AxSpA – an overview document

Intro

I have been struggling with blogs recently as my time has been stretched all over the place so by way of apology below you can download a document which contains the information I wrote as part of the Health Education England modules (this is contained in the  serious pathology of the spine module). These are open access if you work for the NHS.

Please bear in mind the following caveats, I was restricted on word count so it is at best an overview of the condition, it was also part of a wider piece of work (the modules) which means it is written standing on the shoulders of other parts of the module. I hope to get time to expand on this as I did with my RA blogs (here and here and here and here and here!)

As usual feedback is greatly appreciated and any further reading for me please send it my way!

PLEASE REMEMBER – THIS BLOG IS NOT A REPLACEMENT FOR CLINICAL REASONING, IF YOU ARE UNSURE GET ADVICE

Click here to download the document

Find details of upcoming courses for much much more detail on Rheumatology! click here

As usual thanks for reading and don’t forget to check out my other blogs. Sign up for the Rheumatology.Physio newsletter for further resources and updates!

Axial Spondyloarthritis is one of the featured conditions in my “Rheumatology At A Glance” booklet along with 9 others – more details in the shop here.

Related Blogs

An Introduction to Rheumatoid Arthritis for Therapists

Polymyalgia Rheumatica

Gout

Imaging in Rheumatology for Physios

MINI BLOG – Screendem

 

 

 

Osteoporosis – An Introduction For Physios

Intro

Welcome to another series of blogs, this time on the topic of Osteoporosis. These will look to unpack in some detail the important aspects of this relatively common condition and what as Physio’s we should be doing in clinic.

It is an important distinction to make at this point that recognising someone at risk of low bone density (osteopenia/osteoporosis) is very different to recognising the red flag indications of a fracture which may be due to that low bone density. In a red flag situation, the recognition of potentially low bone density will aid in your clinical reasoning but clearly the management will be significantly altered.

As usual feedback is greatly appreciated and any further reading for me please send it my way!

PLEASE REMEMBER – THIS BLOG IS NOT A REPLACEMENT FOR CLINICAL REASONING, IF YOU ARE UNSURE GET ADVICE

What is Osteoporosis?

Osteoporosis is a combination of reduced bone mass and reduced bone quality which understandably results in an increase in the fragility of the bone structure. Imagine the inside of the bone to be supported by scaffolding bars, in Osteoporosis these bars are fewer in number (reduced bone mass) and individually less solid (reduced bone quality).

These changes lead to the bone being at a higher susceptibility to fracture, classically presenting as low trauma (areas such as the wrist or neck of femur) or pathological and sometimes asymptomatic in the spine.

Developing Osteoporosis is multifactorial, those starting at a lower level of bone density and those who are exposed to local or systemic alterations to bone remodelling are the most at risk. i.e. if you reach a lower bone density level in adolescence then the normal loss of density as you age will allow it to fall to a level that increases susceptibility to fracture or exposure to something that accelerates the bone loss will achieve the same result.

Who Gets Osteoporosis?

Most commonly Osteoporosis follows the menopause as Oestrogen has an inhibitory affect on the osteoclasts (these resorb bone). Older adults are also commonly affected as mentioned above a decrease in bone density is a normal (although not necessarily inevitable) result of the ageing process.

A third category are those with an underlying cause for their reduction in bone density, these are often younger people with a history of nutritional deficiencies, drug therapies or inherited causes.

The prevalence of Osteoporosis itself is difficult to determine and likely under reported however in the UK over 1/3 women and 1/5 men will sustain a fragility fracture in their lifetime and at age 75-84 the absolute 10 year risk for sustaining a fragility fracture is approx. 24% for women and 14% for men.

What should we do?

Clearly in cases of a known fracture especially if it is low trauma, we should be considering factors that may have contributed to a lower bone density and I would hope this point doesn’t require labouring significantly.

We should retain some level of suspicion for all the people who attend Physiotherapy and consider if they have risk factors which may lead them to have (or to develop) low bone density. As seen in the above numbers, the likelihood of a fragility fracture is relatively high over a lifetime so I do not believe it unreasonable to consider the factors in every person. We will be asking many of the questions as part of a normal assessment and a process of connecting the dots is not an onerous one.

In our younger attendees recognition of factors contributing to the possibility of low bone density and/or an underlying cause does raise the possibility of more medical urgency. Nutritional deficiencies in conditions such as RED-S for example or familial history of fragility fractures will raise our suspicions. I will cover these in more detail in later instalments.

Investigating

DXA scanning is the gold standard for measuring bone mass, it is usually easily accessible via a community service but local pathways will vary. Using a tool such as the FRAX (fracture risk assessment) can help to assess thresholds for investigation.

Management

Medical management through supplementation of calcium and vitamin D, bisphosphonates and biologics can be used. Physiotherapy has a role using weightbearing physical activity to load the skeletal structure and in falls prevention. (more to come in a subsequent blog).

As usual thanks for reading and don’t forget to check out my other blogs. Sign up for the Rheumatology.Physio newsletter for further resources and updates!

Osteoporosis is one of the featured conditions in my “Rheumatology At A Glance” booklet along with 9 others – more details in the shop here.

Related Blogs

An Introduction to Rheumatoid Arthritis for Therapists

Polymyalgia Rheumatica

Gout

Imaging in Rheumatology for Physios

References

Book by Drs Al-Sukaini, Azam and Samanta https://www.amazon.co.uk/Rheumatology-clinical-handbook-medical-students/dp/1907904263/ref=sr_1_1?ie=UTF8&qid=1538037053&sr=8-1&keywords=rheumatology+a+clinical+handbook

Cauley J – Osteoporosis: fracture epidemiology update 2016, Current Opin Rheumatol 2017, 29:150–156

 Rosen CJ. The Epidemiology and Pathogenesis of Osteoporosis. [Updated 2017 Feb 21]. In: Feingold KR, Anawalt B, Boyce A, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-

Compston, J., Cooper, A., Cooper, C. et al. Arch Osteoporos (2017) 12: 43. https://doi.org/10.1007/s11657-017-0324-5

The Stages of Rheumatoid Arthritis – Established Disease

Intro

This finishes the series of blogs in my RA series that looks to expand upon the article for PhysioFirst which you can read in full here. It has topped 9000 downloads at the time of writing this blog and I am immensely proud of it as a piece of work, it was however hamstrung by a word limit and primarily about the joint dysfunction component of RA. Check out the intro to RA stages here prior to reading this one.

This portion will elaborate on the stage of RA that we are traditionally the most comfortable with, in the literature it has been referred to as the stage after the first two years from diagnosis but this time frame will vary to a degree. People will have very different symptom presentations in this stage and I may have to expand further on this in future blogs.

As usual feedback is gratefully received as are any materials I might be interested in!

PLEASE REMEMBER – THIS BLOG IS NOT A REPLACEMENT FOR CLINICAL REASONING, IF YOU ARE UNSURE GET ADVICE

Established Disease Characteristics

Theoretically we are dealing with a relatively stable disease process at this point which will involve a combination of pain, ongoing inflammation and potentially joint deformity in varying degrees dependent upon the person. In reality there remains the chance of “flares”, acute on chronic periods of inflammation which can signify a lack of control over the condition previously thought to be handled by the current medication regime.

We need to bear in mind when we think about how the person is going to look in this stage that there are likely 5 or more subsets of RA that are as yet undefined. For simplicities sake these might be “erosive”, “non-erosive”, “relapsing-remitting”, “monoarthropathy” and “drug-resistant” (please note I have made these names up to illustrate my point). The number of joints affected, the severity of joint damage (sometimes there will be none) and the regularity of flaring will be affected by multiple factors. Genetics, co-morbidity, time since onset, delay to diagnosis and medication effectiveness (of not more).

Joint deformity is something that will need to be considered in this stage, most likely of the MCPJs and MTPJs but also leading to joint replacements in the usual suspects of the knees, hips and shoulders. It is important to remember that there may be erosive damage without visible joint deformity.

Persistent pain in this cohort is likely under reported in my opinion. These people have had long periods of pain, loss of function, stress and lack of sleep but their pain is often put down to continued disease process whereas there can be no argument against some sensitisation of the nervous system during the period of time when active disease was present.

Symptomatic Treatment

It probably goes without saying after the above section of this blog that this is going to vary significantly from person to person so I have no recipe for you. Umbrella ideas to be considering are education, an exercise program and functional assistance.

Education again is going to vary dependent upon your attendee but don’t assume they have a good handle on the condition, check they know their medicine regimes and that they stick to them! General health advice such as smoking cessation and diet as appropriate. Also consider other co-morbidities especially any that will affect bone or cardiovascular health.

Exercise programs here are again of vital importance, graded exercise programs targeting general strength, cardiovascular fitness, bone density and any functional requirements are key. It may be necessary to be inventive if structural changes prevent specific exercises, lack of wrist extension for example may prevent pushing. With regards to symptom increases there is no evidence that even high intensity exercises are detrimental to symptoms or joints but we need to be pragmatic with increases in the short term. I try to stick to the following advice: pain increases within tolerable levels but not affecting function, swelling/pain/redness is acceptable as long is it reduces back to normal (for the patient) within a few hours and is not worse during the night or first thing in the morning.

Functional assistance can take a few forms, from splints/braces which can be helpful to adaptations of technique or equipment. For example, thickening the handles of cutlery can make it much easier to grip. In all honesty, I often refer to Occupational Therapy colleagues for this portion of management as I have found them exceptionally skilled in this area!

Thanks for reading, I hope you have found this series useful, please sign up to the newsletter here for links to new blogs and extra Rheumatology resources that I find on my travels.

You can now visit my SHOP and find my “Rheumatology At A Glance Booklets“!

Rheumatoid Arthritis Blogs

The Stages of Rheumatoid Arthritis – Early Arthritis

The Stages of Rheumatoid Arthritis – Clinically Suspected Arthralgia

The Stages of Rheumatoid Arthritis

Rheumatoid Arthritis Tendons

An Introduction to Rheumatoid Arthritis for Therapists

Rheumatoid Arthritis and Pregnancy

References

Brosseau L, Wells G, Tugwell P, Egan, M, Dubulouz C, Casimiro L, Robinson V, Pelland L, Mcgowan J. Ottawa Panel Evidence-Based Clinical Practice Guidelines for Electrotherapy and Thermotherapy Interventions in the Management of Rheumatoid Arthritis in Adults. Physiotherapy 2004:84(11):1016-1043

Brosseau L, Rahman P, Poitras S, Toupin-April K, Paterson G, Smith C, King J, Casimiro L, Angelis G, Loew L, Cavallo S, McEwan J. A Systematic Critical Appraisal of Non-Pharmacological Management of Rheumatoid Arthritis with Appraisal of Guidelines for Research and Evaluation II. PLos ONE 2014 9(5)

Christie A, Dahm k, Moe, R, Haavardsholm E, Hagen K. Effectiveness of Nonpharmacological and Nonsurgical Interventions for Patients With Rheumatoid Arthritis: An Overview of Systematic Reviews. Physical Therapy 2007:87(12):1696-1715

Combe B, Landewe R, Daien C, Hua C, Aletaha D, Alvaro-Gracia J, Bakkers M, Brodin N, Burmester G, Codreanu C, Conway R, Dougados M, Emery P, Ferraccioli G, Fonseca J, Raza K, Silva-Fernandez L, Smolen J, Skingle D, Szekanecz, Kvien T, van der Helm-van Mill A, Vollenhoven R. 2016 Update of the EULAR Recommendations for the Management of Early Arthritis. Annals of the Rheumatic Diseases 2016:0:1-12

Lamb S, Williamson E, Heine P, Adams J, Dosanih S, Dritsaki M, Glover M, Lord J, McConkey, C, Nichols V, Rahman A, Underwood M. Williams M. Exercises to Improve Function of the Rheumatoid Hand (SARAH): A Randomised Controlled Trial and Economic Evaluation. Health Technology Assessment 2015:19(19) ISSN 1366-5278

Lee S, Shin B, Ernst E. Acupuncture for Rheumatoid Arthritis. Rheumatology 2008:47:1747-1753

Loof H, Demmelmaier I, Henriksson E, Lindblad S, Nordgren B, Opava C, Johansson U-B. FearAvoidance Beliefs About Physical Activity in Adults with Rheumatoid Arthritis. Scandinavian Journal of Rheumatology 2015:44:93-99

Markatseli T, Voulgari P, Alamanos Y, Drosos A. Prognostic Factors of Radiological Damage in Rheumatoid Arthritis: A 10-year Retrospective Study. The Journal of Rheumatology 2011:38:44-52

Sharif S, Thomas J, Donley D, Gilleland D, Bonner D, McCrory J, Hornsby W, Zhao H, Lively M, Hornsby J, Always S. Resistance Exercise Reduces Skeletal Muscle Cachexia and Improves Muscle Function in Rheumatoid Arthritis. Case Reports in Medicine 2011:2:205691

Van Den Ende C, Breedveld F, Cessie S, Dijkmans B, de Mug A, Hazes J. Effect of Intensive Exercises on Patients with Active Rheumatoid Arthritis: A Randomised Clinical Trial. Annals of Rheumatological Disease 2000:59:615-621

Gout

Intro 

This is a blog I have been meaning to write for a while, embarrassingly Gout occupies just the one slide on my “Recognising Rheumatology” courses despite it being the most common Rheumatological condition. I was lucky enough to watch a webinar by Dr James Prior which brought gout into focus and updated some facts for me I will share with you in this blog.

Gout diagnoses areon the increase, likely due to a combination of greater awareness of the condition in primary care and an increase in multimorbidity amongst the population. This coupled with the increasing first contact roles for Physios means it is definitely a condition to be aware of.

As usual feedback is greatly appreciated and any further reading for me please send it my way!

PLEASE REMEMBER – THIS BLOG IS NOT A REPLACEMENT FOR CLINICAL REASONING, IF YOU ARE UNSURE GET ADVICE

What is Gout? (What’s it all aGout?)

Gout is a type of inflammatory arthritis, it is characterised by acute attacks of pain, redness, swelling and heat of the joint. Onset of symptoms is usually during the night and will peak after 12-24 hours. The pain is severe and many attend A+E with the symptoms, gout has overtaken Rheumatoid Arthritis as the Rheumatological condition with the most hospital admissions per year.

Aspiration of the joint often reveals urate crystals which is what sets off the synovitis. Either an excess of Urea in the body (90%) or a reduced ability to produce Urate which metabolises the Urea causes the formation of these crystals within the joint.

Who Gets Gout? 

Gout prevalence is roughly 2.5% of the population with higher incidences in the North West of England and Wales. 1/14 men and 1/35 women are affected, it is important to note that onset prior to puberty in men is unlikely and onset prior to menopause in women is unlikely. The joint most affected by gout is the 1st MTPJ (big toe) which accounts for 75% of cases.

There are a number of associated co-morbidities including, diabetes, cardiovascular disease, stroke, obesity and poor kidney function. There have been associations with dietary intake, most strongly associated is high alcohol and high red meat intake.

What should we do? 

If this is the first attack then advise the patient to go their GP, initial management of the flare is with NSAIDs and Colchicine followed by a titrating dose of Allopurinol. Physiotherapy in this early stage is of minimal benefit. Education around the condition and symptomatic relief where possible (ice, NSAIDs).

If the patient is already on medication, discuss with them the process. It is very common for a flare to be triggered by starting Allopurinol. It is also necessary for the Allopurinol dose to be titrated upwards until control is gained, ensure this happened in this case. Most management will be within primary care however Rheumatology input is of benefit especially in the early stages of the disease and in refractory cases.

Investigating

Gold standard investigation for gout is joint aspiration to assess for the crystals. Blood testing for uric acid levels is useful in the acute and the chronic stage although it is worth noting that in a proportion of cases this blood testing will be within the normal ranges.

As usual thanks for reading and don’t forget to check out my other blogs. Sign up for the Rheumatology.Physio newsletter for further resources and updates!

Related Blogs

An Introduction to Rheumatoid Arthritis for Therapists

Polymyalgia Rheumatica

Inflammatory Arthropathy Bloods

24 Hours Inflammatory Pattern

References

Book by Drs Al-Sukaini, Azam and Samanta https://www.amazon.co.uk/Rheumatology-clinical-handbook-medical-students/dp/1907904263/ref=sr_1_1?ie=UTF8&qid=1538037053&sr=8-1&keywords=rheumatology+a+clinical+handbook

Dr Priors Webinar (which was excellent by the way, part of a series by Lily and BSR which are free https://www.rheumatology.org.uk/events-learning/webinars )

Becoming A Physio With Inflammatory Arthritis – Part 1

I am delighted and priveledged to be able to host this blog written by Jenni Ward (click here to follow her on twitter) a Physio with a real story to tell. I don’t want to detract from it by writing a long introduction but it is a great demonstration of the complexities of Rheumatology conditions and the effect it can have on someones life. Watch out for the second installment soon discussing how the diagnosis affects her management of her patients.

Take it away Jenni:

I was officially diagnosed with a Seronegative Inflammatory Arthritis when I was 18, but I had been experiencing symptoms since the age of 11 and under Rheumatology with a label of “something autoimmune… but we aren’t sure what” since I was 14. We have retrospectively called this Juvenile Idiopathic Arthritis (JIA) given that it started when I was 11 and we just weren’t entirely sure what to call it.

When I first started University, I had been experiencing on and off flares of my usually well controlled arthritis, which resulted in me starting my first disease modifying anti-rheumatic drug (DMARD), Hydroxychloroquine, two months after I had started uni. My biggest problem has always been stiffness and during these flares I would have up to four hours of early morning stiffness, compared to my usual 60 mins of stiffness. My joints settled down well on Hydroxychloroquine after only a few months.

After about 9 months on Hydroxychloroquine, my immune system threw us a curve ball. I developed bilateral insertional Achilles tendinopathy, dactylitis of my little finger and three episodes of inflammatory back pain (alternating buttock pain, worse with rest, better with movement, fab response to NSAIDs). WAIT… WHAT? Now we were looking at a Spondyloarthritis, a sub-type of seronegative inflammatory arthritis that can affect the spine, entheses and peripheral joints. I had experienced only peripheral arthritis for 8 years and it had evolved into a Spondyloarthritis – though I have always had a stiff back and perhaps the regular use of NSAIDs had masked any back symptoms.

My Rheumatologist started me on Methotrexate, another DMARD but with mild immunosuppressive effects that has no real effect on spines, mainly because my inflammatory back pain episodes were short-lived, and my peripheral joint symptoms were my biggest issue – again stiffness, swelling, pain. Methotrexate helped settled everything back down with a big dose of steroids and everything was really good again.

My joints continued to flare on and off for another year and each time we would increase my Methotrexate dose until I couldn’t tolerate the nausea Methotrexate often brings. It got to the point that I struggled to eat for 3-4 days after each dose and by March 2017 I had more active arthritis with 10 swollen and 15 tender joints. My Rheumatologist decided to add a newer type of medication, collectively called Biologics. There are a few different types of Biologics but Anti-Tumour Necrosis Factor (Anti-TNF) are most commonly used as the first-line biologic. These inhibit a small part of the immune system that causes inflammation, aiming to prevent inflammation from occurring in the first place. I started on an Anti-TNF called Humira which worked very quickly resulting in no active arthritis in just 12 weeks. Unfortunately, I did experience a side effect which meant I had to stop Humira but it also meant we knew what class of medication worked for me.

I qualified in Summer 2017 and started work a few months later in MSK outpatients – my first rotation. By the time I started work, I had been off Humira for 2 months and all my joints had become active again. I was having to get up two hours earlier than needed so my joints wouldn’t be so stiff by the time I had to drive to work and I was relying on intramuscular steroids to tide me over until Humira was out of my system and I could start another Biologic. I was really lucky that my first rotation was in MSK because, looking back, I’m not sure the physical demands of working on the wards would have been possible. Virtually every peripheral joint was stiff, swollen or sore and I had a weird, but very problematic, combination of sternoclavicular and glenohumeral joint involvement on the same side! Good job that this was on my non-dominant side so most things were manageable.

Fatigue was also a big issue and wasn’t something that generally wasn’t much of an issue for me until this point compared to other people with inflammatory arthritis. I think my fatigue was a combination of this rip-roaring flare which was making me get up so much earlier than normal, and just starting my first job.

I started my second Anti-TNF, Benepali, after my first month at work. Like Humira, Benepali worked quickly and effectively for me, settling my joints back down. I had loads of energy again and I didn’t have any morning stiffness. This worked out really well because I started working on-calls and the lack of morning stiffness meant I could get out of bed and get to my patients in the middle of the night without any issue.

I was on Benepali for about four months and then found I was allergic to it… major bummer! But we had figured out a group of medications that worked well for my arthritis, so I was started on my third Anti-TNF – Cimzia. Cimzia has worked just as well Humira and Benepali without the added side effects and I have been on it for nearly 15 months now. I still have some issues with my arthritis – namely flexor tenosynovitis of my dominant hand that has been refractory to steroids, but thankfully is responsive to a combination of Cimzia, Methotrexate and Sulfasalazine. It just goes to show that the immune system can be really determined.

No one’s arthritis is the same, but we are in an age now with the most ever rheumatology medications and there are many more in the pipeline. We are in the best place to manage inflammatory arthritis compared to where we were even just 20 years ago. I’m excited to see where rheumatology goes in the future… will we use blood tests to identify the inflammatory molecules responsible for individual’s arthritis and use molecule-specific medications to target these? Where will the role of rheumatology physio go? What new skills can we gain as physios in rheumatology/MSK?

Thank you Jenni!

I think everyone will join me in thanking Jenni for sharing her story, it brings home to me that despite my own difficulties understanding Rheumatology conditions it absolutely nothing compared to what the diagnosed go through. We must be better at recognising and referring people early enough that our Rheumatology Consultant colleagues can manage their conditions as quickly and as tightly as possible. Part 2 available soon…

As usual thanks for reading and don’t forget to check out my other blogs. Sign up for the Rheumatology.Physio newsletter for further resources and updates!

Related Blogs

Imaging in Rheumatology for Physios

Imaging In Rheumatology – MRI for AxSpA

An Introduction to Rheumatoid Arthritis for Therapists

MINI BLOG – Screendem

MINI BLOG – Spondyloarthropathy Extra-Articular Symptoms

Polymyalgia Rheumatica

Inflammatory Arthropathy Bloods

24 Hours Inflammatory Pattern