Posts Tagged ‘achilles tendon’

So much for a new year’s resolution to avoid surgery in 2015. Surgery on my right elbow is now scheduled for February 6th – we’re waiting until after my son’s wedding at the end of the month. This will be my 6th RA-related surgery. Both elbows give fits including persistent pain and tenderness but the right one has been the bigger beast probably because I’m right handed. In August 2013, first symptoms were noted. An MRI in October 2013 showed a 50% tear in a tendon. Enthesitis is the term for damage in an area where a tendon connects muscle to bone and such soft tissue damage is common in rheumatoid arthritis in general an in my case specifically. The orthopedic surgeon gave a cortisone steroid injection in November 2013. Occupational therapy was done from December 2013 to February 2014 but it was stopped as progress was not realized. Finally, in November 2014 a novel platelet-rich plasma injection was tried to no avail. The orthopedic surgeon, who specializes in hands and elbows, said that all conservative treatments failed to help and surgery would be required. He indicated that the surgery would include an incision across the elbow, removal of the damaged tendon, shaving off damaged bone tissue, and using anchor sutures to reattach healthy tendon to the bone. Anchor sutures involve drilling holes in the bone and inserting anchors which hold special permanent suture material. The arm and wrist will be immobilized for a few weeks. Occupational therapy is already scheduled starting two weeks after the procedure. My rheumatologist wanted to add a new DMARD, CellCept, to help with Rituxamab infusions. But now we’ll wait until after surgery to help avoid any infection complications.

While surgery is always a last effort, it’s time to take care of this ongoing issue as the pain is non-stop and use of the arm is limited. Updates will be posted as the process unfolds.


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Corticosteroids or glucocorticoids are powerful anti-inflammatory drugs commonly used to treat a variety of medical conditions. They are not to be confused with anabolic steroids that are notoriously abused by athletes.1 Anabolic steroids are associated with muscle mass gain and corticosteroids are connected with metabolism and immunity.

Most every RA patient has probably taken oral steroids in the form of pills or a dose pack that tapers down the dose over a period of time. Oral steroids are effective at providing quick reduction of RAsymptoms although long-term use is generally discouraged and even short-term use is being questioned.2 When taking an oral steroid, the drug goes throughout the entire body systemically. But there are other forms of steroids that are directly injected into a specific area of the body in an effort to treat RA related symptoms. Since being diagnosed with RA, I’ve had one steroid injection into my right knee, four into my left hip, one into my neck, and one into my right elbow.

Read the rest of the post at http://rheumatoidarthritis.net/living/steroid-injections-treating-ra-symptoms/

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In an earlier post, I outlined how RA can impact much more than bones including many organs and soft tissues. One group of soft tissues that can be damaged by RA includes those involved with the musculoskeletal system. The musculoskeletal system involves a complex interaction between muscles, bones, joints, and various connective soft tissues – all which can be the target of RA.

Erosion of bone tissues in joints is on of the trademark symptoms of rheumatoid arthritis. Through complex autoimmune biochemical processes, the body’s immune system attacks it’s own tissues like it was a foreign invader. A cascade of signaling chemicals promotes the production of bone cells called osteoclasts that erode bone tissue and surrounding cartilage. This kind of gross damage…

Read more at http://rheumatoidarthritis.net/living/attack-on-connective-tissues/

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In the five some years since being diagnosed with RA, I’ve tried a boatload of treatment options including various NSAIDS (chewed up my stomach), multiple DMARDs (one caused an allergic reaction and am currently injecting methotrexate), and I’m currently on my 7th biological medication – Rituxan infusions.

My rheumatologist always says that the treatment goal is that I hardly pay attention to my joints throughout the day. This sounds like everyday language for the ultimate target for RA treatment which is called clinical remission. This is defined as one or less than on tender joint, one or less than one swollen joint, low inflammation blood tests, and a strong patient self-assessment. Over the five years of treatment, I’ve never gotten anywhere close to these goals. But over the past couple of weeks it’s become clear that Rituxan is working like no other treatment combination has! Pain, swelling, and tenderness are hardly noticeable. My hip doesn’t hurt when sleeping or walking. My knee can pull me up steps. I can get out of bed relatively quickly without much stiffness. My right ankle that’s had 2 surgeries lets me know it’s there but it doesn’t scream at me all day along. The bottom line is that RA is starting to take a back seat in daily life…just like my rheumatologist hoped for! This is the first time in five year to have this experience and for this I am very grateful. It was a long time coming and many starts and stops and trying dozens of drug combinations. Of course, I’ll temper the joy just a little and take each pain free day at a time as you never know what lurks around the bend.

It took a while for me to figure out what was going on with Rituxan. These complex biological processes take time – in fact it’s been 4 months since my first infusion and I was already giving up hope for Rituxan to work. But I was also quite distracted over the past month fighting a battle with chronic and almost daily migraines. We’re not sure what’s causing them although my neurologist believes that genetics, a fight with an autoimmune disease, and the medications used to treat RA may all be contributing. So while RA is finally getting under control after 5 years, we’re busy trying to find the best treatment for the migraines. In addition to the emergency triptans (like Imitrex) to take when a migraine comes on, I’ve been on three different long term preventative medications, and have been into the infusion clinic two times for a cocktail of meds in an effort to break a long migraine cycle – the latest was a 4 day killer over the weekend. I have an MRI/MRA  (image of brain and blood vessels) scheduled next week to rule out any functional issues and we’re seeking insurance approval for botox injections which my doctor said works very well for his patients.

Two steps forward for RA treatment success after five long years and dozens of drugs! For this I will truly thank God as I was getting close to giving up hope as the options were getting few and far between. One step back with the nasty migraines. Such seems to be the life of a patient with a chronic disease. But just like what happened with RA, I believe that the migraines will eventually get under control. Two steps forward and one step back still equals forward progress.

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Rheumatoid_arthritis_jointBone erosion is one of the hallmark symptoms of RA and the biological processes involved in RA often result in the breakdown of bony tissue primarily in joints which are surrounded by a sac called the synovium (see diagram). I have this telltale bone erosion in my fingers documented via x-ray and a dime-sized erosion was found in my heel bone several years ago which caused a sharp bone spur. A surgeon removed the damaged tissue and a pathology report confirmed that it was caused by the erosive processes associated with RA.

But RA can impact other parts of the joint including the surrounding soft tissue – tendons, ligaments, and cartilage. Chronic tenosynovitis, inflammation of the sheath of a tendon is common in rheumatoid arthritis and can result in the permanent damage and tearing of the involved tendons. Such tendon problems caused by RA are well known by the scientific community and are linked to joint deformities (see Sivakumar, et al, 2008; Wakefield, et al, 2007). Tendon problems have even been posited as being one of the most powerful predictors of early RA (Eshed, et al, 2009). Sophisticated imaging techniques developed in the last few decades, such as MRIs and ultrasound, can reveal connective tissue damage in joints caused from RA including tenosynovitis and bursitis (Boutry, et al, 2007). Bursitis, inflammation of the fluid-filled sacs that protect joints (see NIH site), often accompanies tenosynovitis. RA is also implicated as a cause of cartilage damage in knees (see the AAOS site). An MRI taken at the onset of my RA diagnosis revealed cartilage damage in one knee.

Soft tissue damage became apparent after dealing with a persistently cranky elbow that was only getting worse to the point that major pain killers were needed one evening. I learned from an orthopedic doctor this week that I now have tendon tears in my elbow. The good news is that the bones and joint spaces are in good shape and appear to be undamaged from RA. While in non-RA patients the tendons commonly tear due to overuse, the doctor was unsure about the relative contributions of RA and overuse to the tearing. But since I don’t tend to overuse my elbow, except when fishing a couple of times this summer, I can’t help but think that RA is the major contributor – especially in light of previous history. Tendon problems have been a hallmark of my struggles with RA. One of the first symptoms I experienced, even before official diagnosis, was Achilles tendon tearing in both ankles which resulted in two surgeries. This bilateral problem, coupled with other symptoms, ultimately led to seeing a rheumatologist and receiving a diagnosis of RA. Several years later the tendon tearing continued and a third surgery was needed on the right ankle to repair the tendon, remove a bursa sac, and remove damaged bone tissue. Even after those procedures, my Achilles tendons continue to speak rather loudly everyday.

At this point, conservative treatments to the elbow will begin and include use of braces, topical NSAIDs (Voltaren gel), and physical therapy. Cortisone injections may be used if conservative treatments don’t work with surgical repair being the last line of treatment. So we wait and see if the most recent RA treatment (Rituxan) and the newly prescribed elbow treatments can slow down soft tissue damage enough to allow the tendons to heal on their own.

Photo attribution: By Wouterstomp at en.wikipedia [Public domain], from Wikimedia Commons

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The last four days have been a grand time of celebrating our oldest son’s college graduation. It’s been a whirlwind of events including his senior engineering project presentation, three formal ceremonies of various sizes and durations, dinners, and a large party hosted at our house. This meant much physical activity around the yard and house the principal of which was 10 hours of smoking five large pork shoulders for 50 people (it was tasty and you should check out the website http://www.amazingribs.com/).

Tired_brown_bear_050701_01Going into this set of events, a nagging thought persisted…”I’m going to pay for this later.” Sure enough, by Sunday evening I could barely walk, my fingers were swollen and throbbing in pain, and sheer exhaustion washed over my body causing me to collapse. I knew that going to work Monday morning would not be possible.

Many argue that movement and exercise is critical medicine for arthritic joints stating that it relieves pain and stiffness (see these websites – Mayo Clinic, NCHPAD). In addition to potential positive impact on joints and muscles, exercise is obviously important for other reasons include cardiovascular and mental health. But my experience over the years has been that exercise and movement causes rebound pain and stiffness. Yet, I know that I’m missing out on the benefits of exercise.

It’s interesting to read some of the recommendations from medical websites. From WedMD…“Regular exercise can actually reduce overall pain from rheumatoid arthritis.” In my experience with RA, exercise always causes more pain. There are many times when I’ve had to stop movement because the pain got worse. WebMD also makes this statement, “Regular exercise improves functional ability and lets you do more for yourself.” This may be true for some but the functional ability of my ankles and Achilles tendons actually got worse after exercising. The tendons tore at a quicker rate and my orthopedic surgeon and physical therapist both recommended that I avoid any activity that puts stress on the tendons.

Can exercise actually be contraindicated for RA? Kelly Young at RA Warrior has an excellent series of posts about this topic. She concludes, “If you can, you should; if you can’t, you shouldn’t.” At the Health Central RA website, Dr. Borogini wrote a balanced article about the topic and makes an excellent suggestion which is in alignment with Kelly Young’s statement, Rest More When RA Is Active, Exercise More When It Is Not. The Johns Hopkins Arthritis Center website makes a great observation about movement and RA.

Acutely, resting of involved joints can assist with pain management and decrease the inflammation of the involved joint. However, the potential side effects of inactivity include decrease range of motion, loss of strength, altered joint-loading response, and decrease aerobic capacity.

This leaves those with active disease in a real quandary.

The conclusion that must be drawn from the recent set of weekend experiences is that my RA is not under control and I should probably avoid strenuous physical activity. But of course, I already knew that going into the weekend. The difficulty lies in the fact that life must go on and I was not about to miss this once-in-a-lifetime celebration. I just have to be ready to pay the consequences afterwards.

Creative Commons Photo Credit: http://commons.wikimedia.org/wiki/File:Tired_brown_bear_050701_01.JPG

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My rheumatologist believes that I may have a combination of rheumatoid arthritis (RA) and ankylosing spondylitis (AS). I have had a positive rheumatoid factor (RF) test and I present classic examples of inflammation and damage in joints commonly associated with RA including in the proximal interphalangeal (PIP) and metacarpophalangeal (MCP) joints in both hands. Add to that list, symmetrical joint presentation in the wrists, shoulders, hips, and knees along with fatigue and it seems like RA. At the same time, my rheumatologist noted limited spinal mobility and many problems with my ankles and Achilles’ tendons which are common with AS. My first autoimmune symptom, which occurred years before joint problems, was inflammatory uveitis in both eyes. While Achilles tendon problems and uveitis can be associated with RA, they are more commonly seen in AS patients. But a test for HLA-B27, a common genetic test related to ankylosing spondylitis (AS), was negative. These blood tests are not 100% accurate and the official diagnosis in my chart is RA (diagnosis code 714).

photo (8)Muddying the water is the fact that I have been through a slew of RA treatments over the past four years in an effort to find a combination that works for the long term. I’m currently on Actemra infusions and now going back to add leflunomide (Arava) in an effort to capture the earlier success with Actemra. While many RA patients find relief from the most common treatments like methotrexate, Enbrel, and Humira, it seems to elude 30-40% of patients.[i] Every person seems to respond differently to various medicines and doses.

This personal evidence leads me to believe that there may be different sub-types of RA. In a recent conversation at the RA site on HealthCentral, the notion of sub-types of RA was mentioned. We already know that there are different types of inflammatory arthritis including RA, AS, psoriatic arthritis.[ii] And each of these diseases presents different patterns and may be treated with similar and/or different medications. But there seems to be a lack of scientifically defined sub-types of RA.

According to researchers from the Netherlands, “Rheumatoid arthritis (RA) is a heterogeneous disease with unknown cause.[iii] Differences in genetic expressions of RA patients were seen by these researchers lending some credence to a genetic link to sub-types of RA. In an earlier study of the genetics of RA in 1989, researchers found a gene called HLA-DR was found in 83% of 149 patients with classical or definite RA.[iv] But no explanation is given for the 17% of RA patients who did not show the gene. In 2010, a group of researchers found four genetic sub-types of RA.[v] Japanese scientists found genetic differences at the molecular level. They stated, “Data from genome-wide screening, transcriptional profiling, and animal models indicate that RA consists with heterogeneous disease subsets.”[vi] Some researchers even found different emotional responses in RA patients.[vii]

While the causes of RA are not completely evident, most scientists suspect a combination of factors including genetic and environmental (see earlier post on the triggers of RA). Scientists are now beginning to unravel the complexities of RA and find that there may actually be a variety of sub-types of the disease. I hypothesize that future research into RA and other autoimmune diseases will reveal that genetics and environmental factors impact the way individuals present symptoms and respond to treatments. This knowledge may lead to definitions of RA sub-types and better treatments in the future. In the meantime, I’ll keep experimenting with treatments in order to find a combination that works.

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