BONUS CASE: An unusual cause of back pain (thinking beyond the spine)

Dr Chris Wincup talks to Dr Shiza Ahmed & Professor Abhishek Abhishek in this bonus case episode. They discuss an unusual case of acute back pain & reduced mobility. Can you work out the diagnosis?

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Transcript

You're listening to the Talking Rheumatology Spotlight podcast, brought to you by the British Society for Rheumatology. Welcome to this Talking Rheumatology podcast. I'm delighted to be discussing a very interesting case here today, with two colleagues. So I am joined by Dr. Shiza Ahmed and Professor Abhishek Abhishek, who will be discussing an interesting case that was presented at the BSR Case-Based Conference last year, welcome to you both. Thanks very much for your time in discussing this case and if it's okay with you, we'll jump straight into it. So, Dr. Ahmed, perhaps you could start by talking us through this case, and can you perhaps just talk us a little bit initially through how the patient presented to hospital? 

Yes, of course. So first off, thank you so much for the opportunity, so I will, um, go straight into the case. Um, so I was introduced to this patient via, uh, my registrar at the time. So essentially, this was a 76 old female patient who presented to Emergency with a week-long history of back pain and reduced mobility. Um, so we started off by just taking a good history as to when the symptoms appeared, whether they were more sudden onset, and whether there was any preceding illnesses or trauma history, and she denied all of that. And then we also took a history of any constitutional symptoms, but she denied any fevers or sweats or any weight loss, and there were also no neurological red flags in the history. Um, so we dug a bit more about the past medical history, so we found out that she had chronic kidney disease, um, and she did have some cardiovascular risk factors as well. Um, under her medications, she was on diuretics and a couple more, um, antihypertensives and also on statins. And, uh, social history was actually quite important, too. So there was significant element of self-neglect. She hadn't seen many clinicians over quite a few time, wasn't very, um, much in contact with her primary physician either, and there was, um, a history of ETOH excess as well and then we moved on to assessing her. So examination-wise, she looked a very well patient. She was hemodynamically stable, we palpated her spine, and there was just some mild tenderness over the lumbar spine, and there was no focal neurology either. So we weren't extremely concerned about, um, the neurological symptoms or even the back pain, but we were more of thinking at this point whether this could be a fracture of, um, um, or anything. So then we moved on to obviously doing some investigations, essentially so the team sent off some bloods and typical stuff that we would send off in this case, like full blood count, renal profile, liver function tests, and CRP, bone profile was also sent off. Um, and the only interesting thing that came back on bloods was just a rise in CRP. So her CRP initially was 67, and the rest were actually quite unimpressive. Um, so I think at this point, we were already starting to think more like, "Is this or could this be an infection?" Especially with a history of significant self-neglect, um, we couldn't really take a detailed history of any previous infections or previous travel history. There wasn't much history, um, about that anyway and we were, I think, much lower down on the list of differentials, possibly a malignancy as well. So an X-ray spine was done initially, and we, we didn't find any convincing acute fractures on there. There were no, like, lytic lesions and much lower down was malignancy, and at this point, I think our prime re-differential was, this could be a spinal infection, essentially. Could this be a discitis, or could this be something like an epidural abscess? Um, and then an MRI of the whole spine was requested. 

Great. Thanks very much for that nice summary. So you had a patient presenting with, with back pain, um, and you've talked through those initial investigations, resulting in you then moving on to, to do this MRI scan. So can you talk us through what the results of that MRI scan showed? 

Um, so the MRI spine, um, kind of I think, consolidated what we were suspecting initially. So the MRI showed there was some edema and inflammatory changes, um, of the L2, L3 spinous processes and adjacent soft tissue. And there were some previous fractures of T12, um, and L1, but, uh, the symptoms, um, that they weren't really acute to cause these level of symptoms, essentially. The radiologist who reported it, as I've already mentioned, his differentials, which were infection or malignancy. And we were already thinking about that anyway, whether this could be a simple, not, not simple, essentially, but a spinal infection. So, um, she had already been commenced on broad-spectrum antibiotics and theoretically, and then we continued on the IV antibiotics, um, hoping that her symptoms would resolve and her CRP would, would start to improve as well. 

And, and perhaps you can tell us a little bit about what happened next. So, so you mentioned the patient had a high CRP. They were started on antibiotics. What, what, what happened next in this patient's case? 

A few days down the road, when we were expecting things would, things would improve, there wasn't much improvement in symptomatology at all really, and the CRP actually started climbing, and at this point, we were also, we had already thought about a possible malignancy, and serum electrophoresis was negative. Bone profile was essentially all okay. So we were a bit stumped as to why the CRP was climbing, and we had already started to think about whether this could be a hematogenous spread of infection from other sites. So we, for instance, did an echocardiogram to rule out any infective endocarditis. We already did a TB screen, which was also negative. So at this point, we were quite stumped, essentially, as to why the CRP was climbing. There was no difference in her mobility or the pain itself, and clearly, the antibiotics were not working. And so, um, at that time, then we just took a step back. We stopped her antibiotics, clearly they were not working, and just re-evaluated the whole situation. So we went through her history again, and there weren't any new points in the history. Um, and then we, uh, naturally did a repeat examination as to just, just try and ascertain whether we've missed something, and that examination actually just changed, um, our perspective completely. So on peripheral examination, this time around, we were able to, um, identify gouty tophi in the finger pulps over the olecranon bursa and her feet as well. Um, so I, I think this was Dr. Soy's light bulb moment when he sent off, um, a uric acid level that came back as raised at naught point four eight, I think, millimole per liter, and the ESR was significantly raised as well at, 118. Now, this is the point we were starting to think whether this could be axial gout, in fact, and, um, obviously, it's, it's really challenging to obtain an aspirate of the joint, and crystals would normally be diagnostic as per the ACR and, uh, European Alliance of Associations for Rheumatology, uh, classification criteria but, um, naturally, this would have been a very difficult aspirate, CT-guided aspirate, but they're not very feasible. So then we ordered a DECT scan, and that did confirm urate crystal deposition in the lumbar spine. Um, so yeah, she was diagnosed with polyarticular tophaceous gout with axial and peripheral involvement, and we started her on oral prednisolone, and that just made a remarkable difference to her pain, mobility, and her inflammatory markers. So, um, yeah, a, a definitely a good outcome. 

Fantastic. Thank you very much for, for discussing the, the clinical challenge and, and how you approached that very difficult case. Um, so we've got, uh, Professor Abhishek on the, on the call as well. I would like to perhaps direct the next, uh, question towards him, and, and this really is relating to DECT scanning. Um, so, so you mentioned the DECT scanning was important in clinching the diagnosis in this case. Professor Abhishek, can you perhaps tell us a little bit about, uh, DECT scanning and how it can be helpful in, uh, clinching a diagnosis of gout, particularly in challenging cases like this? 

Yeah, thanks for asking me this question. And, and, and dual-energy CT is, um, is a very commonly used investigation in hospital practice. So all of our urology, uh, colleagues and radiologists are using it to characterize the u- the, the renal stones. And dual-energy CT, uh, essentially involves, uh, two energies of beams or two different, um, sort of kinds of, uh, beams going through, um, which helps software work out whether the deposition is urate related or whether it is related to, uh, calcium crystals. So, uh, in patients who have got relatively large deposits of urate, dual-energy CT is quite specific at detecting, uh, urate deposition. So it is really useful in patients who've got, um, atypical manifestations. So sometimes patients present with a large lump near, near their ankle, or, as in this case, happened in the spine. And demonstrating urate crystals in the index area can be really helpful and avoids things like biopsy. Um, many times, gouty tophi can appear as a lump near the ankle or wrist, and, and DECT can be helpful. Again, there are a couple of caveats while we, uh, discuss DECT, it's really important to remember that DECT is not very sensitive for diagnosis of gout. So in patients with early gout, yeah, in patients with, with early gout, in the first couple of year of, of symptoms or in patients with infrequent flares, the DECT may not be as sensitive, um, in helping reach a diagnosis of gout and the alternate, um, investigation, such as, uh, joint aspiration, maybe using ultrasound guidance, if needed, should be really pursued. So, so a negative DECT in early phases of gout doesn't rule out a gout diagnosis, but in patients with atypical, uh, uh, presentation and, uh, spinal involvement, um, or suspicion of, of soft tissue tumor, et cetera, DECT can be really helpful in clinching the diagnosis because it really tells us whether the deposition is urate related or calcium related. 

Fantastic. Thank, thank you very much. And I, I think, uh, as Dr. Ahmed was saying, that in this case, the patient was treated with, with steroids. So perhaps my, my question, Professor Abhishek, relates to, um, management, um, uh, of these type of cases, and, and how would you typically approach, uh, spinal gout, and how may this differ from treating gout affecting predominantly the peripheral joints? 

So in terms of acute flare, this is what this patient had. She had a flare affecting her spinal cord deposits. The treatment is to, is to manage the flare, and generally, these patients have got quite large urate burden. So, uh, and generally, they have comorbidities, like this lady, she has got CKD, um, she is on diuretics, um, and she's elderly. So I think things I generally use, uh, prednisolone, uh, in these situations. Um, the usual starting dose is 30mg a day. Um, and, and normally in, in sort of, uh, peripheral gout, we stop in five or seven days, but in spinal gout, I tend to use a slightly longer course, so 30mg a day for a week, then taper by, um, five milligrams, uh, every few days till the patient, uh, is asymptomatic. Uh, again, there's no need to give a long taper, but maybe this, this patient may require two or three weeks' worth of steroids to settle the inflammation. I think the, the other thing to be, uh, aware of that spinal gout, the tophi in spinal gout can sometimes cause neural compromise, so you must seek input from spinal surgeons, um, and get their advice. I wouldn't recommend getting any surgical input, uh, as in doing an, an operation or anything like that, um, because these tissues don't heal well once they've got urate crystal deposits. Um, but it's, it's worthwhile getting input from, from spinal surgery if you are concerned there may be neural compromise. Apart from that, I don't do anything different in the acute phase, uh, when, when comparing to what I do for patients with peripheral gout. The other thing to sort of really remember is that, it's really important to start a urate-lowering therapy, uh, with a treat-to-target approach, for these patients because if you manage the acute flare, the patient will be better, but the, the deposits of urate crystals will still be there, and, um, they may get larger and cause neurological compromise. 

Thank you. So, with that in mind, perhaps if I move back towards Dr Ahmed, perhaps you could tell me a little bit more about how the patient is now, and what the longer-term treatment plan was for this patient. 

So we started her on some urate-lowering therapy. She was started on a slightly lower dose of allopurinol in the context of her chronic kidney disease, and then she was followed up later on in clinic. And in the first appointment, I think her uric acid level wasn't quite as wh- where we wanted it to be, so she wasn't meeting the target of under 36. So then we had to slowly increase it, being very cautious of her eGFR. And over time, she actually did quite well. She didn't have any, um, flares. On the second, um, appointment, she, she was very well controlled symptomatically. Um, and yeah, she, she did quite well on allopurinol. We didn't have to introduce any other, um, combination therapies. So, and, and she was prescribed her, uh, flare prophylaxis, of course, and, um, she, she did quite well. She didn't have any further symptoms. And I think equally important for her was in, in the context of her social history, we, we had to reiterate the, um, severity of her disease and how the chronicity of her disease can lead to severe complications, like, like Dr Abhishek has already alluded to, for instance, neurological compromise, so that was really important. So I think the pharmacological management, of course, that's important, but in cases where the chronicity of the disease has been very challenging to even cause these kind of symptoms, it's equally important to remember the non-pharmacological management. So educating her on the complications, her lifestyle, I think there was a huge element of her ethanol access, so we had to tackle that very sensitively, and she, she eventually did quite well. And, um, again, exploring the dietary history, I don't think there were any dietary red flags as such, aside from the, um, ethanol access in her background, so she did eventually quite well. 

Thank you. I think this is a, a really interesting case, and perhaps bringing us back to the last question for, um, Professor Abhishek, spinal gout, how common is it? And can you perhaps give us a little bit of insight into the prevalence of this and, and what clinicians might need to be thinking of, uh, in cases of suspected spinal gout, please? 

Yeah, thanks. So, uh, spinal gout is really rare. In my clinical practice, I've only seen a few patients, and they usually are in sort of two groups, uh, as, as Shiza's case was. There are patients with sort of advanced tophaceous gout who've got peripheral tophi, um, and also cause spinal involvement, and they, and they may present with sort of predominant spinal symptoms. These are in, in some ways, slightly easier to investigate and manage because you can image them, or you can see peripheral signs of tophi. That gives a strong clue. The other, uh, bunch of people are, who get unusual spinal crystal deposition for some odd random reason, and, and they may present as a sort of acute facet joint, suspected septic arthritis, or acute, uh, radiculopathy, and these can be really challenging to diagnose, um, and, and manage. And many times, you end up having a sort of aspiration, um, of the affected area or a biopsy to get a diagnosis and exclude infection. So reassuringly, spinal gout is quite rare. Um, I haven't got a prevalence, uh, figure for it, um, but in, in clinical practice, it is rare but it's an important differential that we must have in patients who've got suspected spinal infection, where, where we're not making good progress with, with antibiotic therapy. It generally happens in patients who've got, uh, sort of lots of risk factors for tophaceous gout like this lady, who was elderly, she had alcohol excess, chronic kidney disease, had a diuretic excess, uh, sorry, diuretic use, um, and there was also an element of self-neglect. So, so mostly, nowadays, when patients present with gout flares, etc and they get managed, we don't see many people with spinal gout but these are the rare patients which are most difficult to manage, and that's why the BSR case-based conference is so good at highlighting these rare and challenging cases. 

Thank you very much. That was absolutely fascinating and, and very, very insightful. Thank you, Dr Ahmed, for putting forward such a, an interesting case, and, and thank you, Professor Abhishek, for your expert opinion and guiding us on how we can think about this in, in clinical practice. I'm sure that many of our listeners will have gained a lot from this case, uh, and I want to extend my thanks to you both for joining me today. Thank you. 

Thank you. Thank you, Chris- 

Thank you so much 

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