Foot Problems and Their Conservative Treatment in Rheumatoid Arthritis

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FOOT PROBLEMS AND THEIR CONSERVATIVE TREATMENT IN RHEUMATOID ARTHRITIS Clay Miller, MD, MFA, and David L. Nash, MD

This article presents basic information on the biomechanics of the foot with rheumatoid arthritis (RA)and the pathogenesis of foot deformities commonly seen in RA. The understanding of these concepts form the basis for the application of necessary treatments to prevent and control damage to the rheumatoid hindfoot, midfoot, and forefoot. The major foot deformities in patients with RA are the pronated foot, hallux valgus, depression of the metatarsal heads, hammer or claw toes, tendocalcaneal bursitis, subplantar spur formation, and hallux rigi d ~ ~s, .lo, ~ 14, , l5 Studies show that RA affects the foot initially in 16% of cases,', 8, lo,l4 and in patients who have had a 10-year history or more of RA, nearly 90% to 100% have shown clinical involvement of the feet.lO,l2 For conservative treatment to prevent and control damage caused by RA to the foot and optimize comfort and function, an early accurate diagnosis, maximal pharmacologic and physical management, and patient education with compliance are mandatory. This can best be achieved through a multidisciplinary approach involving a team that may include a physiatrist, rheumatologist, orthopedist, physical and occupationaltherapist, and orthotist, each bringing a unique professional expertise to the care of the patient with RA. PATHOGENESIS

The common foot deformities seen in RA result from the interaction of active synovitis and mechanical stress. The rheumatoid process affects From the Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota

PHYSICAL MEDICINE AND REHABILITATION CLINICS OF NORTH AMERICA VOLUME 5 NUMBER 4 . NOVEMBER 1994

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the intra-articular synovium, the synovial fluid, and the tendon sheath synovium. The hyaline cartilage and bone are subject to enzymatic erosive damage by synovial panus. Degradative enzymes directly attack collagen and the cartilage proteoglycan matrix. The periarticular bone becomes osteopenic. The ligamentous supporting structures are stretched by the swelling and loose tensile strength. Intrinsic foot muscles and tendons are also weakened by this process. Pain often accompanies the synovitis and limits motion, which in turn hastens the weakening process. The stress of ambulation stretches the intermetatarsal ligaments and the forefoot widens. Rupturing of the extensor tendons of the foot can occur and results in dorsal subluxation of the toes on the metatarsal heads. This produces the characteristic hammer or claw toes (Figs. 1 and 2). The fat pad beneath the metatarsals slowly migrates forward leaving only a thin covering over the metatarsal heads. The subluxing metatarsal heads, widening of the forefoot, and displacement of the protective fat pad makes the rheumatoid foot vulnerable to develop metatarsalgia (see Fig. 2). The splay foot refers to widening of the forefoot as a result of metatarsal phalangeal joint swelling and weakening of periarticular ligaments and intrinsic foot muscles by the synovitis. The spread of the forefoot seems to increase with duration of the disease in the presence of metatarsal erosion. This is not affected, however, by lesions in the m i d f ~ o t . ~ Hallux valgus is reported as one of the most common forefoot deformities15(see Figs. 2 and 3). As the subtalar joint pronates in midstance, ground reaction forces push the great toe into abduction. Inflammatory synovitisin the metatarsophalangeal joint of the great toe causes ligamentous laxity and joint instability. These factors weaken the structural integ-

Figure 1. Cock-up deformity of the second toe representing hammer toe commonly seen in RA. (Reprinted from the ARHP Arthritis Teaching Slide Collection. Used with permission of the American College of Rheumatology.)

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Figure 2. Hallux valgus deformities of both great toes and hammer toe deformities. The hammer toes are associated with subluxation of the metatarsophalangeal joints which can lead to metatarsalgia. (Reprinted from the ARHP Arthritis Teaching Slide Collection. Used with permission of the American College of Rheumatology.)

Figure 3. Hallux valgus deformity seen in the RA foot. The lateral deviation of the great toe can lead t o impingement of the other toes and possible skin ulceration due to increased pressure. (Reprinted from the ARHP Arthritis Teaching Slide Collection. Used with permission of the American College of Rheurnatology.)

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rity of the metatarsophalangeal joint and make it more vulnerable to the mechanical stresses of gait-causing lateral deviation of the proximal and distal phalanx of the great toe. The action of the flexor and extensor muscles on the great toe shift laterally as they contract, and as the intrinsic adductors shorten, they overpower the overstretched abductor intrinsic muscles of the foot, causing even further lateral movement of the great toe7 (see Fig. 2). Subtalar joint pronation resulting in valgus deformity occurs early in the RA foot. because the talonavicular ioint is commonlv affected, resulting in a weight-bearinginduced malaiignment.7,lo ~he'ali~nment of the subtalar joint has major implications, because alterations in subtalar joint function have significant impact on both proximal and distal joints of the foot and ankle.13 Valgus deformity occurs as the hindfoot overpronates during ambulation on the weakened, inflamed subtalar joint (Fig. 4). The head of the talus shifts in a plantar and medial direction losing its normal locking mechanism. An increased medial moment occurs causing increased depression of the medial longitudinal arch. The calcaneus then outwardly rotates causing a valgus deformity of the heel during weight bearing. Of note, this instability in the hindfoot can lead to previously discussed hallux valgus, metatarsal head depression, and forefoot deformities. Radiographic evidence shows early involvement of the subtalar joint in the first few years of early RA.18It has been suggested that posterior tibialis weakness contributes to hindfoot valgus and pronation deformities. Keenan et al,13however, showed that patients with valgus deformity of the hindfoot and RA had no evidence of tibialis vosterior deficiencv or weakness. Electromyography studies demonstraied that the tibia&

Figure 4. Valgus deformity of the feet. This occurs as the foot overpronates and the medial longitudinal arch flattens with ligamentous laxity in the RA foot. The calcaneus then rotates outwardly creating this deformity. (Reprinted from the ARHP Arthritis Teaching Slide Collection. Used with permission of the American College of Rheumatology.)

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posterior intensity and duration of activity were increased significantly. Decreases in velocity, stride length, single-limb support time, and delayed heel rise were greater in patients who had hindfoot valgus deformity. The study suggests that the valgus deformity of the hindfoot in RA patients results from exaggerated pronation forces on a weakened and inflamed subtalar joint. Radiographic evidence also showed an association between the valgus deformity of the feet and a valgus deformity of the knees in vatients with RA.13 Hallux rigidus is another common phenomenon in the RA foot.17 The great toe develops a fixed deformity (ankylosis) with osteophyte formation at the metatarsophalangeal joint. This deformity occurs because the great toe is held elevated to avoid painful loading of the medial ray. A dorsiflexion contracture can be seen in the beginning followed by the fixed deformity. The painful heel can occur as a result of inflammation at several areas of tendon attachment. Both the plantar aponeurosis origin and the insertion of the Achilles tendon can be inflamed and painful in the RA foot. The windlass plantar fascial mechanism is responsible for absorbing approximately 75% of the forces transmitted to the foot arches during ambulation (Fig. 5). Bone spur formation can occur at the plantar aponeurosis origin in response to these traction force^.^ This irregularity can increase irritation and pain at the site of the attachment. The bursa between the Achilles tendon and the calcaneous can become inflamed as well as the insertion of the Achilles tendon itself. Both receive repetitive mechanical stress and irritation as the calf muscles transmit force to the calcaneus during toe-off in the gait cycle. The resulting pain can cause

Figure 5. Windlass effect allowing 75% absorption of forces transmitted to the foot arches during ambulation. (From Newell SG, Miller SJ: Conservative treatment of plantar fascial strain. The Physician and Sports Medicine5(11):68-73,1977; with permission of McGraw-Hill.)

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a decrease in push-off and a delay in heel rise, disrupting the normal gait pattern. FUNCTIONAL ANATOMY

During the normal gait pattern, on heel strike, the foot usually strikes the ground in supination and pronates as the foot accepts the full body weight in midstance followed by supination as the limb advances toward toe-off. The foot is linked to the knee in a closed-chain-kinetic function relationship. Any inability of the foot to rotate within its function will affect the natural rotational movements of the knee. The subtalar joint has an axis that lies in the oblique plane at about 40 degrees to the horizontal and 15 degrees medial to the sagittal plane. This allows a wide range of normal joint movements for the foot.1 The midtarsal joints in the forefoot permit rotation between the forefoot and the subtalar joint. In midstance, when the forefoot is flat on the floor, the relationship of the calcaneus to the talus is ideally in a neutral position, neither inverted nor everted. Because of this relationship, normal variations of the forefoot lying either in the inverted or everted position to the transverse plane can be compensated by the rotation of the subtalar joint (Fig. 6). In RA with involvement of the subtalar joint, these compensatory movements are lost and result in abnormal rotatory stresses in the midfoot and hindfoot. Clinically, calcaneal eversion is associated with hindfoot valgus and secondary forefoot varus deviation culminating in a collapse of the medial longitudinal arch. This is the commonly seen pronated rheumatoid foot. Less common is the inverted or varus hindfoot deformity with secondary axial rotation of the tarsals to achieve floor contact with the first ray.

Figure 6. Normal functional biomechanics of the hindfoot. The forefoot in supination at heel strike (A); pronation occurs at foot flat (mid-stance) (B and C). Medial posts correct pronation. (Adapted from lnrnan VT (ed): DuVries' Surgery of the Foot, ed 3. St. Louis, C.V. Mosby, 1973, p 432; with permission.)

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This foot is often quite stiff with weight-bearing forces primarily at the lateral forefoot. The primary foot and ankle motions during normal gait include ankle dorsiflexion and plantarflexion as well as supination and pronation of the foot. Supination and pronation are complex three-dimensional combinations of motion at the foot and ankle. Pronation consists of three movements: dorsiflexion, eversion, and abduction. Supination is composed of the opposite motions of pronation: plantar flexion, inversion, and adduction. Rotation occurs along the longitudinal axis of the foot at the subtalar and midtarsal joints. This rotation is a major component of pronation and supination. At the beginning of stance phase, the heel makes contact with the floor in supination. As the body weight is transferred to the foot in midstance, pronation occurs, acting as shock absorbers. The foot resupinates as the body weight is transferred to the forefoot at toe-off. In RA, the joints become hypermobile. The hypermobile talonavicular joint allows the foot to pronate excessively during weight bearing. Subtalar eversion then follows. Free motion then is allowed at the midtarsal joints and the midfoot locking mechanism. Increased motion then is allowed at the midtarsal joints. Deformities of the subtalar and midtarsal joints occur as a result of the disease process, weakening the intrinsic foot support structure and mechanical weight-bearing forces on the hypermobile foot. FOOT DEFORMITIES AND THEIR TREATMENTS

The goal of treating arthritic feet is to limit foot damage, deformity, and disability, and to restore the highest level of physical function (Table 1). Early diagnosis is crucial to instituting therapeutic management to Table 1. RHEUMATOID ARTHRITIS FOOT DEFORMITIES AND THEIR TREATMENTS Nono~erativeTreatment

Foot Deformitv Hammer or claw toes Metatarsalgia Splay foot Heel pain Excessive pronation Severe pronation

Subtalar collapse Severe deformed feet Severe foot pain AFO

=

Wide toe box shoe, metatarsal pad, metatarsal bar Metatarsal bar on outside of oxford or athletic shoe, metatarsal pad Wide toe box, oxford or athletic shoe Cushioned heel, heel cups, orthotic inserts Oxford or athletic shoe, medial wedging, medial heel counters, custom molded orthotic inserts Oxford shoe, rocker bottom sole, floated heel, medial heel flaring, medial wedging solid AFO, lateral single or double metal bar upright AFO with Y strap, cane, crutch cane or walker Custom molded hind foot AFO Accommodative custom molded shoes, cane, crutch cane or walker Patellar tendon bearing AFO, cane, crutch cane or walker

ankle foot orthosis.

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limit the intensity of inflammation and damage to the foot. Radiographic studies show early joint damage even in the first few years.18The active inflammatory stage of RA can cause pain, swelling, weakness, joint deformity, fusion, joint laxity, contracture formation, and functional limitations. The patient's ability to ambulate and transfer in and out of bed, on and off the toilet, in and out of chairs or cars can all be severely affected. These functional activities can be addressed by the physical and occupational therapists to minimize stress to the rheumatoid foot. INFLAMMATION AND PAIN CONTROL MODALITIES

The acute inflammatory stage of RA can be treated both medically with pharmacologic intervention as well as physical modalities for pain relief. During periods of active inflammation, avoidance of weight bearing and stresses on the affected joints may be necessary and appropriate. Use of splinting and complete bed rest, as well as the use of assisted gait aid devices to protect the joints may also be r e q ~ i r e d .7,~lo, , l4 With gait aids, weight bearing can begin as joint swelling decreases and lower extremity pain has improved. The use of platform crutches not only reduces forces in the lower extremities, but also helps protect the upper extremity joints as well during this period of active joint inflammation. Standard crutches or walkers can be used with mild arthritis in the upper extremities. Superficial heat and cold can also be used for pain control. Mild superficial heat can reduce the pain of acute inflammation. The use of a heating pad, contrast baths, and hydrotherapy at 99°F are helpful in controlling pain. Deep heating of acutely or chronically inflamed joints should be avoided. This may increase the lysosomal enzyme degradation and worsen the joint destruction. The use of deeper heating modalities such as ultrasound and paraffin baths for acutely inflamed small joints of hands and feet can theoretically lead to activation of destructive enzymes. Ultrasound and paraffin to small joints should be avoided in the acute phase of inflammatory RA but could be considered during remission to make collagen a little more pliable and assist in effectively stretching a contracted joint. Contrast baths can provide some comfortby heating affected feet with periodic brief immersions in cold water to prevent swelling from the sustained heating. Vigorous cooling can increase stiffness and may aggravate Raynaud's phenomenon which can occur in RA. Icing or other uses of cold should be used with precaution. Wearing socks to bed or the use of electric heating blankets can be helpful in reducing morning stiffness and pain. Electrically heated socks may be helpful when exposed to cold weather. FOOT PROTECTION

Protecting the foot during the acute inflammatory stages of RA has been known to be helpful. Important goals in joint protection include

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avoiding positions that favor deformity, distributing weight-bearing forces over a greater surface area underneath the foot, and redirecting forces to minimize deformation of vulnerable joints. The use of radiographs and pressure sensors such as the F scan may aid in determining which joints are being affected, as well as what areas of the foot are experiencing increased pressure.16 This may be useful clinically when developing orthoses for joint protection and improving the biomechanics of the foot. Another important way to improve joint protection is through energy conservation. This helps the patient avoid fatigue, which can result in increased forces on the rheumatoid foot. Avoiding stressful activity, resting for short periods during household chores, and a midday nap can all help prevent excessive fatigue. Good nutrition and getting a good night's sleep of from 8 to 10 hours are also beneficial. Other forms of joint protection for the foot include avoiding sitting with the legs crossed, and not sitting with the metatarsophalangeal joints of the feet carrying all of the weight. Relieving weight on the foot can be achieved by supporting calves with a foot support stool.

EXERCISE

Stretching and strengthening exercises are important for contracture deformity prevention to maintain endurance and strength, and preserve as much normal range of motion as possible. The type of range of motion and strengthening exercises needs to be modified based on the stage of active inflammation during RA. Range of motion exercises can be passive, active, or active assistive. Passive range of motion is recommended during the acute inflammation. Active assistive range of motion can also be used as long as pain is avoided. During quiescent phases of RA, more active range of motion and prolonged stretching from 30 seconds to 1minute can be helpful in preventing contracture to risk joints. Ideally, applying heat 20 minutes twice a day prior to stretching is recommended. If pain persists longer than a 2-hour period following exercise, the patient should be aware that their exercises are too intense and need to reduce their time of exercise. It may be helpful to instruct patients on the subtalar neutral position of the foot, avoiding external rotation of the leg during weight bearing, and avoiding foot and ankle eversion during calf stretches. Strengthening during the acute inflammation period should be avoided. Isometric strengthening exercises are best during subacute phases. These help maintain muscle strength and minimize risk to joint integrity. Several repetitions of 6-second isometric contractions twice daily can help maintain muscle strength. Isometric strengthening can help maintain muscle strength in and around the arthritic ankle joint without exacerbating any joint deformity. Inversion strengthening for anterior and posterior tibialis muscles would be the most commonly useful strengthening exercise at the ankle.

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During the quiescent phase of the rheumatoid foot, pool therapy can improve both strength and endurance. Rubber tubing and bands can also be used during this quiescent stage. Strengthening exercises for the tibialis anterior, tibialis posterior, and foot intrinsics help to prevent the collapse of the medial arch. If pain persists for longer than a 2-hour period following exercises than the strengthening exercises are too vigorous. The patients should be instructed how to guide the level of their exercises based on their level of pain. ORTHOSES

Selecting appropriate footwear is extremely important. Appropriate footwear can stabilize hypermobile joints, helping to prevent deformities from occurring. If foot deformities have already occurred, accommodative foot wear can help provide comfort and reduce abnormal pressures on the foot, thereby helping to prevent further progression of the deformity. Generally, accommodating shoes should provide extra depth and width in the toe box and soft leather upper. These shoes are designed to accommodate molded plastazote inserts fit to better distribute weightbearing pressure. Occasionally custom molding and fabrication of a shoe to accommodate more severe deformities are required. The standard oxford or athletic walking shoe is a common choice for RA footwear (Fig. 7). Orthodigital splinting with a silicone rubber putty can be used in cases such as hallux valgus to help support and prevent the further

Figure 7. Examples of footwear used on the RAfoot. (Reprintedfrom the ARHP Arthritis Teaching Slide Collection. Used with permission of the American College of Rheumatology.)

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Figure 8. Orthotic inserts can decrease foot pain at the heel and plantar fascia insertion. (Reprinted from the ARHP Arthritis Teaching Slide Collection. Used with permission of the American College of Rheumatology.)

progression of the deformity. Putty can be molded directly to the patient's toes to protect and correct the def0rmity.l Hammer and claw toe deformities can be accommodated in a wide toe box with a soft leather upper to reduce irritation of pressure on the lateral and dorsal aspects of the toes (see Fig. 7). A metatarsal pad can also be used to elevate the metatarsals and reduce the hammer and claw toe deformities. A metatarsal bar on the sole of the shoe is still used by some to reduce weight-bearing pressure under the metatarsal heads. A metatarsal bar added to the outside of the shoe situated behind the metatarsal heads relieves weight-bearing stress and pain in the RA foot with metatarsalgia. A 0.25- to 0.50-inch bar can be used depending on the severity of the pain. Metatarsal bar greatly reduces the pressure of push-off on the metatarsal heads. One must weigh the potential risk, however, of the metatarsal bar being a potential hazard to causing tripping and falling. In heel pain, local management involves controlling forces that affect the Achilles tendon insertion and the insertion of the plantar fascia. The heel in the shoe should be of a soft rubber cushioning. A firm medial heel counter to resist pronation forces is also desirable. Orthotic inserts can decrease the mechanical forces and pain at the plantar fascia insertion (Fig. 8). Prefabricated heel cups can be tried before considering the more expensive molded foot orthoses. Using a cane or crutch in conjunction with these shoe modifications may also provide some symptom relief.'

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SUBTALAR PRONATION

The oxford shoe with a cushion heel and rocker sole is commonly used to help reduce forces transmitted at heel strike and reduce to a minimum foot and ankle movement during gait. If the cushion heel is too soft, however, it can cause an unsteady gait. The rocker sole provides the ability of the foot to roll over this sole in the toe-off phase of gait with minimal motion at the metatarsophalangeal joint. Progressive pronation deformity commonly occurs in the RA foot in the subtalar joint. This occurs as inflammation progresses in the subtalar joint as well as weakening and inflammation of the tibialis posterior tendon. As the tibialis posterior tendon weakens, the medial arch will progressively flatten as the foot collapses into pronation. In correcting the pronation deformity, one must evaluate the ability to invert the hindfoot to a neutral subtalar position and the flexibility of the forefoot to be able to rotate the medial side of the foot to the floor. Progression of pronation and hindfoot valgus causes the talus to fall downward toward the medial side of the foot in a plantar direction, creating a palpable bony talonavicular prominence at the collapsed midarch region. Shoe modifications can help prevent foot deformities in the subtalar joint as well as early synectomy of the tibialis posterior tendon which can reduce or delay tendon infiltration, incompetence, or rupture.12 Controlling the collapse of the subtalar joint requires firm support. Molded polypropylene orthoses such as a submalleolar foot orthosis with medial hindfoot and forefoot posting can be used. A specific hindfoot orthosis has also been recommended (Fig. 9).9A firm shoe with a stiff

Figure 9. Patient wearing custom-formed leg-hindfoot orthosis used in patients with deformities localized to the hindfoot. (Reprinted from Hunt GC, Fromherz WA, Gerber LH, Hurwitz SR: Hindfoot pain treated by a leg-hindfoot orthosis: A case report. Physical Therapy 67(9):1384-1388,1987; with permission of the American Physical Therapy Association.)

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medial heel counter or added medial buttress can also provide sufficient support to prevent collapse into excessive pronation. In severely deformed feet, shoe and orthotic modifications that accommodate rather than correct the deformity need to be considered. Molded shoes made from a cast positive mold of the patient's feet may be the only way to accommodate the feet. Extra depth shoes with soft leather will help accommodate the forefoot spread and bony prominence of foot and toe deformities. The extra depth shoe also accommodates light-weight foam inserts molded to evenly distribute weight-bearing forces across the sole of the foot. This is particularly helpful with painful and prominent metatarsal heads. Velcro straps for shoe closure are also a consideration, because patients with RA feet often have involvement of the hands. Forefoot supination can cause pronation of the hindfoot and vice versa. In forefoot supination, the first metatarsal segment elevates in relation to the fifth. This causes the calcaneus and the talus to tilt medially and plantarly. Medially wedging the forefoot can help support the supinated forefoot, allowing for the hindfoot to remain in a more neutral position. Supporting the medial longitudinal arch is also important when there is excessive pronation. A medium density foam such as plastazote can be used to support the medial arch and accommodate any bony prominences. In severe pronation, external modifications to the shoe may be necessary to control the medial moment of pronation. This can be achieved with flaring of the medial heel. The flare can extend approximately 318 of an inch to 112 inch from the heel and sole line. A firm supportive material can be added to this medial heel flare extending up the medial side of the shoe, forming a medial buttress which is effective in preventing the foot from collapsing into excessive pronation. A medial wedge can be placed inside the shoe to assist holding the heel in slight inversion and counteract the heel tendency to slip into eversion. Certain RA foot patients may not be able to tolerate rigid foot orthoses yet may need more support than the usual shoe modifications to manage a painful rheumatoid foot deformity. An option would be to use a lateral single-metal-bar or double-bar upright short leg brace with a leather Y strap (Fig. 10). This orthosis can be attached to a leatherheeled shoe and help provide control of the medial moment of the medial longitudinal arch during gait. Hunt et a19describe a case report of a custom molded polypropylene leg-hindfoot orthosis device that successfully reduced subtalar and ankle joint pain and improved gait parameters in an RA patient (see Fig. 9). The custom molded orthosis cups the heel and extends proximally up the posterior medial and lateral side of the ankle supporting the hindfoot. It extends upward to the distal third of the tibia and fibula. It provides control in the frontal plane of the calcaneal eversion and inversion and pronation with bimalleolar contact and medial lateral support of the calcaneus. The apparent advantage of this orthosis is that in patients

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Figure 10. A and 6,Lateral single upright short leg brace with leather Y strap can be used in more severely affected RA feet. (From Rose CK: Pes planus. In Jahss MJ (ed): Disorders of the Foot. Philadelphia, WB Saunders, 1982, p 506; with permission.)

who have limited forefoot involvement, this orthosis allows the foot mechanics in the forefoot to work normally while supporting the subtalar joint. When foot pain becomes too severe even in patients who have custom molded orthotic inserts or custom molded ankle foot orthoses, a patellar tendon-bearing ankle-foot orthosis may be useful (Fig. 11). This orthosis has a molded plastic shell that places body weight on the medial tibia1 flare and patellar tendon. Weight bearing is reduced by approximately 45% in the ankle subtalar joint. This bracing is effective if there is no involvement of the knee. The patellar tendon weightbearing brace can be made of light plastic and can be used with regular shoes. As with all the custom orthoses used for the lower extremity, a cane or platform crutch may be necessary to help unload the stresses on that involved foot and help to improve the pattern of the patient's gait. SUMMARY

In treating the RA foot and common presenting deformities, a multidisciplinary approach is highly recommended. Early diagnosis and preventive measures are crucial in preventing the progression of severely destructive changes resulting in deformities of the feet. This involves the coordinated efforts of the rheumatologist, the physiatrist, occupa-

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Figure 11. Patellar tendon weightbearing (PTB) brace used to decrease weight bearing through foot and ankle by transferring some of the weight-bearing load to the knee. May not be practical with knee arthritis. (Reprinted from Orthopaedic Review Vol. 16:9; 1987, [pgs. 671-6761,)

tional and physical therapists, the orthotist, and the orthopedic surgeon. Careful clinical assessment as to the joints being affected allows the clinician to begin preventative treatment not only through medications but also through the physical medicine and rehabilitation principles discussed in this article. If the RA foot problems do progress, surgical evaluation may be necessary in conjunction with custom-fitted orthoses to correct and support these deformities. Each patient's deformities need to be evaluated independently and close follow-up is necessary to make modifications throughout the lifetime course of their rheumatic disease. References 1. Anderson EG: The rheumatoid foot: A sideways look. Ann Rheum Dis 49(suppl 2):851-857, 1990

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2. Benson GM, Johnson EW Jr: Management of the foot in rheumatoid arthritis. Orthop Clin North Am 2:733, 1971 3. Bouysset M, Tebib J, Noel E, et al: Rheumatoid metatarsus: The original evolution of the first metatarsal. Clin Rheumatol 10:408-412, 1991 4. Bouysset M, Tebib JG, Weil G, et al: Deformation of the adult rheumatoid rear foot: A radiographic study. Clin Rheumatol 6:539-544, 1987 5. Cailliet R: Foot and Ankle pain, ed 2. Philadelphia, FA Davis, 1983, pp 41-45 6. DeLisa JA, Gans BM: Rehabilitation Medicine: Principles and Practice. ed 2. Philadelphia, JB Lippincott Co, 1993, pp 1059-1062 7. Dimonte P, Light H: Pathomechanics, gait deviations, and treatment of the rheumatoid foot: A clinical report. Physical Therapy 62:1148-1156, 1982 8. Geppert MJ, Sobil M, ~ b h n eWH: Ceumatoid foot, part I: Forefoot. Foot Ankle 13:550-558, 1992 9. Hunt GC, Fromherz WA, Gerber LH, et al: Hind foot pain treated by leg hind foot orthoses: In case report. Physical Therapy 67:1384-1388, 1987 10. Jacobs SR: Rehabilitation of the person with arthritis of the ankle and foot. Clin Podiatr 1:373-399, 1984 11. Johnson KA: Surgery of the Foot and Ankle. New York, Raven Press, 1989 12. Johnson KA: Tibialis posterior tendon rupture. Clin Orthop 177:140-147, 1983 13. Keenan ME, Peabody TD, Gronley JK, et al: Valgus deformities of the feet and characteristics of gait in patients who have rheumatoid arthritis. J Bone Joint Surg Br 73:237-247, 1991 14. Kitaoka HB: Rheumatoid hind foot. Orthop Clin North Am 20:593-604, 1989 15. McGuire T, Kumar VN: Rehabilitation management of the rheumatoid foot. Orthop Rev 16(9):83-88, 1987 16. Rose NE, Feiwill LA, Cracchiolo A: A method of measuring foot pressures using a high resolution, computerized insole sensor: The effects of heel wedges on plantar pressure distribution and center of force. Foot Ankle 13:263-270, 1992 17. Vainio K: The rheumatoid foot: A clinical study with pathological and roentgenological comments. Clin Orthop 265:4-8, 1991 18. Van der Heijde DM, Van Leeuwen MA, Van Riel PL, et al: Biannual radiographic assessment of hands and feet in a 3-year perspective followup of patients with early rheumatoid arthritis. Arthritis Rheum 35:26-34, 1992

Address reprint requests to Clay Miller, MD, MFA Mayo Clinic 200 First Street SW Rochester, MN 55905