You are in: eMedicine Specialties > Plastic Surgery > HAND Hand, Rheumatoid HandArticle Last Updated: Feb 25, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 10
 
Author: Michael Neumeister, MD, FRCSC, FACS, Program Director, Assistant Professor, Department of Surgery, Division of Plastic Surgery, Southern Illinois University School of Medicine Michael Neumeister is a member of the following medical societies: American Academy of Dermatology, American Association for Hand Surgery, American Burn Association, American Medical Association, American Society of Plastic Surgeons, Canadian Medical Association, College of Physicians and Surgeons of Alberta, College of Physicians and Surgeons of Ontario, Pacific Dermatologic Association, Royal College of Physicians and Surgeons of Canada, and Undersea and Hyperbaric Medical Society Coauthor(s): Minh-Doan Nguyen, MD, Staff Physician, Department of Surgery, Division of Plastic Surgery, Southern Illinois University School of Medicine; Bradon J Wilhelmi, MD, Endowed Leonard Weiner, MD, Professor and Chief of Division of Plastic Surgery, Residency Program Director, University of Louisville School of Medicine Editors: Anthony E Sudekum, MD, Consulting Staff, Department of Plastic Surgery, St John's Mercy Health Center of Saint Louis; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; David W Chang, MD, FACS, Associate Professor, Department of Plastic Surgery, MD Anderson Cancer Center, The University of Texas; Nicolas (Nick) G Slenkovich, MD, Practice Director, Colorado Plastic Surgery Center at Swedish Medical Center; Subhas Gupta, MD, PhD, CM, FRCS(C), FACS, Professor of Surgery, Chair, Department of Plastic Surgery, Director of Plastic Surgery Residency, Director of Comprehensive Wound Service, Department of Plastic Surgery, Loma Linda University School of Medicine Author and Editor Disclosure Synonyms and related keywords: rheumatoid arthritis, RA, arthritis, rheumatism, synovial hypertrophy, matrix metalloproteinase, MMP, tumor necrosis factor-alpha, TNF-alpha, TNF-a, interleukin-1, IL-1, synovectomy, tenosynovectomy, tendon realignment, reconstruction surgery, arthroplasty, arthrodesis, tenosynovitis, paratenon, synovium, metacarpophalangeal joint, MP joint, MCP joint, rheumatoid nodule, trigger finger, finger triggering, tendon rupture, swan neck deformity, swan-neck deformity, boutonniere deformity, skier's thumb, gamekeeper's thumb, skiers thumb, gamekeepers thumb, hand deformity, synovial proliferation, synovial inflammation, carpal tunnel release, Vaughn-Jackson lesion, caput ulna syndrome INTRODUCTIONSection 2 of 10
 
Rheumatoid arthritis (RA) is a systemic disease that affects synovial tissue. The disease affects approximately 1% of the population, has a female predominance (female-to-male ratio of 2.5:1), and shows increased incidence with age.1 The clinical course of the disease is variable and ranges from mild, self-limited arthritis to a progressive multisystem disease. Joint involvement occurs early in the natural history of the condition. Magnetic resonance imaging can detect synovial hypertrophy as early as 4 months after the onset of synovitis.1 At the cellular level, a pronounced inflammatory reaction with cellular hyperplasia and angiogenesis occurs. As the synovium proliferates and hypertrophies, it alters its surroundings by destroying articular cartilage via an enzymatic reaction, invading subchondral bone, and stretching the soft tissues.2 The initial proliferative stage is characterized by swelling and fibrin deposition that cause pain with motion, decreased movement, and nerve compression. The proliferative tissue is composed of synoviocytes that resemble macrophages and fibroblasts. Accompanying the synovial proliferation is the growth of new blood vessels or angiogenesis to support the new growth and allow leukocyte infiltration. The influx of leukocytes is composed of T cells, B cells, macrophages, and plasma cells.1 The exact role of T cells in synovitis is still unclear; however, some evidence indicates that an overrepresentation of certain major histocompatibility complex class II alleles causes abnormal systemic selection or activation of T cells.1 The disease can progress to a destructive phase, in which the synovium or pannus invades the adjacent tissue and causes tendon rupture and articular damage. A high level of proinflammatory cytokines is also present along with matrix metalloproteinase production. The 2 main cytokines are tumor necrosis factor-alpha (TNF-alpha) and interleukin-1, which induce cellular proliferation, matrix metalloproteinase expression, adhesion molecule expression, and secretion of other cytokines and prostaglandins. Matrix metalloproteinase is a family of endopeptidases that degrades extracellular matrix components and is implicated in the cartilage and bone destruction that occurs in the later stages of RA. Additionally, increased adhesion molecule expression aids in recruiting leukocytes to the joint spaces and may perpetuate the inflammatory reaction. In the final stage, the inflammatory reaction extinguishes and is replaced by fibrosis, which causes tendon adhesions and fixed deformities.3 One of the end results of this pathological inflammation is the disruption of the balance between flexor and extensor tendons, which produces the characteristic hand deformities. While taking the history of a patient with RA, effort should be devoted to elucidating the onset and pattern of disease, the functional limitations, and symptoms, such as pain, stiffness, weakness, and numbness.3 The patient should be asked if the condition limits his or her ability to perform any specific tasks at home and at work. Constant, severe pain suggests that the patient is having an exacerbation of synovial proliferation and inflammation because most patients do not usually have pain at rest. The presence of numbness suggests nerve compression, which is common in persons with RA as a result of swelling around nerves. The surgical treatments for RA include synovectomy, tenosynovectomy, tendon realignment, reconstructive surgery or arthroplasty, and arthrodesis. The main goals for surgical treatment of RA are alleviation of pain, improvement of function, retardation of the progression of the disease, and improvement of appearance.2 For excellent patient education resources, visit eMedicine's Arthritis Center and Hand, Wrist, Elbow, and Shoulder Center. Also, see eMedicine's patient education articles Rheumatoid Arthritis and Understanding Rheumatoid Arthritis Medications. TENOSYNOVITIS OF THE HANDSection 3 of 10
Tendon sheaths are lined by paratenon and synovium; therefore, the tendons are affected by the same disease process as joints. (For education on tendinopathy, please see this Medscape CME activity.) In fact, symptoms of tenosynovitis may occur before those of intra-articular disease. The affected sites are (1) the dorsal and volar aspects of the wrist, because the tendons are covered by synovium as they pass under the flexor and extensor retinaculum and under the wrist, and (2) the volar aspect of the digits, because the tendons are covered by synovium in the fibroosseous canals in the finger.2 Synovitis of the tendons can cause pain, dysfunction, and eventual rupture of tendons. Early in the process, synovial proliferation results in the accumulation of fluid that causes swelling. As the tissue continues to proliferate, the synovium thickens. Furthermore, small fibrinoid rice bodies can develop in the tendon sheath. Hypertrophic synovial tissue begins to invade and weaken the tendon, eventually leading to rupture. Tendon rupture may also be a result of attrition of the tendon from bony spicules and osteophytes. Rheumatoid nodules can also develop within the tendons and within the subcutaneous tissue. Dorsal tenosynovitis in the wrist is usually detected when the dorsum of the wrist becomes swollen. Minimal pain may be present, but bogginess and crepitus can be appreciated with palpation. This swelling may even be the first sign of RA and may involve any combination of extensor tendons. In early cases, spontaneous remission can occur. Furthermore, rest, steroid injections, or medical management may induce remission. As dorsal tenosynovitis becomes more apparent, the likelihood of tendon rupture increases. Tenosynovectomy is usually recommended if symptoms do not improve after 4-6 months of medical therapy. After a tenosynovectomy, tendon rupture rarely occurs and complications are infrequent, yet postoperative adhesions may occur. Tendon adhesions result in an extensor lag of metacarpophalangeal (MP) joints or decreased active finger flexion. Swelling is less obvious in wrist flexor tenosynovitis because of the thicker skin on the volar aspect of the hand. Decreased passive and active motion of the fingers is caused by impairment of the free-gliding movement of the flexor tendons through the sheaths as the thickened synovium proliferates. Proliferative synovitis in flexor tendon sheaths can cause compression of the median nerve and can produce the symptoms of carpal tunnel syndrome. Tendons can also adhere to each other and may rupture. To avoid the consequences of prolonged median nerve compression, early carpal tunnel release and tenosynovectomy is recommended in patients in whom conservative means have failed. FLEXOR TENOSYNOVITIS IN THE FINGERSSection 4 of 10
Synovial proliferation produces discrete rheumatoid nodules on tendons, which can result in trigger finger. The size and location of these nodules on the flexor tendon determine the degree of triggering. Type 1 is similar to nonrheumatoid stenosing tenosynovitis, in which the tendons catch at the first annular pulley during flexion secondary to small, localized hyperproliferation of the synovium. In type 2, the nodules form in the distal palm and cause the finger to lock in flexion. When nodules are present on the flexor digitorum profundus (FDP) tendon near the second annular pulley (over the proximal phalanx), the finger locks in extension. This is type 3. Generalized tenosynovitis within the fibroosseous canal causes type 4 trigger finger. Active motion is more restricted than passive motion, and contracture and stiffness result. Tendon rupture can also occur with prolonged disease. Flexor tenosynovectomy and nodule excision are recommended for all types of tenosynovitis and trigger finger. TENDON RUPTURESection 5 of 10
The 2 main causes of tendon rupture are chronic attrition of the tendon over a bony prominence and synovial invasion of the tendon. The most frequent sites for extensor tendon rupture are at the distal end of the ulna or at the Lister tubercle, which acts like a fulcrum for the extensor pollicis longus (EPL) tendon. Sudden loss of finger extension or flexion is the cardinal sign of tendon rupture. Usually, it is painless and can occur during normal use of the hand. Patients with RA frequently ignore the new development because it may be subtle in the context of the other constraints on their normal function. Commonly affected extensor tendons are the EPL, extensor digiti quinti, and extensor digiti communis. Multiple extensor tendon ruptures are usually initiated by attrition of a single tendon and progress in a radial manner, frequently beginning with the small finger extensor. EPL tendon rupture may not significantly affect the thumb interphalangeal (IP) joint extension because this motion is controlled by the intrinsic muscles and by the EPL. In contrast, extension at the thumb MP joint is usually reduced because the extensor pollicis brevis cannot compensate for deficient EPL function. To test for EPL tendon rupture, palpate the tendon at the wrist while the patient extends the thumb with the palm resting on a flat surface. Active testing may also reveal some weakness and pain at the site of rupture. Significant deformity or functional loss is an indication for repair by end-to-end repair, tendon graft, or tendon transfer to avoid flexion contraction.2, 1 Tendon transfer with the extensor indicis proprius or extensor carpi radialis longus is the preferred method.2 No deficit in independent index finger motion or wrist extension results using these tendons. Furthermore, this transfer avoids the complication of adhesion formation that can occur with tendon grafts. End-to-end repair is not usually possible because of the delay that frequently occurs between the time of the injury and the time the patient presents for treatment. Extensor tendon rupture due to RA also frequently affects the small finger, causing extensor lag at the MP joint. Loss of extensor digiti quinti function reduces small finger extension at the MP joint by 30-40°. Any greater loss usually indicates the extensor digiti communis tendon has also been affected. The Vaughn-Jackson lesion is a sign of loss of extension in the little and ring fingers due to rupture of these tendons at the distal ulnar head, which can result from caput ulna syndrome. Small finger extension can be tested by having the patient extend the small finger while the index, middle, and ring fingers are held in flexion. A small finger extensor tendon rupture from RA should be repaired early because this defect generally leads to multiple tendon ruptures. Repair is usually accomplished by attaching the distal tendon end to an adjacent extensor tendon.2 Dorsal tenosynovectomy and removal of bony spicules that may have worn down the tendon are also required to eliminate the ultimate cause. When diagnosing extensor tendon ruptures secondary to RA, 3 other sequelae of RA that mimic this problem should be considered. First, MP joint dislocation produces a fixed deformity with a flexed and ulnarly deviated finger. Second, volar and ulnar subluxation of the extensor tendons into the gutters between the phalanges limits extensor function as the extensors essentially become flexors in this position. In this condition, the patient can sometimes maintain MP extension actively after the finger is passively extended. Finally, paralysis due to posterior interosseous nerve compression can also cause symptoms similar to extensor tendon rupture when it affects the common extensor muscle. Differentiation between tendon rupture and paralysis can be difficult, and the most reliable diagnostic maneuver is to test for the presence of MP joint extension while flexing the wrist (tenodesis effect). Because the tendon is not in continuity when it is ruptured, wrist flexion does not restore MP joint extension. The diagnosis of flexor tendon rupture is more straightforward. The flexor pollicis longus is the most common flexor tendon to be affected by RA. Patients with this condition are not able to actively flex the thumb IP joint. The diagnosis can be slightly complicated if chronic stiffness or hyperextension is present in this joint. Similarly, loss of function in the proximal IP (PIP) joint or the distal IP (DIP) joint suggests rupture of the flexor digitorum superficialis (FDS) or profundus, respectively. Rheumatoid nodules can limit FDP function and produce symptoms similar to FDP tendon rupture; therefore, this diagnosis should be considered. A palpable nodule can aid in differentiating between these conditions. Furthermore, when the flexor tendon is ruptured, the affected finger also has a more extended posture in the resting position. To make the diagnosis of concomitant FDP and FDS tendon rupture, passive motion of the finger must be present in the absence of active motion at the DIP and PIP joints. The flexor tendons can rupture at multiple sites in the hand, including the wrist, palm, and fingers. Surgical exploration is usually required to determine the exact location of the rupture. Treatment of flexor tendon rupture varies with the degree of functional disability. Rupture of the FDP may not require repair if the DIP joint remains stable, despite compromised active flexion. The treatment of a rupture of the FDP tendon is also complicated because, through restoration of the FDP tendon, the FDS tendon or PIP joint may become compromised, resulting in a stiff and functionless finger. The treatment of most FDP ruptures is best served with a tendon or arthrodesis at the DIP joint. FDS tendon rupture alone usually does not require repair because the functional loss is minimal. Rupture of both the FDP and FDS tendons does require surgical intervention because the functional loss is obvious. In the wrist and palm, the ruptured tendon can be sutured to an adjacent tendon, but within the fibroosseous canal in the finger, this is not an option. Primary repair is seldom an option because of the significant restriction of the tendon within the canal. Also, tendon grafts have traditionally yielded poor results.2 Staged tendon reconstruction can usually be effective, but this technique is also fraught with poor results.2 A last-resort treatment for older patients with severe disease may be fusion of the PIP and DIP joints in a functional position. THE METACARPOPHALANGEAL JOINT IN RHEUMATOID ARTHRITISSection 6 of 10
The condylar structure of the MP joint, which permits motion in 2 planes, makes the MP joint inherently more unstable than the IP joints; therefore, the distorting effects of RA are more pronounced. The classic deformities associated with RA of the MP joints are ulnar drift, which is made up of ulnar shift and ulnar deviation, and volar dislocation. The cumulative effects of various factors contribute to these deformities. Initially, the MP capsule and ligamentous structures are stretched by the proliferation of the synovium, which loosens the collateral ligaments and decreases joint stability. Normally, in the flexed position, minimal lateral movement occurs at the MP joint, but, with increased laxity of the collateral ligaments, up to 45° of lateral deviation occurs in this position.2 With loss of MP stability, other forces on the MP produce the characteristic ulnar drift. For example, wrist collapse contributes to ulnar drift. Weakened radiocarpal ligaments cause radial rotation of the metacarpals and carpus on the radius, which results in ulnar deviation of the MP joint via the Z mechanism. This phenomenon describes the consequence of an imbalance of opposing forces at a joint; when a particular joint is continuously angulated in one direction, the joints on either side of it will adopt the opposite position if no physical impediments are present.2 Moreover, the extensor tendons can be shifted or dislocated in the ulnar direction and contribute to the ulnar drift. The normal ulnar shift of the fourth and fifth extensor tendons during flexion of the MP joints is exaggerated when the radial side of the transverse lamina fibers stretches as a result of synovial proliferation. Volar dislocation or subluxation is also caused by weakening of the collateral ligaments and by weakening of the dorsal extensor mechanism when the extensor tendons are dislocated between the metacarpal heads. As a result, no force counters the extrinsic and intrinsic flexors, and a flexion contraction at the MP joint occurs, which is evident by prominent metacarpal heads. Conservative treatment is advised for RA of the MP joints to see if control can be gained with medication therapy alone.2 Recurrence is always a possibility postsynovectomy, and approximately 30-50% of patients may undergo spontaneous remission. Synovectomy is indicated in the RA patient who is refractory to 6-9 months of medical treatment and has persistent MP joint synovitis with minimal joint deformity and minimal radiographic evidence of RA. Additionally, extensor tendon relocation with synovectomy is indicated for an RA patient who also has early volar subluxation and ulnar drift, especially if the patient is young and the disease is not rapidly progressing. Subluxed extensor tendons fall into the ulnar gutters of the MP joint. The patient may not be able to extend this finger once it is in the flexed position. However, the finger can maintain extension if passively placed into this position. The arthroplasties of the MP joint can incorporate reconstruction of the soft tissues only or involve complete joint replacement. Soft tissue arthroplasty usually incorporates an element of synovectomy with MP joint stabilization, such as reconstruction of the radial collateral ligament or tendon realignment. Joint replacement is indicated for MP joint deformity or subluxation when pain is not controlled or function is impaired. Various MP joint implants are available for joint replacement. The MP joint replacement procedure involves making either a transverse incision across the entire dorsum of the hand at the MP level or individual longitudinal incisions over each MP joint. Less chance of interference with the lymphatics and venous outflow occurs with the individual longitudinal incisions, but the transverse incision is most commonly used for ease of access. The dissection is carried down to the paratenon level. An incision is made on the ulnar aspect of the extensor tendon, and the tendon is reflected radially. Care is taken to not breach the integrity of the capsule at this time. An incision is made longitudinally in the capsule of the MP joint. Using a periosteal elevator, the metacarpal head is freed of any soft tissue attachments to the metaphyseal flare. Using an oscillating saw, a true cut is made, maintaining 90° in line with a long access of the metacarpal and in the coronal plane. The metacarpal head is then discarded. An electrical burr or a Christmas-tree type of rasp can be used to ream the medullary canal. The medullary canal of the proximal phalanx is then identified through a burr hole on the articular surface of the base of the phalanx. Osteophytes are removed from the proximal phalanx at this time with a rongeur. The intramedullary canal of the proximal phalanx is reamed. Care is taken so that the rectangular opening for both the metacarpal and the proximal phalanx are square in line with the axial direction of both the metacarpal and phalanx. Appropriate sizes are then placed inside the medullary canals. Using a no-touch technique, the definitive prosthesis is then introduced. The capsule is repaired, and the extensor tendon is subsequently aligned. Some authors prefer to reconstruct the collateral ligaments at this time. Care is taken at the initial dissection to preserve as much of the collateral ligament as possible. The skin is then closed using nylon suture, and a splint is applied with the fingers in extension and in a neutral position. Approximately 4-5 days after the procedure, the patient is fitted for a dynamic outrigger splint that maintains extension in an appropriate anatomical position of the fingers while the patient undergoes active flexion exercises. Night splints are manufactured to maintain the fingers in extension. Splinting is required for the next 4-8 weeks. Follow-up radiographs are obtained to confirm the appropriate positioning of the implants. Crossed intrinsic transfer of the extensor tendons from the ulnar side to the radial side of the adjacent finger to increase stability is another surgical option. Intrinsic release to alleviate intrinsic tightness eliminates the dorsal digital expansion tightness that is one of the subluxing forces on the MP joint. Finally, MP joint arthroplasties can provide long-term relief. A patient with good hand function in the absence of pain is not a candidate for arthroplasty, even if obvious MP joint deformity is present, because surgery may not improve the hand function and could decrease grip strength. THE PROXIMAL AND DISTAL INTERPHALANGEAL JOINTS IN RHEUMATOID ARTHRITISSection 7 of 10
The swan-neck and boutonniere deformities are common in, but not unique to, patients with RA. In the swan-neck deformity, the DIP joint is flexed and the PIP joint is hyperextended. The boutonniere deformity is characterized by the opposite, with DIP joint hyperextension and PIP joint flexion. Both are caused by an imbalance of the forces on these joints due to synovial proliferation. The swan-neck deformity can be classified by the extent of functional loss secondary to loss of PIP joint mobility.2 In type 1 swan-neck deformity, the PIP joint can be completely flexed and little functional loss or MP joint involvement occurs. The nidus of the type 1 deformity can be at the DIP or PIP joint. In the first case, stretching or loss of the terminal extensor tendon attachment at the DIP joint results in DIP joint flexion because of the unopposed action of the FDP tendon, similar to what occurs with the mallet-finger deformity. A relative shortening of lateral bands, which migrate dorsally, occurs. At the PIP joint, the volar plate becomes lax, and the transverse retinacular ligament attenuates and fosters the hyperextension at the PIP joint and migration of the lateral bands. Alternatively, the PIP joint can primarily hyperextend because of a stretched volar capsule or FDS rupture, which eliminates the counteracting flexor forces at this joint. The lateral bands sublux to the dorsal side. The terminal tendon generates less force. Consequently, the DIP joint is flexed. The surgical approach used to correct the abnormality should be decided based on the causative mechanism, ie, whether it is due to an initial DIP or PIP joint deformity.2 DIP joint fusion is recommended for correction of the swan-neck deformity secondary to loss of the extensor pull at the DIP joint (mallet-finger deformity). Repair of the extensor tendon is not advised because this procedure cannot eliminate the causative disease and the repaired tendon will be subjected to the same degenerative processes. The second type of swan-neck deformity is caused by MP joint abnormalities, in which the swan-neck deformity is positional. When the MP joint is subluxed and deviated, the tightness of the intrinsics causes hyperextension of the PIP joint and flexion of the DIP joint. Upon examination, extension and radial deviation of the MP joint restricts PIP flexion. With progression of the disease, the PIP joint becomes stiff independent of the MP joint position. Correction of this deformity must address the tightness of the intrinsics, not just PIP hyperextension. With mild disease, intrinsic release can relieve the problem, while more severe cases may also require MP joint arthroplasty. In the third type of swan-neck deformity, PIP joint flexion is reduced in all positions. With this type, hand function becomes compromised because of a decreased ability to grasp objects. Despite this functional loss, little radiographic evidence of joint destruction by RA can be demonstrated. The surrounding soft tissues (ie, extensor mechanism, collateral ligaments, skin) limit PIP joint function; therefore, the initial treatment goal is to restore passive mobility by joint manipulation, lateral band mobilization, skin release, or a combination thereof. Gentle intraoperative joint manipulation to passively flex the PIP joints while the patient is under anesthesia can help to restore function. Usually, this treatment is performed in addition to intrinsic release, MP arthroplasty, or flexor tenosynovectomy. The adjunctive treatment determines whether the hand is splinted postoperatively. With joint manipulation, dorsal skin release may be required if the overlying skin is excessively stretched from attempts to flex the PIP joint. Skin necrosis may ensue; therefore, make a releasing incision distal to the PIP joint. If manipulation is not adequate (80-90° of PIP joint flexion), then soft tissue release is indicated. A good procedure is lateral band mobilization in which dorsally displaced lateral bands are released from the central slip of the extensor mechanism. Additionally, flexor tenosynovectomy or tenolysis is often needed to correct for stiff flexor tendons that are the result of either synovial proliferation or tendon adherence secondary to limited motion. The last type of swan-neck deformity involves stiffness of the PIP joint with radiographic evidence of joint destruction by RA. Salvage procedures, such as joint fusion and arthroplasty, are usually indicated at this stage. The choice of procedure should be determined by the extent of involvement of the surrounding soft tissue, flexor tendons, and adjacent joints and by the identity of the affected finger.2 For instance, the index finger PIP joint should be fused because lateral stability is important in this digit. Furthermore, weak ligamentous support or tendon ruptures are also indications for fusion, instead of arthroplasty. Conversely, patients with small or ring finger PIP joint involvement should benefit from arthroplasty in order to maintain a strong grip, provided the patient has no contraindications for this procedure. The same disease processes also cause the converse deformity, the boutonniere, in which the PIP joint is flexed and the DIP and MP joints are hyperextended. This abnormal finger posture usually starts with PIP joint flexion that leads to the changes in the other joints. Specifically, synovial proliferation in the PIP joint stretches and weakens the extensor mechanism; therefore, full extension cannot be maintained. Then, the lateral bands are displaced volarly and the oblique retinacular ligaments are shortened, which causes hyperextension of the DIP joint. In compensation for increasing PIP joint flexion, the MP joint hyperextends. Generally, if the problem is corrected early, passive treatments are adequate. In the later stages, salvage procedures are indicated. With mild boutonniere deformity, minimal distortion of the joint positions and functional loss occur. A slight extensor lag (10-15°) is present at the PIP joint with slight hyperextension at the DIP joint and no involvement of the MP joint. Surgical treatment usually consists of extensor tenotomy, which should not threaten existing function while increasing DIP joint flexion. With moderate boutonniere deformity, the flexion deformity at the PIP joint increases to 30-40° and the MP joint begins to hyperextend in order to compensate. At this stage, reconstruction of the extensor mechanism by shortening the central slip and moving the lateral bands dorsally is indicated to restore PIP extension and hand function. Certain criteria should be met before correction is attempted, including good dorsal skin, smooth joint surfaces, functional flexor tendons, and the ability to passively correct the PIP joint.2 If wrist deformity is present, it should be corrected before addressing the PIP extensor mechanism. Conversely, PIP joint flexion should be corrected before MP joint arthroplasty because achieving adequate MP joint flexion while the PIP joint is also flexed is difficult. When the PIP joint can no longer be passively extended, the boutonniere deformity is severe. Fusion of the joint or arthroplasty is now warranted. Fusion of the PIP joint should be performed so that the treated finger is in a functional or flexed position. The degree of flexion should increase from the index (25°) to small (40°) finger.2 Postfusion, MP joint function is often regained. If PIP joint arthroplasty is chosen in order to maintain motion, the extensor mechanism should also be repaired. This option is particularly useful for boutonniere deformities of the small and ring fingers to maintain or improve grip strength. The deformities of the thumb that arise from rheumatoid arthritis are similar yet, in many ways, different from those of the fingers. Significant forces are placed at the IP, MP, and carpometacarpal (CMC) joint of the thumb in daily activities that promote significant degeneration in the face of proliferative synovitis of RA. Nalebuff has described 5 types of deformities of the thumb associated with RA, and Ratliff described a sixth type.
The treatment of these specific deformities depends on the severity of disease in each involved joint. Fixed joint deformities with bony destruction are usually more amenable to fusion than arthroplasty. However, in general, in an attempt to preserve motion, fusion of 2 joints in tandem is considered the last-stage effort. IP joint fusion is tolerated extremely well and maintains function. The IP joint should be fused at 0-20° of flexion. MP joint arthroplasty is recommended at the CMC joint or IP joint about to be fused. This preserves the motion of the thumb for prehensile tasks. Pathology isolated to one joint, such as in a type 4 deformity, can be surgically treated with an arthroplasty or volar plate advancement. A type 6 deformity requires fusion to regain stability. Bone grafts may be required to restore adequate bone stock. CMC joint arthroplasties are a good option for significant deformities of the thumb if the disease initiated at the CMC joint (ie, type 3 deformities). Ligament reconstruction with tendon interposition offers a stable joint with preservation of motion. Occasionally, fusion of the CMC joint may be required if significant bone destruction is present with poor residual bone stock. RHEUMATOID ARTHRITIS OF THE WRISTSection 8 of 10
RA can affect any tendon sheath or joint in the body. Often, distal appendage deformities are the result of the proximal joint pathology. This is no truer than in the wrist. Significant wrist synovitis and destruction results in dysfunctional pain, weakened grip, and distal finger deformities. Therefore, correction of the wrist pathology is usually required before, if not at the time of, MP joint or finger reconstruction efforts. Pathology of RA of the wrist is somewhat predictable and usually follows a progressive pattern. The ulnar side of the wrist is most commonly affected with synovitis that destroys the ulnar carpal stabilizing ligaments. The triangular fibrocartilage complex is attenuated, and the distal radial ulnar joint becomes eroded as the dorsal capsule is disrupted. The proliferative synovitis results in dorsal subluxation of the distal ulna, volar subluxation of the extensor carpi ulnaris tendon, and supination of the proximal carpal bones. These signs are collectively known as caput ulna syndrome. Destructive synovitis at the radial side of the wrist results in (1) attenuation of the radioscaphocapitate ligament with rotary subluxation of the scaphoid and (2) ulnar translocation of the carpal bones. The carpal height collapses, and bony destruction of the wrist ensues. Clinically, the hand deviates radially and maintains a supinated position. This imbalance causes ulnar drift of the phalanges on the metacarpals as the extrinsic forces of the extensors and flexors pull the fingers into this position. Therefore, the pathology of the wrist promotes distal finger deformity. Correction of the wrist pathology before correction of the fingers is often prudent to prevent recurrences of the finger deformities. Early treatment of synovitis of the wrist consists of synovectomy at the ulnar carpal or radial carpal sites. This procedure may help control pain, slow the progression of the disease, and maintain motion. RA of the wrist that has progressed beyond simple proliferative synovitis may require more radical treatments. Destruction of the distal radial ulnar joint may require excision of the distal ulna and reconstruction of the triangular fibrocartilage complex. Tendon transfer reconstruction of the ruptured extensor tendons often associated with caput ulna syndrome can be performed in the same setting as the resection of the distal ulna and synovectomy. A few reports have indicated that the Sauve-Kapandji procedure may be more appropriate in younger patients. This procedure provides a fusion of the distal radius and ulnar head and excision of the ulnar neck. This procedure may be more beneficial to those patients who do not have significant ulnar translocation of their carpus. Stabilizing techniques for the distal ulna following resection include using a segment of the radial carpal volar ligament or slips of the extensor carpi ulnaris or flexor carpi ulnaris tendons. Stabilizing procedures following excision of the distal ulnar head may help prevent complications such as painful forearm rotation. With destruction of the radial carpal joint, wrist fusion becomes a very functional and viable option. Numerous methods are used for wrist fusion, including the use of Steinman pins, 62-gauge Kirschner wires, plates, and screws. These techniques require the use of autologous bone graft from the iliac crest or allograft bone material. The exact position the wrist should be in following fusion is controversial. Most surgeons prefer to fuse the wrist at an angle of approximately 10° of dorsal flexion. UPDATE ON RHEUMATOID ARTHRITIS OF THE HANDSection 9 of 10
The treatment of RA has undergone much advancement. The selective costimulation modulator abatacept demonstrated efficacy for treating rheumatoid arthritis in early clinical studies. Smolen et al from the Medical University of Vienna discussed the results from the ASPIRE trial to delineate the predictors of joint damage in patients with early RA treated with high dose methotrexate with or without cantonment infliximab.4 Conclusions indicated that high C-reactive protein levels and high erythrocyte sedimentation rates or persistent disease activity were associated with greater radiographic progression in groups taking methotrexate only, while little radiographic progression was seen in patients receiving both methotrexate and infliximab, regardless of the abnormal levels of those traditional predicators. O'Dell et al found an improved response rate to the treatment of RA in patients who are seropositive when using doxycycline plus methotrexate relative to methotrexate alone. In a review by Turesson and Matteson, the authors indicate that the genetic profile of the patient may have significant implications on the treatment of RA because of the activity of the enzymes relative to the metabolism of drugs such as methotrexate and azathioprine are, in part, genetically determined. The MRI has been used to identify subtle changes within joints that were otherwise not picked up on routine radiographs. Approximately 8% of patients who develop RA have normal radiographic findings, whereas the MRI may pick up subtle changes. In one study, high-resolution ultrasonography detected early erosions in 7 times more patients than did normal radiography.5 Studies have looked at the role of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) may have a substantial role in the pathogenesis of the rheumatoid arthritis disease. Feldmann et al described a therapeutic effect of the combination of etanercept and methotrexate compared to early treatment with either one alone in patients with RA.6 This study indicated that radiographic scores improved with this treatment.6 The TNF is also thought to prevent the activation of osteoclasts, which degrade joints by the receptor activator nuclear factor k-B (RANK). The medical therapies with medication such as TNF inhibitors hold significant promise in stopping the progression of the disease seen with RA. However, a significant number of patients are not responsive to the inhibitors of TNF. Edwards et al are employing anti–beta-cell therapy in the treatment of RA.7 Such medications that target specific cells may hold significant promise in the treatment. O'Brien et al have written an impressive review on the hand function in patients with RA.8 The goal was to identify specific physical therapy regimens that may offer improvement in the function of patients' hands relative to their activities or daily duties. This study suggests that the role of strengthening hand exercises offer significant improvement in the overall function of patients with RA. If surgery is not an option, medical management should be pursued in conjunction with a rather thorough physical therapy in order to maintain and preserve function of the hands. For education on advances in arthritis and related conditions presented at the 71st annual meeting of the American College of Rheumatology, please see this Medscape REFERENCESSection 10 of 10
Article Last Updated: Feb 25, 2008 |
