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Okay. Hi guys. Can you hear me? Okay, be nice to have some feedback. Okay, perfect. So, welcome to another bleeding event. And today we've got uh Doctor Ali, one of our uh rheumatologists uh who's going to be currently presented to us about acute rheumatological emergencies, quite a niche topic. So it'll be helpful to get, get a leg up on it. Um And I hope you guys enjoy and without further, I do, I'll hand over to Dr Ali. Thanks. Tell her. So, um Hi everyone. I'm Sabrina. I'm one of the Rheumatology registrars at Guilford at the moment. Um Thank you so much for the invitation. Um The plan for today's webinar is basically going to be a case based discussion of some acute rheumatology presentations that you might see on the take. Um But also um in general practice, for instance, things that you need to be aware of. So we'll talk about relevant differentials, investigations and management. I've got four cases to get through. So hopefully we'll have time for all of them. And I think it might be easiest if we, if we have questions after each case and if you can just put your questions in the chat, we can briefly go through them once I've done each case. So the first case um is a 75 year old patient who is known to rheumatology for rheumatoid arthritis and is um seen in clinic. Um for this, she has been quite well controlled for several years on sulfaSALAzine and hydroxychloroquine, which are a couple of dumb odds that we use quite commonly. Um, recently though she's been flaring quite often and she presents to the clinic saying she's had a few days of joint pain, headache and fatigue as well. When she's examined in the clinic, she has some mild synovitis in her wrists. Um Nothing much else to find on examination and blood tests done after the clinic show a CRP of around 30. So the doctor who sees her in clinic um says you're flaring with your rheumatoid, let's put up yourself a Saleh seen and that is the plan that is initiated. She doesn't want any steroids at this stage. So she doesn't get any a week later. However, she then presents to her GP with some neck stiffness, she feels quite uncomfortable although she's constitutionally well. So she's a febrile BP is um normal for her. Um So the G P isn't too worried about her but says, let's organize the cervical spine, X ray. You might have some spondylosis iss, there's no other red flag features here, but he does also organize some further blood tests as well a few days later. However, she then presents too, I casualty with a transient loss of vision in her left eye. The ophthalmologist look at the back of a ride, they look at the retina, they can't find any significant abnormalities. So they sent her along to the main hospital to get a CT head which is negative. And someone suggests that maybe she should have a rheumatology review on the ambulatory care unit. So this is where I first meet this patient on the ambulatory care unit where she's got quite a prominent left temporal artery with some tenderness as well. She's got concurrent scalp tenderness and PMR symptoms. So neck stiffness and shoulder stiffness too. She's got night sweats, occasionally drenching and a repeat of her blood test showed a CRPF 53 with an ESR of 80. And of course, she still has that headache which she mentioned in the clinic and got slightly lost amongst her joint flare. Her temporal artery ultrasound showed a positive halo sign. So this lady has giant cell arteritis, which is probably one of the, you know, communist rheumatological emergencies. But it's one that you definitely need to know about. It is an acute or subacute onset vasculitis of medium or large arteries. And the reason why it's an emergency is because there's a risk of irreversible bilateral visual loss, you can progress to stroke, aneurysms, etcetera. So it is time critical. There's a few baseline criteria that you would um take into account when you're looking at whether a patient could have G C A or not. Um Usually they above the age of 50 which is actually a conservative estimate. Normally, actually, patient's are above the age of 60. Um, but yes, any new headache in a patient above the age of 50 you have to rule out or at least think about G C A. The vast majority of patients have an abnormal CRP or ESR I think there's a lot of emphasis placed on E S are being abnormal and a lot of people wait for the ESR to come back before they make any decisions, which can take a little bit longer than the CRP. Um For rheumatologists, we actually usually disregard the ESR to be honest, we go much more by the CRP. Nowadays, it's very sensitive in G C A. And so I would urge you all to do the same. Um Occasionally you can get patient's who have a normal CRP and E S are who have G C A, but this is really quite rare. So, um in the vast majority of cases, you would expect to see an abnormality here. It's usually acute or subacute onset and there are some typical symptoms which will, will go into in a second. So what are you looking for in these patient's cranial symptoms you probably know about. So they often have a headache which can be temporal occipital. Um but it can also be quite generalized and non specific. They may have jaw or tongue claudications, which is quite a serious symptom. And it's important to elicit that this is actually claudications that we're talking about. So pain that is worse on chewing, worse on talking, not just jaw pain, which is actually very common in the elderly. Scalp. Tenderness is also uh an important sign to elicit because it's actually an early indicator of scalp ischemia. And if left untreated can actually go on uh to become scalp necrosis. In very severe cases of G C A visual symptoms are important, obviously, because it indicates complicated DCA as well. So you could have a whole range of things. Double vision, Amoros, iss uh monocular visual loss, which can then progress to become by uh binocular visual loss. You can get optic neuritis or optic atrophy. And that's actually what the ophthalmologists are looking for. Most of the time when you, when you, when they have a look at the slit lamp at the back of the eye as well. Um and evidence of central retinal artery occlusion, you can get ophthalmoplegia. And in fact, you can get cranial nerve palsies as well with G C A. So that's another important um thing not to miss when you're seeing patients with new cranial nerve um findings is do their CRP if it's raised to think about G C A constitutional symptoms are usually present in these patient's. So they might, they might have a fever, but usually they're quite tired. They've noticed weight loss if it's been going on for long enough and a lot of them will have sweats as well. And you may have some signs of large vessel vasculitis, which of course, not all patient's with G C A have, but it may occur alongside. So you can look for breweries or listen for breweries in the carotids or subclavian vessels and think about limb claudications. So, do they get any numbness when they're using their arm? Do they get pain when they're walking? Uh For example, so in terms of what the patient feels like, they often always say they feel unwell. So, you know, you often get referred patient's who've got a bit of a headache, crp of like 10. Um and it's query G C A and but they are otherwise fine in G C A. Often they do really feel quite poorly. You expect raised inflammatory markers and there's often other clues in the blood tests to look for, to suggest there's an inflammatory process going on. So, anemia, thrombocytosis iss sometimes you can get hypoalbuminemia if it's quite severe, this is just a photo of a thickened temporal artery. So if you see that, then that's obviously a big clue as to whether there could be something going on, but it's not present in everybody. A temporal artery ultrasound is the first line investigation. If you're suspecting um someone with G C A this is a temporal artery ultrasound. On the right here, you can just about make out this um where the arrows are that's called a halo. Its an echolucent halo. That's what confirms the diagnosis of G C eight. It indicates wall um inflammation just after that. On the right. Can you see there's an area of stenosis where there's no flow on the Doppler. So that's a complication of long standing G C A as well. So Temple ultra ultrasound is quite sensitive if done within the first few days of a patient starting steroids, the longer you leave it, the less likely you are to see a halo on that um on that scan. So if there's a high pretest probability that the patient's got G C A, the temporal artery ultrasound is negative um sorry, positive. You would then say yes, this patient has got G see A, you don't need to go any further, you stop there. So those patients' do not need a biopsy. But if the converse happens, if you have a patient, you're suspecting G C A N, the ultrasound is negative, you may then want to go ahead and do a temporal artery biopsy. Remember that temporal artery biopsies are also not um completely 100% accurate. You might have skipped lesions within the temporal artery. So you may miss cases of G C A if you're relying on those alone and that's why the pretest probability is quite important. Your clinical instinct as to whether you think this patient has got G C A or not, usually the biopsies have to be done within two weeks to get a positive result. Um but it depends on where you work and how available that is to you. So I've included this, this is the South end G C A probability score which a lot of trust they're using now um in their G C A pathways to try and make life a bit easier for you guys and work out whether it's likely that a patient actually has G C A. So you can see there's lots of factors it takes into account. Um and the cut off score above which it is likely that G C A is, the diagnosis is nine. So in my trust that I work at the moment below nine, it's not even considered worth referring to rheumatology. But I think if you're still suspicious, it's always worth a discussion because there's always that odd case that will slip through the net. But generally, this is a very useful way of looking at G C A. So what are you gonna do about it? If the patient does not have any visual symptoms or jaw claudications, you give them steroids without delay, even if you're not sure if it's the diagnosis. A few days of steroids is not the end of the world. If they go blind, that's much more serious. So give them oral prednisoLONE 40 mg stat and continue that once a day and contact rheumatology. If they've got visual symptoms, it's managed slightly differently. Um So if it's evolving visual loss, you would pulse them with methylprednisolone. So you give them a status of 500 mg of IV and continue 60 mg of oral prednisoLONE as well. Draw claudications. I would also give 60 mg, we would then institute a weaning regimen, make sure they've got a PPI on board. Um and some at CAL D three in the longer term, steroids have used as a mainstay of treatment, but we can also use I'll six inhibition. So you would have heard of tocilizumab in the context of COVID, but it's been originally used for rheumatoid arthritis in G C A. Really? Um it is used as a kind of steroid sparing agent in patient's who flare um on steroids and you're not able to control their inflammation, but that's later down the line. So that's the end of the first case. Um Does anyone have any questions? Well, if you think of any, just just pop them in the chart and we can come back to it. So I'll carry on for now. So the second case is a patient that most of you will recognize. We see this all the time on the take. This is a 77 year old man um admitted to hospital with a full and long lie. He's got a past medical history of ischemic heart disease. He's got a bit of heart failure, BPH and osteoarthritis. And he's on sort of relevant drugs for that on examination. Um, it's documented that he's got some abdominal discomfort. Um, and he's got a palpable bladder. He's a little bit hypertensive, um, is in fast af with a temperature of 38.1. Uh, and he's saturating 96% on air. So, not too bad. He's got, um, site raised inflammatory markers. So white cells are 14 crp of 280 he's got an AKI so created another 190 baseline of around 90. His chest X ray doesn't show any evidence of infection. And um he has a bladder scan which shows quite a large residual volume. So he's catheterized and quite reasonably, he's treated with fluids and IV antibiotics for your oh sepsis. So day to into his admission, he's now on an elderly care award. His CRP is 200. So it has come down but it's not come down dramatically with intravenous antibiotics. He's then starts complaining of left knee pain and someone goes to examine him. It is a swollen left knee. He's got a restricted range of motion. It's quite warm a bit, erythema tous and he's got known osteoarthritis in this joint. So the team wonder whether he might be having a flare of his own way and they ask her repeat X ray. So an X ray in this case would probably be only helpful to exclude a fracture because this guy has had a fall and he's now got a swollen knee. It's not going to tell you anything in the context of his osteoarthritis. But you can see here that there's very severe osteoarthritis in this joint, he's got, um, joint space narrowing in the medial compartment. He's got quite extensive osteophytosis. Um, and also there's quite a lot of chondrocalcinosis. I can't point with my cursor, but I'm sure you can see that there's this in the cartilage is where there should just be clear space. There's a lot of chondrocalcinosis and kind of white change there. Now, this is not unusual osteoarthritis. Chondrocalcinosis is a known feature where you've got C P P D or calcium pyrophosphate crystals depositing in the mini sky and in the cartilage. Um and that can lead to kind of flares of osteoarthritis and joint pain. But nothing really that gives us a clue as to what's going on with this patient. So how are you going to approach a hot swollen joint? So you should approach them all in the same way. And that's really the main, the main learning point here. So, hot swollen joint is any acute joint, swelling and significant pain of less than two weeks duration. And the approach here should be the same for any joint apart from the axial skeleton. Okay. So that includes usually the hips as well. Um So any acutely hot swollen joint as we've been told multiple times during our training is septic arthritis until proven otherwise, especially there's restriction in movement. Remember that a joint can be septic if the patient does not have a fever. And if you've got a high clinical suspicion, you've still got to make sure you rule that out. It can also be septic in a not very erythema tous, not very hot or swollen joint as well. So, you know, especially the patient is immunocompromised, for example. So it's always important to keep it in the differential. The key is to aspirated the joint. Um If it is a native joint, do not aspirate joints which are prosthetic or have metal work in them, speak straight to orthopedics for that. But if it's a native joint, it's really helpful if you're able to aspirated. And I think knee aspirations is something that all trainees should learn how to do. Um I'm always happy to teach anyone who wants to learn it, but it's really important to do that early and preferably before they've had antibiotics. So, what investigations are you going to do? So you're gonna send that sign of your fluid that you've drained for microscopy culture and sensitivities and you're gonna do a gram stain, which can be done very quickly. If you take the sample to the lab, they can literally look at it straight away if you're really suspicious. And if you're really keen, um and you should also always send it for cytology, for crystals at the same time. Okay, because that saves the patient from having that done again. Um Polarizing like microscopy will be done for those, for those samples to look for crystals. You should send blood cultures, um and any other relevant cultures. Um So urine sputum, whatever it might be and routine bloods, obviously you would send that might change your antibiotic choice depending on if they've got renal impairment or liver, liver impairment. A your rate is often sent in these patient's because you think ok, they might have gout. But actually, it's really important to realize that you're, it does not have any diagnostic value in whether or not a patient has got gout or not. Um It often falls in an acute gout flare. So a normal, you're a gas ID level does not exclude gout. If it's less than 200 it's really very unlikely to be gout. But still you can't say that it is, it is or it isn't on that basis alone. Okay. Pro calcitonin is obviously something which has come in more, more and more nowadays um with regard to ruling out infection. But when it comes to a septic joint, you can have a septic joint with a normal pro calcitonin. So it's not yet there in terms of being able to definitively exclude it. Imaging. Um Yes. So we, like I said, we often do X rays to try and rule out things like fracture. You might see some signs of osteomyelitis on an X ray. Um but often it's not advanced enough for that to happen. So, if you're really worried and MRI is what would be useful because it can pick up early osteomyelitis and of course infusion, et cetera. So the differential diagnosis of acutely hospital and joint septic arthritis at the top, um and then crystal arthritis probably comes a close second in terms of the common things that we see um in hospital reactive arthritis is also quite common. You can get a mono arthritis in a condition that would usually have a polyarticular presentation. So for example, rheumatoid can present with Justin e or just an elbow, for example. And then you can have trauma which can cause ahem arthros iss, you can occasionally get spontaneous hemarthrosis as well in patients who are on warfarin or I T P or that sort of situation. So this is what the fluid looked like from this patient's knee aspirate when he eventually had it done. Um he had it stained and it showed gram negative rods. So he's got E coli in his knee and that was consistent with his blood and urine cultures. So essentially, he's got your oh sepsis which is seeded then into his joint as a secondary septic joint. His microscopy was also positive for um positively by refrigerant crystals that is consistent with the diagnosis of pseudo gout. And the point I wanted to make here is that often when you have osteoarthritis in a joint, you will have some CPPD crystals in that joint, even if they don't have an acute pseudo gout flare. So in this case, we'd obviously be sending this patient for a wash out and that's what happened. You wouldn't then need to concurrently treat him for a pseudo gout. Okay. It would be slightly different if, for example, we did the same aspirate and he had negatively by refrigerant crystals, he's then got gout. So you don't get gout crystals in a joint unless you've got active gout in that joint. So that's the difference between those two pathologies. In that case, I would send the patient for the washout, but I would probably still cover him for a gout flare. Does that make sense to everyone? So that's probably the most important take home message in this um in the set of cases because it's common to see um hot swollen joints in A and E on the take. And really the key thing is learn how to aspirate these joints. It'll really make your life easier as you go through your training. Okay. Next case. So this is a 55 year old lady um seen in E D with a rash on her face. Um She saw her GP initially and he thought okay. Yes. Um She's got a rash but she's got some other symptoms. So we better send her in to hospital. And the main thing that he was worried about is that she was getting really fatigued and she felt quite weak and short of breath when she was walking on an incline. Her symptoms have been going on for about a month, but it was acutely getting worse. She didn't have anything in the way of past medical history. She didn't, hadn't taken any new medication. So the ent doctor who sees had notices that she's got, um, a little rash. Um She's got some joint tenderness over her fingers, but not a lot of um sign of itis or inflammation. She's got some peeling skin on her hands as well and some crepitations in both her lung bases, most noticeably he finds that she is weak, so she's got weakness, affecting her upper and lower limbs and actually a little bit in her neck flexes as well. She says it's really difficult for me to hold my head up, which is obviously an important sign to elicit. She does not have any dysphasia. She does not have Ray knows she does not have fever or chest pain. So I'm saying those things because those are important negatives for you guys to ask about or important, you know, symptoms for you guys to ask about. So this is what her rash looks like. Um Sorry about the quality of the photo, but it's um it's all I could find with a good male. A rash. So um you can see that there, there's a little bit on her forehead as well. But if you look closely, you can see her lids are closed and she's got what we would describe as a heliotrope rash on her eyelids as well. Okay. So her CK comes back at 1800 which is obviously very elevated. She's got a mildly raised CRP. So she's referred to rheumatology, which is appropriate. We ask for a number of investigations. So she's week. So we need to demonstrate evidence of inflammation. The way we do that is with imaging. So we get an MRI we try and demonstrate it functionally. And the way I would do that is by getting an E M G, we send off some bloods. So a myositis immunoblot which if you're requesting it in hospitals, it is called an extended myositis panel. She also has a CT neck, chest abdomen pelvis and we ask for a baseline forced vital capacity as well. I should say that she had some baseline immunology which just showed an A, an A which was positive one in 6 40 but everything else was pretty much negative. So what does her, what all these investigations um find? So her ct chest abdomen pelvis shows evidence of early institutional lung disease. There is no lymphadenopathy and no evidence of malignancy. Her E MG does show some membrane instability and myelopathic changes in the proximal muscles, which is where you would expect to find um changes in the upper and lower limbs and the MRI of her thighs. As you can see here shows this diffuse T two signal which was increased across almost circumferentially but mostly in the anterior compartment consistent with um irisitis. She goes on to have a pet scan and the reason for this is really to exclude a malignancy and her extended my slightest panel comes back with Auntie Jo one antibody positivity. This is a classical antibody associated with dermatomyositis and something called the anti synthetase syndrome, which will go into in a second. Her HMG coa reductase antibodies are negative and that is associated with a sort of statin induced um myositis, but it can also be present in the absence of a patient taking statins. Interestingly, uh it causes a necrotic myopathy. So, idiopathic inflammatory myopathies um are kind of a range of heterogeneous, a range of disorders with lots of, lots of symptoms that can present in a number of different ways. You can get fatigue, you can get arthritis. Proximal weakness is obviously much more um suggestive of an inflammatory myocyte. You can get distal weakness in other conditions, but those tend to be neurological. Um there is a condition called inclusion body myositis, which is not inflammatory and tends to give you a much more distal picture of weakness. So it's important that you're demonstrators proximal dysphasia is is important but worrying sign of more severe myofascitis. Um Raynaud's phenomenon, you can get skin changes, classical skin changes. We've kind of alluded to a little bit. So you get the heliotrope rash, you can get um a little rash. You can get, got transport fuels on the knuckles, which are these discolorations on the knuckles that are raised. And you can also get some nail changes and mechanics hands and this patient actually did have mechanics hands, those with that was appealing, um peeling skin on her fingers, fever, shortness of breath because it is associated with interstitial lung disease and weight loss. So, quite a wide range, the anti synthetase syndrome um is characterized with a few antibodies in particular, but it tends to give you a bit more of a um distinct phenotype. So you get arthritis fever, ray, nose mice, itis I L D and mechanics hands. But there's a lot of overlap between all of these symptoms. So what are you expecting to find when you do blood tests on these patient's? So remember if a patient is week for whatever reason, just do A C K if it's raised. Obviously, it tells you that there may be inflammation going on. But there are cases of my sight is in which the CK can actually be normal. Um And patient's are often wasted at that point because they're muscle bulk is not high enough to mount. Then an inflammatory response doesn't mean they don't have active myositis. Ferritin tends to go up if you've got as an acute phase response and the L T tends to go up and this often confuses people as well because they think, oh, there's something going on with the liver but A L T, don't forget, is a skeletal muscle enzyme as well. And so that it's probably not coming from the liver at all. Um, it's usually from the muscle. You can get a raised troponin T and that can, that can be present in skeletal muscle, but it can also a trop I can be used to screen for cardiac involvement in myositis, which can also happen. You should do an A and A because you know, it's useful to see whether that's positive but it can be negative. And a myositis immunoblot is often done. And I've, I've list some of the antibodies below. You don't have to know what each of them are. I often have to look them up myself because there's just so many. But um it's just important to realize that a lot of antibodies are present and they are associated with sort of distinct phenotypes of disease. So I talked about the anti Sympathy Syndrome. That would be the anti Trna antibodies I've highlighted in the middle there, but you can get other forms of myositis that are associated with other things. Um um for example, Tiff one gamma antibodies associated very strongly with malignancy related myositis. So in those patients', you would definitely want to rule that out. So the key points to take away from this case, um recognizing uh the importance of a race C K in the context of a proximal weakness. I'm sure you all know that um ask about extra articular features that's really important to try and elicit whether it is indeed an inflammatory myositis. And what do you mean myositis? Could there be an overlap with another condition you can get, for example, lupus with a concurrent myositis. But unless you ask about the symptoms of lupus, you're not going to actually work out that that might be the diagnosis based on investigations. I've shown you all the investigations that we would check for a patient with myositis. So useful for you guys to know what those are. And if you're seeing a patient who's coming into hospital with suspected myositis, I would always do a forced vital capacity. These patient's can deteriorate very quickly on the wards and often the FBC is what is going to be going down because of diaphragmatic weakness. Another tip is that it's often worth asking a patient if they can lie flat because if they can lie flat comfortably, they probably don't have diaphragmatic weakness when they come into hospital because you actually need your diaphragm rather than, you know, you're, you're suppressing most of your intercostals in a supine position. So that's a good tip to ask them that if, if they can do that early escalation of deterioration, again, this comes back to the FEC and if you notice that it's falling less than 50% of when they first presented, you need to get I T U involved as they might need intubation. The last point is to look for malignancy. So, dermatomyositis especially is really strongly associated with malignancy in adults. And so we often end up doing pet scans on these patient's colonoscopies. Um to look hard for the condition for the underlying cancer. Sometimes it precedes cancer. So we don't find it, but we keep a close eye. We might get them into remission with the dermatomyositis. And then a few years later, they have a flare and that flare might actually represent the cancer then coming, you know, being able to be found. So really important to be vigilant in the monitoring of these patient's okay. So that's the third case. Any questions there guys? Okay. So we'll go into the last and final case. So this is a 65 year old man who is a Ukrainian descent. He works as a builder um in Central London. He has known B 27 positive A S. So ankylosing spondylitis on Adeline um AB which is an anti TNF um monoclonal antibody. So he's seen an A and E because he's generally not feeling great, his back pain and stiffness from his A I S is not really well controlled, but he's also noticed some shortness of breath. Um He's been quite feverish lately and he's quite myalgic. So when he's seen in A and E, he's a febrile, his sats are around 94% on air. So sort of borderline. Um He has a normal BP, heart rate of around 90. He has a raised inflammatory response to his white cells of 14.1 with a crp of 80 usually around 20. So higher than usual for him in the context of his A S this is his chest X ray. So you, I think you can just about make out he's got some consolidation um or patchy shadowing on the right side, but also a little bit on the left. So he's treated um with intravenous antibiotics for a community acquired pneumonia, bilateral pneumonia. Um And someone does send a TB Ellis spot which was negative because they, because of his background. So he actually had the antibiotics um in A and E and he was in hospital for less than a day. He wasn't requiring oxygen and he didn't look too unwell. So they sent him home. Um They let us know about him because his A s was not particularly well controlled. So I actually arranged to see him the next day when I met him, he was on all antibiotics from hospital. Still not feeling well actually. Um on further questioning, he was quite feverish at home. He'd been having sweats, he was still short of breath, but he did not have any chest pain examining him. He had some crepitations. So a little bit more on the right than on the left. Consistent with the findings on his chest X ray. He had a soft systolic murmur, um, and looking at his legs, he actually had a rash which looked like this. So it's probably not as dramatic as this, but definitely had a particular rash which was nonblanching on his lower legs. So we sent off some investigations. He still had a raised inflammatory response. So his white cells were a little bit lower but still elevated. His CRP was 95. So it hadn't really come down with the antibiotics at all. Um He had some changes as I discussed earlier clues as to whether there's something else going on. He was anemic, he was mildly hypoalbuminemic and his platelets were not too bad actually. So they weren't low, which is the main point here because he's got a particular rash. Um His urine dip showed blood and protein and his anchor, which you may have thought might be relevant. In this case was actually negative. He had um an A N A of one in 1 60 which is a weekly positive A N A may not be significant uh with a negative E N A which is the test that you would want to do when someone's got a positive DNA, you're suspecting they may have a connective tissue process. You check their DNA, which has a lot of other antibodies which may be relevant. And then his complement was also sent now complement our acute phase proteins. So in the context of some an inflammatory response, you would expect that the compliment would be elevated in this patient. His complement, see three you can see was low and his C four was, was normal. So at this point, there was one test that I wanted immediately to know what that was. Does, could anyone have a guess as to what we think might be going on here or what test you might want to do? Um I'll give it, I'll give it a minute to see if anyone can think of it. No guesses. Okay. So the one test that I would ask for straight away in the context of this patient in this scenario, with these blood tests would be a blood culture. So nothing rheumatological, just very simple and it was positive for one of the hatchet group organisms. I can't remember which one. So I just said the group and we got an urgent echocardiogram which confirmed infective endocarditis. In this patient. He had aortic valve vegetations and the findings on the chest X ray, which was presumed to be a cap was actually consolidation secondary to septic emboli. Okay. So he was admitted under cardiology for intravenous antibiotics and his anti TNF was discontinued. So that's a short case. But I thought it really illustrated a few points. Um The first thing is to do the basics really well. So take a proper history and examination. I don't think that was done in this case to a great extent because the chest X ray was done quite early. And so it was assumed, okay, this patient's got a cap. Um And really, if you really talk to him and explored a bit more about his symptoms was, you know, there's something a bit more serious going on. Um uh murmur was also not detected initially. He is immunocompromised. And that's the key point here. So always take blood cultures in an immunocompromised patient if they're presenting with, you know, an inflammatory or infective sounding history, even if they're a febrile when they see you. And that's often what happens is that they don't tend to be fibril. Um So no one gets the culture done, but actually, it might really be relevant. Okay. The other point that this case illustrates is that there's a really wide range of mimics and rheumatology. Not all acute rheumatology is rheumatological and there's a lot of infection and malignancy which can present to rheumatology acutely. So it's always worth keeping that on your differentials list. A lot of people will look at a particular rash and say that looks like vasculitis. This is anca vasculitis because anchor remember takes a few days to come back. So you would not have had that result at the outset the negative anchor, but really, you know, it had nothing to do with, it was important to send it. But um that's not the diagnosis here and you would have potentially made this patient quite sick. Um If you had kind of completely disregarded his symptoms as a as a vasculitis, your analysis is also a very important test. It's a simple one, but it's important to document it for blood and protein. If there is blood, send it for red cell casts, microscopy. If there is protein, send it for protein creatinine ratio and do that at the beginning when you're first seeing the patient, it's really, really helpful. Um And it often isn't, isn't really well documented or clear. Okay. And the last thing I just wanted to say was about isolated, see three deficiency. So a bit more of a niche point but quite useful one to know about because there's not a lot of causes of low C three um in the absence of a low C four. So if it's just see three, which is down, endocarditis can do that because it activates the complement. Um Lupus can also do that although it tends to be C three and C four which go down together, that's the more common pattern than Lupus. But you can get a C three which is just down on its own. And um cryoglobulinemia is the other one which can cause an isolated, see three deficiency can also cause a particular rash. All of those three conditions can cause a particular rash. So that's just a good way, a good test to do because you can actually get compliment back on blood test quite quickly. It's not, it doesn't take a long time like the antibody tests. Um So it can be useful in um in cases like this. Okay. So, um that's all I wanted to say. Um I hope that was helpful for you guys. Um Just a very quick run through of some cases which all of these are genuine cases that I've seen in the last couple of years. Um It just goes to show that it's rheumatology is not actually difficult. It's just about keeping a very um broad mind as to what the underlying condition might be and not jumping to conclusions and like I said, just doing the basics really well. Okay. So if anyone's got any questions about any of those cases, please just put it in the chat, um or you can email me afterwards if that, if that works for you. Um And if anyone's at Guilford and you're interested in learning a bit more about joint injection, just email me, please because we can set something up if you would like. Thank you. Thank you so much. That was, that was, that was great. Um Really insightful. Um Thank you for giving us your time and uh on a random evening, um uh would you be able to stick around for a couple of minutes just in case there are any questions? Yeah, sure, no problem. I think there's one question already. So what does it mean to send a patient for a wash out. So that's a good question. Essentially. That's when a patient has septic arthritis, they go to theater and literally, that's what they do. They wash out the joint. So with lots of saline, they clear out all the puss and, um, muck that's in the joint and then wash it out with lots of saline. And, uh, I think historically, they used to um, use intra-articular antibiotics. I'm not sure if they do that anymore. Um But yeah, that's what they do and sometimes patient's require more than one wash out because you can get a re accumulation of, of puss in the joint. Um Yeah, that's what, that's what the orthopedic surgeons do. So, septic arthritis, um It really can destroy the joint in ours today's. Um So that's why we take it so seriously. Um And if it's missed, it can be quite um quite serious for the patient. Um When should we test the C three C four? So not, I mean, it's not something that I would expect you guys to be testing for routinely. Um I think if you saw a patient who had existing lupus, which of course we do see patients who already have a diagnosis of lupus, I would definitely test for C three and C four because if it is normal, that makes me less worried as a rheumatologist that this patient has active severe lupus going on. Um If it's low, it's much more likely that they're having a flare of their lupus. So that's really helpful to decide what treatments to do next. Um And then I guess when you're dealing with unusual presentations, like for example, a particular rash is a good time to do it because as I said, um those some of those conditions can lead to a low C three by all means test for C three C four. You know, it's like I said, you'll get the test back quite quickly, but I wouldn't be doing it in your standard box, standard patient. Any other questions guys can ask me anything. It doesn't have to be on these cases just in general, you guys, if I if I could button and quickly say, could you please provide some feedback so that we can sort of improve in the future and it will help Sabrin also? Yes, that would be great. Thank you everyone for in advance for giving me some feedback. Why would Lupus not be a differential for the Dermatomyositis case? It absolutely would be that's a really good point. Um So that's kind of what I was alluding to when I mentioned about asking um about features in the history which would point more towards Lupus. So if it was pure, so sorry, if it was Lupus with mice, ITIS, I would expect you to have some other features of Lupus. Now, I didn't talk about Lupus as a separate case, but some of those things would be, for example, um or ulceration, you might get pleuritic chest pain, you might get um abnormalities on your blood tests, including thrombocytopenia, leukopenia. So all of those clues which would lead you a bit more towards lupus with overlap myositis. But I think having a heliotrope rash in addition to the mail, a rash that's unlikely in lupus. That tends to be more with dermatomyositis mechanics. Hands again tends to be more towards a myositis type presentation. But ultimately, the immunology is kind of what pushes you towards, um, you know, the myositis being, being the main diagnosis because AJO one is very typical for dermatomyositis. You wouldn't see that in Lupus. Um Yes, I think the caveat is always in rheumatology. You can get unusual things, you can get overlaps, but you have to kind of make a decision as to what broad category the patient is fitting into. Um, and then proceed from there rather than trying to work out the intricacies of the immunology. That's not really what you need to do. The thing is, is it doesn't look like a myositis. Is it a dermatomyositis? Yes. Possibly. Is it Lupus myositis? Yes, possibly. But at that point, it doesn't really matter because your initial investigations are what's important. Okay. Cool. I think that's probably all the questions. Um But yeah, I'm sorry, I should turn my camera on. So if anyone's working at Guilford, um and this is what I look like. So if you see me in the corridor, just catch me. Um And if you want to come to some rheumatology clinics or, you know, like I said, if you want to learn a bit more about joint injections, just let me know and I'm happy to happy to help. Thanks very much guys. Thank you so much guys. 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