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Rheumatoid Arthritis of the Foot and Ankle - Essay Example

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This essay "Rheumatoid Arthritis of the Foot and Ankle" discusses Rheumatoid arthritis (RA) as a systemic autoimmune disease that causes chronic inflammation of the joints. RA is a chronic inflammatory disease that causes pain, stiffness, and swelling in the joints, frequently symmetrical…
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Rheumatoid Arthritis of the Foot and Ankle
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RHEUMATOID ARTHRITIS Rheumatoid arthritis (RA) is a systemic autoimmune disease that causes chronic inflammation of the joints. RA is a chronic inflammatory disease that causes pain, stiffness, and swelling in the joints, frequently symmetrical (if one foot has it, the other one will). While rheumatoid arthritis can last for years, patients may experience long periods without symptoms. Typically, rheumatoid arthritis is a progressive illness that has the potential to cause joint destruction and functional disability (Shiel, 2006). In RA, the joint lining (synovium), normally smooth and shiny, becomes inflamed, painful and swollen. The disease, which lasts over a long period of time, can cause damage to cartilage, bone, tendons and ligaments (DynoMed.com, 2000). SIGNS AND SYMPTOMS Foot deformities are very common in RA. These deformities may affect patient functional foot, especially hallux rigidus and calcaneal valgus (Bal, et al. 2006). Human foot is more susceptible to arthritis because the human foot contains 33 joints. About 90 percent of RA patients will complain of problems with the midfoot and forefoot while 67 percent will have problems with the hindfoot and ankle. The ankle is usually the last joint to be involved with RA (DynoMed.com, 2000). RA causes inflammation in the lining (synovium) of joints, most often the joints of the feet. The most common symptoms of RA in the foot are pain, swelling, and stiffness. Symptoms usually appear in several joints on both feet. The signs of inflammation can also include a feeling of warmth around affected joints. In some patients, chronic inflammation results in damage to the cartilage and bones in the joint. Serious damage can lead to permanent joint destruction, deformity, and disability (FootPhysicans.com, 2007). With the progress in the disease the feeling of pain in the joint or in the sole or ball of the foot will increase. The joint may be warm and the way the patient walk may be affected. In addition the patient may develop corns or bunions, and the toes can begin to curl and stiffen in positions called claw toe or hammer toe. Corns, or even ulcers, may develop on the foot. Metatarsalgia, a general term for pain in the sole or the ball of the foot, is also very common. This indicates that RA is affecting the metatarsal joints of the toes. Hindfoot and ankle pain often involves the posterior tibial tendon. The ankle itself is usually the last joint in the foot to be involved with RA (DynoMed.com, 2000). As the disease progresses in the foot region, the joint space becomes narrow and bone begins to rub on bone, leading to painful arthritis. Besides, deformities may occur resulting in loosening of the ligaments and capsule lining of the joint. If the housing of the joint or the capsule loosens up considerably, the joints mostly in front of the foot may dislocate. This can cause painful swelling on the bottom of the ball of the foot that can make walking even more terribly uncomfortable. Later the big toe begins to deviate and bunions may form on the inside of the big toe (footandankle.mdmercy.com, N.D.). In cases where the hindfoot (back of the foot) and ankle are affected, the bones may shift position in the joints. This can cause the long arch on the bottom of your foot to collapse (flatfoot), resulting in severe pain and difficulty walking. Because RA affects the entire system, the patient may also feel feverish, tire easily, and lose appetite (AAOS, 2001). AETIOLOGY The exact cause for RA is still unknown, but there are many thoughts about what might contribute to it. A sudden and traumatic injury such as a broken bone, torn ligament, or ankle sprain can cause the injured joint to become arthritic in the future. According to Cotran et al, (1994)"...RA is triggered by exposure of an immuno-genetically susceptible host to an arthritogenic microbial antigen". Heredity, or the genes from the parents, may be a determining factor in who gets rheumatoid arthritis. Roth explains that this "genetic predisposition appears to be related to the histocompatibility genetic marker HLA-DR4, especially in those patients who maintain high titers of immunoglobulin M (IgM) rheumatoid factor" (1994). According to Kumar and Clark (1998), the genetic contribution to the cause of RA is estimated at 15-30%. Another set of researchers consider certain infections or chemicals might cause the disease. Several studies are being done to conform this. The initiator of the RA process is an infectious or noxious agent which is yet to be fully identified and confirmed (Kumar and Clark, 1998). Once this agent initiates an acute inflammatory synovitis, an auto-immune reaction results (Panayi, 1986). In yet another set of studies it was proposed that with the infiltration of T cells, inflammatory mediators and lytic cytokines are released locally which destroy the joint (Cotran et al, 1994). Instead of normal resolution after the acute response, the inflammatory process becomes chronic and self sustaining, even though the initiating factor has long disappeared (Cotran et al, 1994). Some people also think hormones may play a role in the manifestation of RA. But this, too, is still uncertain, even though women are more apt to suffer from RA than are men. Studies point out that symptoms develop as the result of many other factors as well, including: bacterial and viral infections; the use of prescription and/or illegal drugs; contact with certain chemicals; traumatic injury such as a broken bone, torn ligament, or sprained ankle; bowel disorders such as ileitis and colitis; and obesity, which often aggravates arthritic conditions (DynoMed.com, 2000). PATHOLOGY Rheumatoid arthritis normally progresses through three stages of disease development. The first stage includes synovitis then joint destruction starts and finally ends up in deformity (Apley and Solomon, 1993). Once the initial synovial inflammation occurs, the synovium becomes hypertrophied to form granulation tissue (pannus), which spreads over the cartilage surface causing destruction. In the 'bare areas' of the joint where bone does not get the coverage with cartilage, pannus directly invades into the bone resulting in marginal erosions. In the final stages, a fibrous or bony ankylosis of the joint takes place (Yochum and Rowe, 1993). DIAGNOSIS The manifestation of symptoms in the same joint on both feet or in several joints is an indication that RA might be involved. When the doctor first identifies the symptoms of RA, the patient is diagnosed on the basis of a clinical examination as well as blood tests. To further evaluate the patient's foot and ankle problems, the surgeon may order x-rays and/or other imaging tests (FootPhysicans.com, 2007). Along with plain x-rays, radioisotope bone scans, using technetium- labeled diphosphonate complexes may be used to indicate increased uptake around inflamed joints due to the increased blood flow. However, they do not offer any great advantage over a plain x-ray in the diagnosis and assessment of rheumatoid arthritis (Dieppe et al, 1985). TREATMENT A study conducted by Vidigal et al. in 1975 reported that Hallux valgus was very common and occurred with similar frequency to disease in the other metatarsophalangeal joints. Although not exclusive to rheumatoid arthritis, hallux valgus must have been caused for the most part by the rheumatoid arthritis and if so, then it is suggested that the provision of suitable shoes for patients may be less costly than subsequent surgical treatment. Forefoot involvement with hallux valgus and lesser metatarsophalangeal joint subluxation and dislocation are among the most common findings in different studies. Reconstruction usually requires lesser metatarsophalangeal joint excisional arthroplasty and first metatarsophalangeal joint arthrodesis. Midfoot tarsometatarsal and intertarsal involvement is treated with orthotic devices and intertarsal fusion for advanced arthropathy. Hindfoot involvement frequently leads to pes planovalgus deformity that may require isolated talonavicular arthrodesis if treated early or triple arthrodesis for advanced destruction (Abdo and Iorio, 1994). While treatment of RA focuses on the medication prescribed by a patient's primary doctor or rheumatologist, the foot and ankle surgeon will develop a treatment plan aimed at relieving the pain of RA-related foot problems. The doctor decides one or more options of the following depending on the patient: Orthotic devices: In this treatment, the surgeon often fits the patient with custom orthotic devices to provide cushioning for rheumatoid nodules, minimize pain when walking, and give needed support to improve the foot's mechanics. Accommodative shoes: This is among the most common treatments followed. These shoes are used to relieve pressure and pain and assist with walking. Aspiration of fluid: When the patient is suffering from inflammation and pain in a joint, the surgeon may aspirate (draw out) fluid to reduce the swelling and pain (FootPhysicans.com, 2007). Drugs: Some drugs can help control the disease. A rheumatologist will often suggest Nonsteroidal anti-inflammatories. These may include Acetylsalicylic acid (aspirin); Ibuprofen; Indomethacin; Naproxen; and Tolmetin (DynoMed.com, 2000). Steroid injections: Injections of anti-inflammatory medication may be applied directly to an inflamed joint or to a rheumatoid nodule. However these are also associated with several side effects. Surgery: Patients may have to undergo multiple surgeries based of the manifestation of RA. Often the pain and deformity associated with RA in the foot is relieved through surgery. The foot and ankle surgeon will select the procedure best suited to the patient's condition and lifestyle (FootPhysicans.com, 2007). Surgery is a most common way to treat RA of the foot and ankle, such as bunions and hammer toes. In many cases, however, the most successful surgical option is fusion (arthrodesis). Fusion is often performed on the great toe, in the midfoot, in the heel, and in the ankle. In this procedure, the joint cartilage is removed; in some cases, some of the adjacent bone is also removed. The bones are held in place with screws, plates and screws or a rod through the bone. The surgeon may then implant a bone graft from the hip or leg. Eventually, the bones unite, creating one solid bone. There is loss of motion, but the foot and ankle remain functional and generally pain-free. Replacing the ankle joint with an artificial joint (arthroplasty) may be possible. However, this is a relatively new surgical technique. Whether it will be as successful in the long term as hip or knee replacement surgery is not yet known (AAOS, 2001). Since RA is a progressive autoimmune disease it currently has no cure. RA in the foot and ankle is a very serious problem. As the disease progresses the joints undergo severe deformities. However, medications, exercises, and surgery can help lessen the effects of the disease and may slow its progress. It can be diagnosed at the early stages and with the help of the physician a patient can slow down the disease progression. References Abdo, R.V. and Iorio, L.J. 1994. Rheumatoid Arthritis of the Foot and Ankle. J Am Acad Orthop Surg.1994; 2: 326-332. American Orthopaedic Foot and Ankle Society (AAOS), 2001. Rheumatoid Arthritis of the Foot and Ankle [Online] Available: http://orthoinfo.aaos.org/fact/thr_report.cfmThread_ID=332 [Accessed on 15 March 2007]. Apley, A.G., Solomon, L. 1993. Apley's System of Orthopaedics and Fractures. (7th ed). Butterworth-Heinemann Ltd, Oxford. Bal, A., Aydog, E., TolgaAydog, S. and Cakci, A. 2006. Foot deformities in rheumatoid arthritis and relevance of foot function index. Clinical Rheumatology Vol 25, No. 5 September, 2006: 671-675. Cotran, R.S., Kumar, V., Robbins, S.L. 1994. Robbin's Pathological Basis of Disease. (5th ed). W.B. Saunders, Philadelphia. Dieppe, P.A., Doherty, M., Macfarlane, G.M., Maddison, P.J. 1985. Rheumatological Medicine. Churchill Livingstone, Edinburgh. DynoMed.com, 2000. Rheumatoid foot and ankle. [Online] DynoMed encyclopedia. Available: http://www.dynomed.com/encyclopedia/encyclopedia/foot_and_ankle/Rheumatoid_foot_and_ankle.html [Accessed on 16 March 2007]. footandankle.mdmercy.com, N.D. Rheumatoid Arthritis: Foot and Ankle Conditions. [Online] The Institute for Foot and Ankle Reconstruction at Mercy Available: http://footandankle.mdmercy.com/conditions/rheumatoid/rheumatoid_arth.html [Accessed on 16 March 2007]. FootPhysicans.com, 2007. Rheumatoid Arthritis in the Foot and Ankle. [Online] February 19, 2007 American College of Foot and Ankle Surgeons. Available: http://www.footphysicians.com/footankleinfo/Rheumatoid_Arthritis.htm [Accessed on 17 March 2007]. Kumar, P. and Clark, M. 1998. Clinical Medicine. (4th ed). W.B. Saunders, Edinburgh. Panayi, G.S. 1986. The aetiopathogenesis of rheumatoid arthritis. In Scott, J.T. (Ed) Copeman's Textbook of the Rheumatic Diseases. (6th ed). Churchill Livingstone, Edinburgh. pp. 595-603. Roth, R.D. 1994. Rheumatoid Arthritis. In Oloff, L.M. (Ed) Musculoskeletal Disorders of Lower Extremities. W.B. Saunders, Philadelphia. Shiel, W.C. 2006. Rheumatoid Arthritis. [Online] 16 October 2006 MedicineNet, Inc. Available: http://www.medicinenet.com/rheumatoid_arthritis/article.htm [Accessed on 15 March 2007]. Vidigal, E., Jacoby, R. K., Dixon, A. S. Ratliff, A. H. and Kirkup, J. 1975. The foot in chronic rheumatoid arthritis. Ann Rheum Dis. August; 34(4): 292-297. Yochum, T.R., Rowe, L.J. 1987. Essentials of Skeletal Radiology. Williams and Wilkins, Baltimore. Read More
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