakness um with a, with a big disc protrusion? Ok. So this, so this patient, so we know that um obviously all the nerve roots um in the lumbar spine, we we know that particular nerve roots control particular muscle groups. And um we know that people with a large L4 5 disc can present with a foot drop. Um So if you remember your um my atoms, your myotome controlling your ankle, dorsiflexion is your L4 nerve root. So if you have a large disc protrusion, pressing the exiting L4 foot drop, and if you remember that scan, I showed the, the, the criteria I showed you right at the beginning, if patients have lower back pain and leg pain and even without bladder or bowel symptoms, if they have a progressive or a significant focal neurological deficit, this is treated the same as a Quina syndrome. And they often call this major motor radiculopathy. So this is a foot and the most common, most common one is a foot drop. So this is treated essentially the same as a Cor Ana syndrome. Um again, essentially because this can be irreversible. And again, for a young person to have a permanent foot drop can be hugely disabling. Um So, so essentially, the answer is no, the management would not change. He again would have um an emergency MRI out of our. And again, if that demonstrated as we saw a large L4 5 disc which would fit with his symptoms, which it would, as we've said, um compression, the exiting L4 nerve root could cause would cause a foot drop. Then again, he would have emergency surgery um to prevent that foot drop becoming a AAA permanent deficit. Um So no, the answer is the man would not change. Um And I think this is, this is my, my last slide. This is a nice, this is slightly out of date because they've just released that new, that new thing. But this is something I've had saved on my phone for many, many, many years and produced by the SPNS. So the society um of um British Neurosurgeons and the British Association of Spinal Surgeons, and they've had this posters up in lots of A&E departments. It's, it's a really nice um clear thing you can Google it. Um and it's, it's just a quick guide about identifying cord quina syndrome. Um kind of guidance for MRI though, as I've said that now is the, the new guidance says it should be done within four hours and then the the the the kind of possible results. So it's either cord quina which needs treatment, might have other spinal pathology, which does need discussion with a spinal surgeon though not an emergency um or, or may not explain the symptoms at all. And, and essentially the referring team needs to look for for other problems which would explain why they've had similar symptoms to quina. Um Like I said, this is a nice thing to have on your phone as a quick, as a quick guidance. Um And I think that is my, I think that's my last slide. So um hope that was useful for everyone, like I say much more about sub, right? Because Cor Quina for the most part is a um does tend to be a, a reasonable reasonably. Um uh I won't say simple because the, the key thing is identifying it. But um but, but once you have identified it, it does seem it's kind of a, a bit easier to figure out what's going on and to treat it. Um So yeah, I don't know if anyone's got any questions, anything that wasn't clear about either of those? Thank you very much for that. Um MS Ingles. And if any, if anyone has any questions, feel free to put them in the chat or meet yourself as well? Oh, that's fine. Thank you. And before before you guys leave, you could fill out the um feedback form. I'll just post the QR code. Uh Can you guys see that? Cool. I'm not sure any questions. Thanks. Everyone who contributed. It makes it um uh nice when you track. So thank you to everyone who, who answered some of the questions. It's very good. Ok? And if no one has any questions, then see you guys tomorrow, we've got another session. You've got Jack tomorrow. Jack's very good as well. So you'll learn a lot from Jack tomorrow. Thank you very much. It was really nice to have it quite interactive as well. A lot of um back and forth which it was nice as well. Um Yeah, have a nice evening. I'll close the session in 23 minutes. Any last minute questions that might take a while to write, chuck them in otherwise. Thank you.