THE HISTORY OF HAND THERAPY AND HAND rehabilitation began during World War II when the Surgeon General, Major General Norman T. Kirk, determined that severe hand injuries and surgeries were worthy of specialized treatment. This led to the development of nine “hand centers” in select military hospitals across the country where officers trained in plastic, orthopedic, and neurologic surgery were designated to repair wounded hands. These surgeons realized that postoperative therapy was as critical to recovery and socioeconomic well-being as the surgery itself and worked closely with therapists to develop specialized protocols and technical manuals to manage this patient population.

By the mid-1970s, there were occupational and physical therapists in the United States and Canada who were only treating patients with upper-quarter injuries. About that time, a group of six occupational and physical therapists joined together and created the American Society of Hand Therapists (ASHT). In 1984, ASHT established a certification committee to develop a framework for hand therapy certification. This committee discovered guidelines established by the National Organization for Competency Assurance (NOCA) for organizations who offer professional certifications. This led to the first practice analysis, which formed the basis of the scope of practice. The results of the practice analysis were subsequently used to develop the original blueprint for the certification examination (which determined the percentage of content included in the examination). In 1987, ASHT voted to move forward with a hand therapy certification, and the first exam was administered in 1991, which marked the first cohort of Certified Hand Therapists (CHTs).

One of the NOCA guidelines for certification programs is administrative independence, meaning that an organization should not certify its own members. This led to the incorporation of the Hand Therapy Certification Commission (HTCC), which functions administratively as a separate entity from ASHT. In 2008, HTCC conducted a detailed practice analysis of CHTs in the United States and Canada, and from this analysis the current definition and scope of practice for hand therapy was established.

To become a CHT, a licensed physical or occupational therapist must have a minimum of 3 years of clinical experience, including 4,000 hours or more of direct practice in hand and upper extremity therapy. In addition, the CHT candidate must successfully pass a comprehensive examination of advanced clinical skills and theory in upper-quarter rehabilitation. Because of changes in the profession and advancement of evidence-based practice, every CHT is required to demonstrate ongoing professional development and competency by recertifying every 5 years. To date, HTCC has certified over 6,000 physical and occupational therapists in the United States, Canada, Australia, New Zealand, other U.S. territories, military bases, and other countries.¹

The wrist and hand are very complex structures, and the pathophysiology is quite diverse (). The carpus (wrist) is made up of eight bones, more than 20 joints, 26 ligaments, and the triangular fibrocartilage complex. The hand consists of 19 bones, a vast array of ligaments including the biomechanically intricate pulley system and extensor mechanism, and intrinsic and extrinsic muscles, tendons, and nerves. An appreciation of the surface anatomy of the hand is critical in its physical examination (Figs. 31–1 and 31–2).

With constant use and abuse, it is little wonder that the wrist and hand are subject to trauma, degenerative disorders, and overuse syndromes. Damage to the wrist and hand can have serious consequences and may create permanent limitations in function and participation.

For the purpose of this chapter, the pathophysiology of hand injuries has been divided into soft tissue disorders, degenerative disorders, fractures and dislocations, and nerve compression / neurovascular syndromes. In addition, a brief discussion of pain in hand rehabilitation is included.

Wrist Instability and Ligamentous Injuries

All carpal bones rotate in specific directions when under load. The direction of the carpal bone depends on many factors, including the position of the carpal bone when loaded, the direction of the load, the congruency of the articular surfaces, the magnitude of the load, and the status of the capsule and ligaments, which links the carpal to the surrounding structures. The tendons surrounding the carpal bones may also contribute to the degree of motion. Any injury or disease that modifies the carpal geometry, articular position, and ligament integrity or tendon/muscle dysfunction will change the mechanics and degree of carpal motion, resulting in instability.³ Determining the appropriate classification of carpal instability is controversial, as none are ideal. Larsen and colleagues⁴ published an analytical scheme which seems to be a useful tool in the assessment of carpal instability. According to Larsen et al, there are six categories that need to be examined: chronicity, severity, etiology, location, direction, and pattern, and all categories should be addressed when describing the instability.

Chronicity is a critical factor in prognosis and potential for healing and has been broken down into acute (<1 week from the time of injury or the initiation of a nontraumatic instability), which provides maximum healing potential; subacute (1–6 weeks), where the deformity is still reducible but the ligaments have decreased healing potential due to retraction or necrosis; and chronic (>6 weeks), where there is little healing potential and the possibility of primary ligament healing and an acceptable reduction is unlikely. Severity refers to whether the deformity is fixed. The more fixed the deformity, the more severe. Static deformities, defined as malalignments as seen on static radiographs (posteroanterior [PA] and/or lateral), can be reducible or irreducible. Any malalignment only seen on stress or motion radiographs is dynamic. Although carpal instability is often the result of trauma, certain diseases such as rheumatoid arthritis (RA) may result in a similar disorder; however, ligament ruptures as a result of RA mean that normal healing is unlikely.^3,4 Location of the instability may or may not coincide with the location of the initial injury. It is important to note whether a single joint or multiple joints are involved. Direction of the carpal malalignment is a critical consideration. The most commonly recognized directions are described as (1) DISI (dorsal intercalated segment instability), where the lunate appears extended relative to the radius and the capitate; (2) VISI (volar intercalated segment instability), where the lunate appears abnormally flexed; (3) ulnar translocation, when a portion or the entire proximal row is displaced ulnarly; (4) radial translocation, when the proximal row is displaced radially beyond normal; or (5) dorsal translocation, when the carpal condyle can be displaced dorsally, often as a result of a misaligned distal radius fracture. Finally the pattern of instability represents the synthesis of the previous five categories.

There are four major patterns of carpal instability: (1) the carpal instability dissociative (CID) involves a major derangement (fracture, ligament avulsion, or both) between bones of the same carpal row; (2) the carpal instability nondissociative (CIND), when there is dysfunction between the radius and proximal carpal row or between the proximal and distal carpal rows; (3) the carpal instability complex (CIC), where there are components of both CID and CIND; and (4) carpal instability adaptive (CIA), where the reason for the carpal malalignment is not located in the wrist but rather proximal or distal to it. A good example of a CIC pattern would include perilunate dislocations due to a ligament injury that coexists at both the radiocarpal and intercarpal levels, often resulting in a scapholunate or lunotriquetral dissociation, or both, with an ulnar translation of the lunate. A good example of a CIA pattern would include a carpal malalignment seen as an adaptation of a normal carpus to a malunion of a distal radius fracture.^3,4

The most common CID is scapholunate dissociation (Fig. 31–3) due to rupture of the mechanical linkage between the scaphoid and the lunate, and results from an injury involving wrist hyperextension, ulnar deviation, and midcarpal supination. When the scapholunate joint is completely dissociated creating abnormal carpal kinematics, the forces across the wrist cannot be distributed normally and this results in progressive degenerative changes. Eventually long-lasting carpal malalignment with irreducible subluxation of the scaphoid induces degenerative osteoarthritis that precludes successful ligament repair or reconstruction. This is known as scapholunate advanced collapse (SLAC) wrist, which is treated by relieving pain through a combination of bony excision or intercarpal fusion or both.^3,5

Injuries to the ulnar collateral ligament (UCL) of the thumb metacarpophalangeal (MP) joint are common, especially among skiers and athletes who participate in ball handling sports. The mechanism of injury is a sudden thumb valgus force caused by a fall on an outstretched hand with the thumb in a radially abducted position, commonly seen when a person falls skiing while gripping a ski pole^6–8 (Fig. 31–4). Most UCL injuries occur at the distal insertion of the ligament on the proximal phalanx. Stener’s lesions, which occur when the distal portion of the ruptured UCL displaces proximally and is trapped superficial to the proximal edge of the adductor pollicis aponeurosis between the UCL and the bone, occurs in 64% to 87% of complete ruptures and necessitates surgical intervention, as persistent instability of the thumb can lead to decreased pinch grip strength, persistent thumb pain, and/or secondary osteoarthritis. Patients with UCL tears present with tenderness, ecchymosis, and swelling along the ulnar border of the thumb MP joint.^6–10

Examination of the injured thumb should include a thorough examination of neurovascular function as well as range of motion of the MP and interphalangeal (IP) joints. More specific examination of the MP joint should include a valgus stress of the joint in full MP extension as well as in 30 degrees of MP flexion. This may be difficult to assess in the acute injury due to pain, swelling, and patient guarding, and injection of a local anesthetic may be beneficial in examining the acutely injured thumb. Absence of a firm endpoint on MP joint valgus stress testing may be considered the most reliable indicator of a complete UCL tear; however, traditionally authors have cited a 30-degree valgus laxity or a 15-degree difference between the involved and uninvolved thumb as criteria for diagnosing a complete UCL injury.⁸ Laxity at 30 degrees of MP flexion and full extension is indicative of a complete rupture of both the proper and accessory ligaments; however, if there is laxity in 30 degrees of MP flexion only, an isolated proper collateral ligament is likely.^6,8,9

There is general agreement that acute, partial ruptures of the UCL can effectively be treated by 4 weeks of continuous immobilization in a thumb spica cast or orthosis while leaving the IP free (Fig. 31–5). This 4-week period is followed by 2 weeks of additional immobilization in a thumb spica orthosis during which time active range of motion is initiated. Prognosis is excellent, although it is common for patients to have ongoing symptoms for up to 6 months following the injury despite the lack of laxity on examination. Athletes can often return to play 2 to 4 weeks after injury with a protective orthosis.^7–11

Surgical repair or autograft reconstruction is recommended for patients with complete tears, as conservative care often fails and results in chronic pain, instability, and weakness. The surgical technique for complete tears depends on the location of the tear and chronicity of the injury and is beyond the scope of this chapter. Postoperative management includes a short arm thumb spica cast for 4 weeks followed by a custom orthosis for two additional weeks. Range of motion (ROM) is begun when the cast is removed, and full ROM is expected by 7 to 9 weeks postoperatively. Radially directed pressure on the thumb tip and resisted pinch are restricted for 12 weeks, at which point full unrestricted activity is allowed with the exception of contact sports, where use of a protective orthosis and/or taping is recommended.^7,10,11

Muscle and Tendon Disorders

Intersection syndrome is an inflammatory disorder that occurs where the muscle bellies of the abductor pollicis longus (APL) and extensor pollicis brevis (EPB) cross over the tendons of the extensor carpi radialis longus (ECRL) and extensor carpi radialis brevis (ECRB) approximately 4 cm proximal to the radial tubercle.^12–15 It is considered an overuse syndrome common in rowing, canoeing, racket sports, weight lifting, and skiing. Intersection syndrome is characterized by pain, tenderness, swelling, and redness on the dorsal radial aspect of the distal forearm and is often associated with crepitus during flexion and extension of the wrist.^12–15 Typical findings on ultrasound include peritendinous edema and synovial fluid within the tendon sheaths as well as thickening of the APL, EPB, ECRL, and ECRB tendons^12,13 (Fig. 31–6).

Conservative management for intersection syndrome includes steroid injection into the second dorsal compartment, use of a forearm-based wrist extension or thumb spica orthosis, and activity modification with emphasis on restricting activities requiring repetitive wrist flexion and extension. Prognosis is very good with conservative management; however, the second dorsal compartment can be surgically released in recalcitrant cases. A postoperative wrist extension or thumb spica orthosis is worn for up to 2 weeks after surgery followed by progressive mobilization.^14,15

De Quervain’s disease was first described in 1895 by Fritz de Quervain, a Swiss surgeon, and involves the tendons of the APL and the EPB within the first dorsal compartment on the radial aspect of the wrist.^14–17 These tendons pass through a fibro-osseous tunnel formed by a shallow groove in the radial styloid process and dense tissue composed of transverse fibers of the dorsal ligament (Fig. 31–7). The entrapment of these tendons is a relatively common disorder caused by repetitive radial abduction of the thumb with simultaneous ulnar deviation of the wrist and/or repetitive radioulnar deviation of the wrist, which is associated with hammering, cross-country skiing, or lifting a child or pet. De Quervain’s disease is also common during pregnancy, during the postpartum period, and during lactation likely due to an increase in fluid retention, which may increase the pressure within the fibro-osseous tunnel. Overall, women are more likely to develop de Quervain’s disease, which is thought to be related to the angulation against the roof of the retinaculum, which is greater in females.^14,15,17,18 Tension on the tendons is said to produce friction in the rigid retinacular sheath resulting in inflammation, tendon thickening, and subsequent narrowing of the fibro-osseous canal. Aberrant tendons—variations in tendon anatomy and their sheaths, including the presence of a septum separating the APL and EPB tendons (present in about 40% of the population)—are thought to predispose certain individuals to this condition and may explain poor response to conservative management in those individuals.^15,17

The diagnosis of de Quervain’s disease is based on patient history and clinical examination. Patients typically present with pain and swelling over the radial aspect of the wrist, which is aggravated by resisted motion of the thumb and/or radial deviation and extension of the wrist and passive ulnar deviation. There is often tenderness over the first dorsal compartment with visible fullness or swelling indicative of thickening of the extensor retinaculum.¹⁷ Special tests include Eichhoff’s maneuver, Finkelstein’s test, and the wrist hyperflexion and abduction of the thumb (WHAT) test.^15,17,19 Corticosteroid injections provide relief in 50% to 80% of cases^14,15,17 and have been shown to be much more effective than the use of an orthosis alone.^14,17 A forearm-based thumb spica orthosis is used to promote rest and prevent motions that exacerbate symptoms. Typical therapeutic management includes patient education about activity modification; modalities for pain relief, tendon gliding exercises, and mobilization with movement have been shown to be effective.^14,17,18,20

Surgical management involves the dorsal release of the sheath that covers the first dorsal compartment. Careful consideration of the presence of a subseptum should be identified and also released if present. Surgeons agree that leaving the volar portion of the extensor retinaculum is important to prevent volar subluxation of the tendons over the radial styloid.^15,17 Care must also be taken to identify and protect the superficial radial nerve as it crosses the radial styloid. Postoperative management includes a thumb spica orthosis in 20 degrees of extension for up to 2 weeks followed by a gradual return to activity as tolerated.^15,17 Formal, ongoing, supervised hand therapy is rarely necessary following release, although avoidance of any heavy activity for 4 to 6 weeks is recommended.

Trigger finger/thumb is one of the most common causes of hand pain and disability. Although synovial proliferation and fibrosis of the flexor sheath are triggering factors, there is no consensus about its true cause and the etiology remains unknown. The patient presents with a thickening of the A1 pulley and in the flexor tendons, primarily the flexor digitorum profundus (FDP); however, thickening may occur in the flexor digitorum superficialis (Fig. 31–8). In most patients, a tender nodule can be palpated at the site of the A1 pulley.

The condition causes painful popping or catching in the finger or thumb, and the digit will lock into flexion at times, which requires passive manipulation into extension.^15,17,21 Trigger finger is more common in women on the dominant side, and the most commonly affected digit is the thumb. There is also a higher incidence of trigger finger in patients with diabetes mellitus (DM) and RA.^14,17,21 Supervised hand therapy programs, targeting differential gliding of the FDS and FDP tendons and orthosis management, have been shown to be less effective than corticosteroid injection in reducing pain and triggering. Corticosteroid injections tend to be the first line of management in trigger fingers and have shown a success rate of 60% to 90%.^15,17,22 If nonsurgical management fails, open release and percutaneous release of the A1 pulley are current surgical options. Open release has been performed for more than 100 years and is considered the gold standard of care with a high rate of success and minimal morbidity or recurrence. Sato et al²¹ compared corticosteroid injection to percutaneous and open releases in their randomized control trial. They compared the results of 150 fingers that were randomly assigned and allocated to one of the three treatment groups with a 6-month follow-up. Their results demonstrated significantly higher cure rates for open and percutaneous releases than corticosteroid injection. The trigger cure rate for patients in the injection group was 57%, and the injection group demonstrated a rate of trigger finger relapse of 12.5%, which necessitated a second injection. The group then received a second injection, which increased the cure rate to 86%. No relapse occurred in either the percutaneous or open release groups, and remission of the trigger was achieved in all cases. It should be noted that the patients in the injection group experienced a lower incidence of pain in the first month of follow-up compared to those in the open and percutaneous groups, which had similar incidences.²¹ Wang et al²² found similar results in their comprehensive review. They reported that they found no difference in treatment failure or complications between percutaneous release surgery and open release surgery and that patients undergoing percutaneous releases were less likely to have treatment failure than patients treated with corticosteroid injections.²² Postsurgical management includes a small hand dressing with the digits free. Immediate motion is encouraged the day of the surgery, and patients are also encouraged to use their hand for light activities. Sutures are removed at 7 to 10 days, and patients may resume unrestricted hand use within 3 to 4 weeks following surgery. Supervised hand therapy is rarely necessary except for those patients who presented with fixed flexion contractures prior to surgery.^14,15

Jersey finger is a closed flexor tendon injury and occurs when the FDP is avulsed from its insertion on the volar aspect of the distal phalanx (Fig. 31–9).

Close FDP ruptures are common in contact sports versus noncontact sports where the distal interphalangeal (DIP) joint is forced into extension while the fingers are actively flexed, most commonly when pulling on a jersey. Jersey finger can happen to any finger; however, the ring finger accounts for 75% of these cases.^23–25 Diagnosis of a closed FDP injury can be made with physical examination. The finger will be painful and swollen, and the patient will lack isolated DIP flexion of the affected digit.²⁴ Treatment of FDP injuries solely with the use of an orthosis is not recommended, and early direct repair (within 10 days of injury) is preferred to restore active flexion at the DIP joint.^23,24,26 Primary repair of avulsed FDP tendons is not an option after 6 weeks due to retraction of the tendon. At that point a variety of surgical options are available; however, the techniques vary in terms of cost and technical difficulty, and not one technique is considered to be superior to another. It is important to note that obtaining full motion following delayed surgical repair of a jersey finger is unusual.^23,25,27 Detailed postoperative management of flexor tendon injuries is beyond the scope of this chapter; however, postsurgical management includes supervised hand therapy to maximize range of motion and strength outcomes. General guidelines include use of a dorsal blocking orthosis positioned in 10 to 30 degrees of wrist flexion, 40 to 60 degrees of MP joint flexion, and full IP extension, which is worn continuously for 4 to 6 weeks following surgery. For the first 3 to 4 weeks, home exercises include active range of motion of the elbow and shoulder while the patient remains in the orthosis. Multiple protocols exist based on surgical management and healing potential of the repaired tendon; however, initial protected passive motion of the involved digit is consistent among all flexor tendon protocols. At 3 to 4 weeks the orthosis is modified to bring the wrist into neutral flexion and extension. The protocols differ at this stage and may include removal of the orthosis on an hourly basis to initiate exercises, which may include ongoing passive range of motion, place and hold (where the digit is passively flexed and the patient attempts to actively hold that position), and/or active tendon gliding exercises which includes active differential gliding of the FDS and FDP tendons. At 4 to 6 weeks the dorsal blocking orthosis is discontinued and the use of a nighttime volar orthosis may be initiated. The exercise program progresses to include gentle active blocking exercises.²⁷ Resistance and strengthening exercises are generally initiated around 8 weeks. Heavy resistance (lifting over 10 pounds) manual labor or return to full sports activities may take 10 to 12 weeks.^24,27

The most common closed tendon injury in athletes is a mallet finger, which occurs with forced flexion of the DIP joint during active extension when the top of the finger strikes a ball (Fig. 31–10). The extensor tendon is torn at its insertion on the dorsal aspect of the base of the distal phalanx, with or without avulsion fracture. Seventy-four percent of mallet finger injuries involve the dominant hand, and more than 90% of injuries were found in the ulnar three digits.^28,29 If left untreated, this injury can lead to a swan-neck deformity where there is hyperextension of the proximal interphalangeal (PIP) joint due to tendon imbalances.^23,28 Isolated tendon injuries may be treated with uninterrupted immobilization with the use of an orthosis in slight hyperextension of the DIP joint or with percutaneous pinning using Kirschner wires (K-wires) for 6 weeks. There are many variations in the design of orthoses for the treatment of mallet finger, but the principle is the same. For the use of an orthosis to be successful, the ruptured end of the extensor tendon must have continuous contact with the bone to allow for secondary healing. If the orthosis is removed at any time and a gap occurs between the bone and the ruptured tendon, the period of immobilization in the orthosis must be started over or surgical repair is necessary. After 6 weeks, the orthosis and/or the K-wires are removed; however, the patient should continue wearing an orthosis at night and during sports activities for an additional 6 weeks.^23,28–30 An excellent outcome is the absence of pain with full range of motion at the DIP joint; a good outcome is considered when there is less than a 10-degree extensor lag; a 10- to 25-degree extensor lag with no pain is considered a fair outcome; and greater than a 25-degree extensor lag or persistent pain is considered a poor outcome.

A Boutonnière deformity consists of flexion of the PIP and hyperextension of the DIP joints^27,30,31 (Fig. 31–11). Understanding the anatomy and biomechanics of the extensor mechanism of the finger is critical in determining appropriate management. Three muscles contribute to the extensor mechanism of the finger: the extensor digitorum (ED), the lumbricals, and the dorsal interossei. Radial and ulnar sagittal bands stabilize the ED as it crosses the MP joint. In addition to stabilizing the MP joint, the sagittal bands assist with MP extension through a lasso effect. After the ED crosses the MP joints, it splits into three structures: the central slip and two lateral strips. The central slip inserts on the dorsal aspect of the middle phalanx and extends the PIP joint. The lateral slips traverse the radial and ulnar aspects of the finger and insert into the lateral bands. The lumbricals originate on the FDP tendons, travels volarly to the MP joint and then along the radial aspect of the finger, and terminate in the lateral band. The deep heads of the dorsal interossei give rise to the lateral tendon, which passes superficially to the sagittal bands. The lateral tendon gives off transverse fibers, which flex the MP joints, and then contributes to the oblique fibers and the medial bands of the interossei, which extend the PIP joint. The lateral tendon then joins the lateral slip of the ED and the lumbrical tendons to form the lateral band.³¹ Distal to the PIP joint the lateral bands are anchored dorsally by the triangular ligament and volarly by the transverse retinacular ligament, which prevents volar or dorsal subluxation of the lateral bands. At the distal aspect of the middle phalanx, the lateral bands come together dorsally and join to form the terminal tendon that inserts at the base of the distal phalanx and extends the DIP joint.

A boutonniere deformity occurs due to disruption of the central slip and triangular ligament as a result of blunt trauma, an open laceration, or a volar dislocation of the PIP joint. An injury to the central slip and triangular ligament allows the lateral bands to migrate volarly with PIP joint flexion. Over time, a PIP joint extensor lag develops, and if not treated properly, the lateral bands become fixed volarly resulting in a permanent flexion deformity. As the lateral bands migrate volarly, they also move proximally due to the pull of the lumbrical and interossei muscles, which increases the tension on the terminal tendon resulting in hyperextension of the DIP joint.^29–31

Conservative, nonsurgical management is recommended for patients with an acute, closed dorsal boutonniere deformity. This consists of placing the PIP in an extension orthosis continuously for 6 to 8 weeks to allow the central slip to heal. Active DIP flexion and extension exercises are performed frequently throughout the day to pull the lateral bands dorsally and counteract the proximal migration of the lateral bands.^29–31 After continuous use of an orthosis for 6 to 8 weeks, PIP flexion exercises are initiated; however, the PIP extension orthosis is continued at night for an additional 4 to 6 weeks. Chronic boutonniere deformities may also respond well to orthotic management, provided the patient is able to achieve full passive PIP extension through serial casting or use of a dynamic orthosis over a 6- to 12-week period. Active DIP flexion and extension remains a critical component of treatment for the fixed deformity. Once the patient achieves and maintains full passive PIP extension with a PIP extension orthosis over 6 to 12 weeks, gradual progression of PIP flexion is initiated.^29–31

Surgical management is recommended for patients with acute, closed injuries that are not amenable to a full-time extension orthosis. The PIP is positioned in full extension and a K-wire is placed across the joint and left in for 4 to 6 weeks. Once the K-wire is removed, progressive PIP flexion exercises are begun. Surgical repair of chronic boutonniere deformities is complicated and there are multiple surgical options; however, patients with a boutonniere deformity often have full finger flexion and full grip strength, and have few functional limitations. Surgical intervention may lead to an extension contracture and poor functional outcomes; therefore, surgery for a boutonniere deformity is not always in the best interest of the patient.^29–32 Therapeutic management following surgery is dependent on the choice of surgical technique.

Arthritis affects nearly one in five adults, and it is anticipated that this number will increase to 40% by the year 2030. It is the leading cause of disability in adults in the United States and the most common joint disorder throughout the world. Osteoarthritis (OA) affects over 27 million Americans and is found more frequently in women, the majority of whom are over the age of 45.^33,34 OA is a result of mechanical, biochemical, and cellular factors. The most common joints affected in the upper extremity are the DIP joints and the carpometacarpal (CMC) joint of the thumb. In addition, 50% of individuals with DIP involvement also have PIP involvement^34,35 (Fig. 31–12).

RA affects all racial and ethnic groups throughout the world and is estimated to affect 1.3 million adults in the United States. It is a chronic systemic disease characterized by synovial inflammation (synovitis) and tissue proliferation, most commonly seen in the wrist, MP, and PIP joints. There is also inflammation (tenosynovitis) and synovial proliferation in the extrinsic tendons and tendon sheaths. The synovium causes cartilage to lose its ability to absorb forces, which, in time, results in mechanical disruption of the joint surfaces. RA can affect individuals of any age, and juvenile RA (JRA) is one of the most common diseases in children.^33,34,36,37 Women between the ages of 35 and 45 are involved four times more frequently than men.³⁸ Typical deformities in adults include volar subluxation of the ulnar aspect of the wrist, ulnar subluxation of the carpals, ulnar drift of the fingers at the MP joints, swan-neck deformities (hyperextension of the PIP joints and flexion at the DIP joints), boutonniere deformities as previously described, and zig-zag deformities of the thumb.^37,38 Deformities found in JRA are highly variable. Children may present with wrist flexion and wrist ulnar deviation, or wrist ulnar deviation and MP joint radial deviation, which is opposite of what is seen in adults, while other children may demonstrate similar deformities as to what is seen in adults. Careful consideration of all potential deformities must be taken when treating children with RA (Fig. 31–13).³³

The use of an orthosis is common in the conservative management of both OA and RA to decrease pain, minimize deformities, decrease inflammation, decrease stress on the joints, provide support to facilitate function, and assist with joint stability.³⁵ Orthoses that allow a small amount of motion promote less cartilage damage and better joint recovery. In addition, properly aligning joints with an orthosis provides cartilage protection, facilitating pain reduction and increased function during daily activities.³⁵

Initiating joint protection principles early in the disease process of OA and RA is of critical importance. There is strong evidence to support the efficacy of joint protection instruction in decreasing joint stress and damage to involved joints by altering work demands, educating patients on proper joint alignment, and the use of adaptive equipment.^33,35,36 For more information on joint protection for arthritis, the reader is referred to the work of Beasley in 2012 (Fig. 31–14).³⁵