Plastic surgery

PART VIII

HAND

CHAPTER 79  TENOSYNOVITIS DISORDERS OF THE UPPER EXTREMITY

MARY C. BURNS AND MICHAEL W. NEUMEISTER

Tendonopathies of the upper extremity are extremely common disorders encompassing a large variety of conditions from tendon strains to ruptures or lacerations. The most common tendinopathy is tenosynovitis or inflammation of the tendon sheaths. Inflammation may arise from a number of causes as categorized in Table 79.1. It is important to understand that inflammation is a continuous process that involves a cascade of events leading to variable clinical symptoms and signs. Acute inflammation involves a vascular response, fluid exudate and swelling, cellular exudate with phagocytosis, and alterations in tissue composition. The exudates associated with inflammation differ from normal interstitial fluid by having a greater protein content and higher specific gravity (over 1.020).1

The fate of acute inflammatory conditions, however, depends upon the treatment and cessation of the inciting caustic agent or activity. Upon cessation, the inflammation may resolve completely leaving normal tissues behind. Alternatively, the acute inflammatory response may result in a number of pathologic states, including (A) organization of the exudate leading to fibrosis, (B) tissue destruction and secondary healing by repair/scarring, (C) chronic inflammation, and (D) in the case of infection, suppuration.

LATERAL EPICONDYLITIS

Lateral epicondylitis, or tennis elbow, is a common condition of the lateral elbow. First described in 1873 by Runge, lateral epicondylitis is the direct result of strain at the fascia and origin of the extensor muscles of the forearm.2 Active extension against resistance, such as occurs when one hits a tennis ball with a back hand shot (hence the term “tennis elbow”), presumably results in microtrauma to the origin of the extensor carpi radialis brevis (ECRB), the extensor digitorum communis (EDC), and the extensor carpi ulnaris. Although the specific etiology is unknown,3 it is postulated that this disease results from micro-tears at the origin of the common extensor muscle mass. Many reports believe that these small tears are caused by overuse, repetitive or cumulative injury, and strain of the common extensor origin at the lateral epicondyle. Continued use of the upper extremity results in continued strain and re-injury to the muscle origins.4,5 This can lead to degeneration and possible avascularity at the muscle origin, which in turn, theoretically, leads to chronic inflammation causing the injured areas to remain weak and painful. Ironically, however, inflammation is not a characteristic histologic finding of lateral epicondylitis, but fibrosis and mucinoid degeneration of the origin of the extensor muscles have been documented.6 Table 79.2 highlights the histologic changes observed at the origin of the extensor muscles of the forearm.

Patients generally present with pain and localized tenderness of the extensor origin and lateral epicondyle of the humerus (Figure 79.1). The onset may be acute or insidious, and it is more common in males between 40 and 50 years of age. Generally, there is increased pain with wrist extension or with gripping. Activities requiring full elbow extension and forearm pronation aggravate the discomfort that may radiate down the posterior forearm or proximally over the lateral upper arm above the elbow. The pain may also be accentuated by extreme wrist flexion from the passive stretch of the ECRB muscle or by active contraction of the wrist extensors.

During the initial examination of the patient, the surgeon should also evaluate the range of motion (ROM) of the elbow, assess crepitus of the radiohumeral joint, observe for bursitis and osteochondritis of the capitellum, and rule out radial tunnel or posterior interosseous nerve entrapment.

There is limited value in obtaining further diagnostic studies for lateral epicondylitis. One may consider plain radiographs if degenerative elbow changes are considered or identified on physical exam. Similarly, magnetic resonance imaging scans may identify articular pathology or masses, but generally these tests are not indicated for clinically confirmed lateral epicondylitis. Nerve conduction and electromyogram studies may be useful if radial tunnel or posterior interosseous nerve entrapment is suspected. These nerve entrapments are not uncommonly found in patients with lateral epicondylitis. Injecting a local anesthetic agent around the extensor origin and lateral epicondyle confirms the diagnosis but the diagnosis is usually made at physical exam. The lateral epicondyle and the proximal radius are the origins of the extensor muscles of the forearm. The extensor carpi radialis longus (ECRL) has its origin just above the lateral epicondyle on the humerus and the intermuscular septum. The ECRB originates from the lateral epicondyle (common extensor origin) and the lateral ligament of the elbow.

FIGURE 79.1. Location of pain in “tennis elbow.” Lateral epicondylitis is characterized by point tenderness over the lateral epicondyle. The patients often complain of weakness, pain on wrist extension, and lateral elbow pain.

The natural history of lateral epicondylitis is variable. Many authors believe that over time (1 to 2 years), the condition burns itself out and therefore no specific treatment may be warranted.The level of discomfort, however, dictates the treatment. If the condition is mild, and the patient can tolerate benign neglect, improvement with anti-inflammatory medication is probable. In general, patients are offered physical therapy, splinting, and oral anti-inflammatory medication. The physical therapy regimen includes stretching the extensor muscle origin and gradual loading. Counterforce braces or forearm support bands are common splints utilized for lateral epicondylitis (Figure 79.2). The counterforce brace essentially changes the origin of the muscles to a more distal site. The brace acts to decrease the force of muscle contraction by inhibiting muscle expansion, thereby reducing tension at the origin of the muscle. This essentially off-loads the muscle origin, prevents repetitive trauma at this site, and allows healing. Most therapists will have patients wear the counterforce brace throughout the day, particularly when performing activities utilizing the extensor muscles. The brace can be removed during periods of inactivity and when they are sleeping. The brace is typically applied approximately 2 cm distal to the lateral epicondyle and should fit with a comfortable amount of pressure. Maximum contraction of the wrist extensors is avoided. A brace that is applied too tightly may result in swelling of the distal forearm and hand, compression of the posterior interosseous nerve, and pain. When lateral epicondylitis is severe, complete immobilization may be necessary. A wrist cock-up splint or even a long-arm splint with the elbow at 90° of flexion may be warranted. The Richard wrist cock-up splint maintains the wrist in extension to off-load the extensors. Orthoses have been described in various positions ranging from neutral to 45° of wrist extension. The rigid wrist orthosis, however, is fraught with noncompliance and is therefore limited to only the more severe cases of lateral epicondylitis.

FIGURE 79.2. Nonsurgical treatment for lateral epicondylitis. A static band at the origin of the ECRB off-loads the epicondyle.

Steroid injections have been utilized for the treatment for lateral epicondylitis. The duration of the effects of the steroid injection, however, is variable.7 Most patients respond favorably within the first 6 weeks but recurrence of the pain is common. The steroid is injected at the site of the maximum tenderness at the lateral epicondyle. Typically, 1 cc of dexamethasone or Kenalog is injected into this area. No significant difference has been demonstrated between different steroid preparations. Most surgeons wait for a period of 2 to 3 months before re-injection at this site and limit the number of injections to 3 or 4, mostly because of the secondary effects of the steroids on the overlying soft tissue. The steroid injections can result in significant atrophy of the fat and overlying skin and may also result in hypo-pigmentation of the area.

Some authors have tried platelet-rich plasma or even the patient’s own blood injected into the lateral epicondyle. Gossen et al. compared corticosteroid with platelet-rich plasma injections in patients with refractory lateral epicondylitis for at least 6 months.7 The long-term outcomes were similar in both groups following the injections but it was generally felt that the corticosteroid injection was more effective in reducing the pain in the short term. Autologous blood injections were thought to initiate an inflammatory response at the lateral epicondyle with subsequent fibrosis that improved the condition by decreasing strain at the origin. Edwards and Calandruccio injected autologous blood in 28 patients and demonstrated an 80% reduction in pain over 9 months.7 Missra and Delco injected buffered platelet-rich plasma into patients with lateral epicondylitis with similar findings comparing corticosteroid and the platelet-rich plasma.7

Botulinum toxin A has been injected into extensor muscles to induce paralysis as a means of off-loading the muscle’s origin.8 Other topical agents have been used for lateral epicondylitis, including topical nitrates, steroid creams, and salicylate creams; however, no randomized controlled studies have been performed with these agents.17

Surgery For Lateral Epicondylitis

The surgical treatment for lateral epicondylitis is restricted to those patients who have failed conservative measures and have been treated for 6 months to a year or are significantly disabled as a result of the discomfort.

A 2 to 3 cm incision is made over the lateral epicondyle and the extensor fascia is incised. Any degenerative muscle or granulation tissue is debrided. The prominent lateral epicondyle is shaved with an osteotome. Care is taken not to disrupt the collateral ligament of the elbow. Hemostasis is secured and the fascia is repaired. The wounds are typically closed with a resorbable sutures and a bulky dressing is applied.

Variations to the procedure include resecting the sensory nerves to the lateral epicondyle, transposing the anconeus muscle over the shaved epicondyle. To denervate the lateral epicondyle, the incision is usually extended proximally to identify the arcade of nerves that innervate the lateral epicondyle in the elbow. The nerves are resected and allowed to retract proximally or are buried in the brachialis muscle.8

DE QUERVAIN’S TENOSYNOVITIS

The anatomy of the first dorsal compartment is variable. There may be multiple slips of the abductor pollicis longus (APL) tendon which may insert in a variety of locations around the basilar joint, including the thumb metacarpal, the trapezium, the volar carpal ligament, the opponens pollicis, and abductor pollicis brevis (APB) (Figure 79.3). The extensor pollicis brevis (EPB) tendon is also housed within the first dorsal compartment. The EPB tendon, however, may travel in its own separate compartment within the first dorsal compartment along with the APL tendon. This septation of the EPB tendon seems to increase the probability of acquiring de Quervain’s tenosynovitis, and it may also increase the probability that conservative measures will not be successful and that surgical decompression is warranted. The treatment of de Quervain’s tenosynovitis is usually conservative at the first presentation. Nonsteroidal anti-inflammatories, corticosteroid injections, and off-loading of the APL and EPB tendon are the mainstay of treatment in de Quervain’s tenosynovitis. Failing all nonsteroidal anti-inflammatories, most patients should receive a trial of corticosteroid injections into and around the first dorsal compartment. This steroid is injected around the radial styloid, which is the site of greatest constriction. Most studies quote steroid injections’ success rates of 50% to 80%.9,10

Repeat injections may be required if the symptoms fail to resolve. Most surgeons will offer second or third injections at 3- to 4-month intervals. Corticosteriod injections, however, may result in atrophy of the overlying soft tissue or hypo-pigmentation of the skin and may not be suitable for those with dark pigmentation. The surgical treatment for de Quervain’s tenosynovitis requires an incision over the first dorsal compartment and its retinaculum to provide frictionless glide of the APL and the EPB tendons. A longitudinal or transverse incision is made at the level of the radial styloid over the first dorsal compartment (Figure 79.4). The subcutaneous tissue is dissected with blunt dissection to avoid injury to the superficial radial nerve which must be retracted to appropriately visualize the thickened retinaculum over the first dorsal compartment. The incision in the retinaculum is made on the dorsal aspect of the first dorsal compartment so that the released APL tendon does not subluxate forwardly upon abduction of the thumb or flexion of the wrist (Figure 79.4B). The EPB must be identified and the potential separate secondary tunnel within the first dorsal compartment visualized and released or the patients’ symptoms may not resolve subsequent to the surgery. The release of the first dorsal wrist compartment is extended to the basilar joint and then proximally into the forearm. This procedure can be performed under local anesthetic, regional anesthesia and is often considered an office procedure. Following closure of the wound, a gentle wrap is applied to the wrist and the patient is encouraged to start gentle active and passive ROM the following day. Postoperative physical therapy is usually not required but may have a role if hypersensitivity or if limited motion is noted.

FIGURE 79.3. Anatomy of de Quervain’s tendonitis. The first dorsal compartment houses the abductor pollicis longus and the extensor pollicis brevis. There may be multiple slips of the abductor pollicis longus. The extensor pollicis brevis may also be compartmentalized in a separate sheath within the first dorsal compartment.

INTERSECTION SYNDROME

Intersection syndrome is a rare tendonitis syndrome observed at the junction of the outcropping muscles and the tendons of the second dorsal compartment. The outcropping muscles include the APL and the EPB as well as the extensor pollicis longus muscles. The second dorsal compartment is comprised of the ECRL and ECRB tendons. The area of intersection between these two compartments is approximately 4 cm proximal to the radial carpal joint (Figure 79.5). Patients present with pain and swelling in this area. The most likely etiology is that of repetitive trauma, such as using a hammer or any repetitive radial and ulnar deviation of the wrist as well as abduction and extension of the thumb. The tenderness and swelling at the site of intersection occurs as the APL and APB tendons glide over the ECRL and ECRB tendons. The friction that arises from this intersection results in acute inflammation and, in severe cases, may even have an audible crepitus on flexion and ulnar deviation of the wrist. There is some controversy about the true pathology that causes the pain. Crunburg and Regan felt that friction was not the etiology of the intersection syndrome but rather a tenosynovitis of the second dorsal compartment alone.24,25

Examination of a patient with intersection syndrome reveals tenderness and swelling 4 to 6 cm proximal to Lister tubercle. Palpable or audible crepitus may be observed but significant pain is predictable on flexion and ulnar deviation of the wrist.

Treatment

Intersection syndrome is usually self-limited. Off-loading the second dorsal compartment and the first dorsal compartment is often sufficient to resolve the symptoms. Static wrist splinting with the wrist in a neutral position is commonly preferred by many therapists, although slight extension and abduction of the thumb may also help off-load the offending tendons (Figure 79.6). Nonsteroidal anti-inflammatories and occasionally steroid injections have been employed. Surgical release of intersection syndrome is rarely needed. If conservative modalities fail to resolve the tenosynovitis, surgical decompression of the second dorsal compartment and the outcropping muscles is warranted. The procedure involves a longitudinal incision 6 cm proximal to the Lister tubercle on the extensor surface of the forearm. The subcutaneous tissue is deepened with blunt dissection to preserve the superficial sensory nerves and veins. The second dorsal compartment is released freeing up the ECRL and ECRB tendons. The fascia of the first dorsal compartment is also released. Occasionally, the EPL fascia is released as well. A distinct bursa over the muscle bellies or tendons is usually not identified. After closure of the wound, the wrist is wrapped in a soft dressing, which can be removed in 48 hours and the patient can start active and passive ROM. Prolonged splinting is not necessary.

TRIGGER FINGER

Trigger finger is also known as stenosing tenosynovitis and is one of the more common disorders of the hand. Stenosing tenosynovitis of the thumb was first described in 1850 by Notta and documented as a size discrepancy between the flexortendon and retinacular sheath, resulting in tendon entrapment (Figure 79.7). The exact etiology of the trigger finger is unknown but it is commonly believed that thickening around the A1 pulley, a nodule formation within the flexor tendon, or a combination of both results in active triggering of the finger as the fullness of the tendon catches on the thickened A1 pulley. As a result of the repetitive motion friction between the A1 pulley and the flexor tendons, the pulley may become significantly thickened and undergo cicatricial fibrocartilaginous metaplasia. There is an upregulation of collagen type 3 relative to the normal type 1 collagen found in the A1 pulleys. Other histologic changes at the A1 tendon sheath include fibrous tissue without leukocyte infiltration, extracellular mucoid collections, fraying, degeneration, cyst formation, and lymphatic or plasma cell infiltration.11,12,13 The true underlying etiology of primary trigger finger is unknown. There are a number of associated conditions listed in Table 79.3 that may result in triggering.

FIGURE 79.4. Surgical release of the first dorsal compartment. A. A longitudinal incision (2.5 cm) is made along the first dorsal compartment to expose the abductor pollicis longus and extensor pollicis brevis. B. The retinaculum of the first dorsal compartment is released on its dorsal side to prevent tendon subluxation.

Triggering is not always associated with a thickening of the A1 pulley. The proximal aponeurotic pulley system may also be thick and result in triggering. The pain and discomfort is usually associated with a more proximal site than the A1 pulley.

FIGURE 79.5. Intersection syndrome. Inflammation in intersection syndrome causes pain and tenderness approximately 4 to 10 cm proximal to the radial carpal joint.

Patients can present with variable stages of trigger finger. Table 79.4 describes Green’s classification of trigger finger. Tenderness over the A1 pulley is a common finding often associated with an inability to grasp objects. Occasionally, there is swelling around the volar aspect of the metacarpal head. The term triggering refers to a clicking sensation the patient has as a result of the size discrepancy of the flexor tendon and the overlying retinaculum sheath of the A1 pulley. Many patients believe that their clicking is at the proximal interphalangeal (IP) joint, but in reality the pathology is at the A1 pulley site. As the condition progresses, there is an active locking of the finger as the flexor tendon is unable to glide back underneath the A1 pulley to allow for extension of the finger. Further progression of the disorder results in the inability of the patient to even passively correct the locking of the finger in the flexed position. For unknown reasons, the ring finger is the most commonly affected followed by the long finger and the thumb. Approximately 20% of nondiabetic patients have multiple digit involvement and women are more commonly affected than men. A statistically significant relationship between occupation and development of idiopathic trigger finger has not been found.

FIGURE 79.6. Conservative treatment for intersection syndrome. Anti-inflammatory agents and a splint that off-loads the first and second dorsal compartments are employed.

FIGURE 79.7. Trigger fingers. The A1 pulley of each digit is the site of pathology in trigger fingers.

Reverse triggering is a condition why the finger has an inability to flex because of the size discrepancy of the flexor tendon and the A1 pulley. In essence, the digit is locked in the extended position rather than the flexed position. Partial tendon injury is the most common cause of reverse triggering. Congenital triggering of the thumb has been associated with an aberrant nodule within the flexor tendon which is unable to pass underneath the A1 and oblique pulleys of the thumb. Carpal tunnel and trigger finger are common comorbid conditions.12 Diabetes is also associated with an increased incidence of both conditions. Repetitive trauma in overuse can result in inflammation around the A1 pulley with significant swelling and constriction of the tendon sheath. Free glide of the tendons is inhibited, friction is increased, and greater inflammatory process ensues resulting in the thickening of the pulley. The hypovascular area between the A1 and A2 pulleys compounds poor blood flow and attrition to the tendons that may result in nodule formation distal to the A1 pulley. Nodular fullness of the tendon forcibly rubs against the proximal distal edges of the A1 pulley causing further inflammation, and pain is produced by clicking or popping of the finger.12

Treatment

Conservative measures in treating trigger finger include immobilizing the tendon, nonsteroidal anti-inflammatories, and steroid injection. In some cases, nonsteroidal anti-inflammatories may relieve the symptoms and no further treatment is required. As the condition progresses, the tenderness and the triggering of the finger often respond to a single steroid injection. The effectiveness of a single steroid injection ranges from 50% to 90%. Commonly used steroids include betamethasone, dexamethasone, methylprednisolone, and triamcinolone; however, little data support one corticosteroid over another. Ray et al. compared dexamethasone with triamcinolone in a prospective randomized study and concluded that triamcinolone has a faster onset but a shorter duration of action. The corticosteroid is injected in and around the A1 pulley, with care taken not to enter the flexor tendon. As the needle is introduced into the flexor tendon, resistance is felt within the syringe. The needle is drawn back until no resistance is noted and the steroid is injected to bathe the A1 pulley. The duration of action of the corticosteroid is variable, ranging from weeks to years. Complications of corticosteroid injections include tenderness, joint stiffness, bruising, fat atrophy, infection, pulley rupture, and tendon rupture.

Splinting for trigger finger is uncommon but may be designed to restrict tendon glide through the A1 pulley until the inflammatory process resolves. Atell et al. reported 77% success rate with splinting in patients who presented with triggering for 6 months or less.

Hand-based splints that immobilize the metacarpophalangeal joints in extension leaving the IP joints free are the most commonly used orthosis for trigger finger (Figure 79.8).

FIGURE 79.8. Nonsurgical treatment of trigger finger. To off-load the friction between the flexor tendon and the A1 pulley, a hand-based splint is designed to immobilize the metacarpophalangeal joints.

Surgical Treatment

Refractory triggering requires surgical release of the A1 pulley. The two main types of release of the A1 pulley include open incision and percutaneous release.11-15 The open technique utilizes a longitudinal or oblique 1.5-cm incision over the A1 pulley at the affected digit (Figures 79.9A–C). Subcutaneous tissue is deepened with blunt dissection down to the flexor sheath. The A1 pulley is identified and transected in its entirety and the release may even include the leading edge of the A2 pulley. Appropriate glide of the tendon should be confirmed prior to closure of the wound. Appropriate skin closure and soft dressing is applied, and immediate ROM is initiated. The percutaneous release of the A1 pulley utilizes an 18G to 19G needle that is inserted over the A1 pulley while the patient maintains the hand with the metacarpophalangeal joint extended. The needle is inserted under local anesthetic down to the A1 pulley which is then scored back and forth with the double end of the needle to completely release the pulley. Again, the patient should demonstrate no further triggering following the procedure. The digital nerves of the thumb and index finger may come to lie very close to the entrance site of the needle; therefore, care must be taken not to injury these nerves. Bain et al. reported superficial scoring of the flexor digitorum superficialis tendon in 75 of 83 cadaveric digits using percutaneous methods.16 Bain et al. as well as Pope and Wolfe found incomplete releases in their cadaveric studies and felt the technique should be used cautiously for the thumb because of the proximity of the digital nerves.16,17

Complications have also been noted for the open surgical technique for trigger release. Complications include stiffness, tenderness, wound infection, incomplete release, bowstringing, reflex sympathetic dystrophy, and digital nerve laceration.

OTHER TENDONOPATHIES

Other uncommon tendonopathies of the upper extremity include flexor carpi radialis (FCR) tendonitis, flexor carpi ulnaris tendonitis, extensor pollicis longus stenosing tendovaginitis, and EDC tendonitis. The FCR has a rather thin synovial sheath in the forearm. As the FCR tendon dives dorsally under the trapezium, the fibrous canal thickens and may result in stenotic tenosynovitis. The condition may be exacerbated by basilar joint osteoarthritis, scaphoid fractures, de Quervain’s tenosynovitis, and volar ganglion. Conservative treatment is commonly employed successfully. Wrist splinting in a neutral position, nonsteroidal anti-inflammatory medication, and occasional steroid injections are common treatment options for FCR tendonitis, which usually presents with tenderness directly over the distal aspect of the FCR tendon. Occasionally, patients also have tenderness on flexion of the wrist or on forced extension of the wrist. Failing conservative measures, surgical release involves dividing the sheath through a longitudinal incision over the FCR.

FIGURE 79.9. Surgical release of trigger thumb. A. An oblique incision is made over the A1 pulley. B. The A1 pulley is exposed. C. A longitudinal excision through the A1 pulley is made to fully release the tendon.

The treatment option for tenosynovitis of the third, fourth, fifth, or sixth dorsal compartments is similar to that of the first dorsal compartment.

Postoperative Care

Rehabilitation goals following postoperative treatment of tendonopathies include monitoring wound status, decreasing edema and inflammation, desensitization exercises to decrease hypersensitivity, increasing ROM, facilitating tendon glide, scar remodeling, and returning the patient to pain-free functional use, including work and sporting activities.

Typically, the immobilization period following surgery should be minimal. Formal therapy is usually not required postoperatively; however, consideration should be given to a referral for a one-time therapy visit to provide edema control as well as for instruction in the proper exercise techniques and precautions. In some cases, if the pain level is significant or if there is significant limitation in the ROM, a referral for more formal therapy may be warranted. A therapist knowledgeable in these conditions and surgical techniques will be able to assist the patient in regaining full ROM and in decreasing pain levels. Formal therapy can offer pain control techniques that may include the use of thermal agents such as heat and ice. Ultrasound or transcutaneous electrical stimulation (TENS) may also prove to be beneficial for patients with a significant amount of pain. An upper extremity therapist can provide scar remodeling techniques as well as assist with progressive strengthening while respecting the patient’s pain level. Therapy can also assist with patient education on how to modify provocative activities as well as to teach proper ergonomic measures for returning to work or sporting activities. In addition, there may be options for a therapist to recommend soft supports to help transition a patient through the early postoperative pain and into the strengthening phase that may in turn minimize the chance of recurrence.

TRIGGER FINGER RELEASE

Trigger finger release typically does not require immobilization. Active ROM is initiated immediately after surgery and generally the patient will achieve full ROM within 3 to 5 days following surgery. As stated previously, a one-time referral to a hand therapist will be beneficial for wound management, edema control, and proper instruction in ROM, including differential tendon glide and intrinsic stretches. A common postoperative complication following trigger finger release is a loss of composite extension, which can ultimately lead to contracture if not treated early. This is common in patients who present with a preoperative contracture or in the digit that was locked in flexion. In cases where full extension is not present, extension splinting may be necessary. A custom fit extension splint can be fabricated to wear at night and as needed during the day. If there is significant loss of passive extension, a dynamic splint such as an LMB spring extension splint can be used.

Following suture removal, scar massage and desensitization exercises may be initiated. Progressive strengthening may be introduced at 3 to 4 weeks after surgery. In general, recovery after trigger finger release will only be 3 to 4 weeks; however, it is important to inform the patient that it may take up to 6 months for all of the swelling, stiffness, and tenderness in the palm at the incision site to completely go away.

DE QUERVAIN’S RELEASE

Edema control and active and passive ROM exercises are occasionally required after de Quervain’s release. Exercises should include wrist flexion and extension as well as wrist radial and ulnar deviation. The ultimate goal of ROM exercises will be to gradually achieve a pain-free Finkelstein’s position of thumb flexion with wrist ulnar deviation. Initially, a thumb spica splint may be fit for up to 2 weeks after surgery to prevent subluxation of the APB and EPB in the first dorsal compartment after release.

One significant postoperative complication that may occur following de Quervain’s release is irritation/injury to the dorsal sensory branch of the radial nerve (DSBRN). Hypersensitivity of this nerve can be quite painful for the patient and can ultimately affect functional use of the hand. Instruction in proper desensitization exercises will be crucial in an attempt to decrease hypersensitivity of the DSBRN. Other pain control or desensitization techniques such as TENS and fluidotherapy may also be beneficial. Adherent painful scar at the incision site may be another postoperative complication that will affect rehabilitation. Several scar management techniques such as scar compression, scar mobilization, silicone gel sheeting, and Kinesio tape may be utilized for this condition.

INTERSECTION SYNDROME

Edema control and active and passive exercises may be initiated within 24 hours of a release of intersection syndrome. Typically, immobilization is not required; however, if the patient is experiencing significant pain, a thumb spica splint with the IP free can be fitted to wear between exercise sessions and at night.

LATERAL OR MEDIAL EPICONDYLECTOMY

Although the vast majority of epicondylitis patients respond to conservative measures, a small percentage of patients will continue to have debilitating pain after 6 to 12 months. These patients may require surgical intervention. Postoperative immobilization may be warranted to off-load the extensor origin and reduce pain for the first 3 to 10 days. The immobilization may be in the form of continuing the surgical bulky dressing or having the patient fit with a custom-made orthosis to immobilize the elbow, forearm, and wrist. Splinting is not commonly required but occasionally pain relief is maximized with the elbow positioned in 90° flexion and the wrist in neutral. Active and passive ROM exercises may be initiated at 7 to 10 days after surgery beginning with isolated joint motions and gradually increasing stress to EDC and radial wrist extensors. Full composite motion should be achieved by 4 weeks after surgery. Thermal agents, ultrasound, or TENS may be utilized for pain management as needed. The patient is instructed in scar massage, scar mobilization, and desensitization exercises. At 6 to 8 weeks, progressive strengthening and resistive exercises may be introduced. Gradual progression to normal use, including ergonomic modifications for work and sports will occur between 8 and 12 weeks. It will be important to progress slowly and work within a pain-free range to ultimately achieve full normal pain-free use of the affected extremity.

References

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2.  Boyd HD, McLeod AC Jr. Tennis elbow. J Bone Joint Surg Am. 1973;55:1183-1187.

3.  Gellman H. Tennis elbow (lateral, epicondylitis). Orthop Clin North Am. 1992;23:75-82.

4.  Verhaar J, Walenkamp G, Kester A, et al. Lateral extensor release from tennis elbow. J Bone Joint Surg Am. 1993;75:1034-1043.

5.  Nirschl RP, Pettrone FA. Tennis elbow: the surgical treatment of lateral epicondylitis. J Bone Joint Surg Am. 1979;61:832-839.

6.  Regan W, Wold LE, Coonrad R, et al. Microscopic histopathology of chronic refractory lateral epicondylitis. Am J Sports Med. 1992;20:746-752.

7.  Price R, Sinclair H, Heinrich I, Gibson T. Local injection treatment of tennis elbow: hydrocortisone, triamcinolone, and lignocaine compared. Br J Rheumatol. 1991;30:39-44.

8.  Lin YC, Tu YK, Chen SS, Lin IL, Chen SC, Guo HR. Comparison between botulinum toxin and corticosteroid injection in the treatment of acute and subacute tennis elbow: a prospective, randomized, double blinded, active drug-controlled pilot study. Am J Phys Med Rehabil. August 2010;89(8):653-659.

9.  Harvey FJ, Harvey PM, Horsley MW. de Quervain’s disease: surgical or nonsurgical treatment. J Hand Surg (Am). 1990;15:83-87.

10.  Weiss APC, Akelman E, Tabatabai M. Treatment of de Quervain’s disease. J Hand Surg (Am). 1994;19:595-598.

11.  Sato ES, Gomes Dos Santos JB, Belloti JC, Albertoni WM, Faloppa F. Treatment of trigger finger: randomized clinical trial comparing the methods of corticosteroid injection, percutaneous release and open surgery. Rheumatology (Oxford). January 2012;51(1):93-99.

12.  Lundin AC, Eliasson P, Aspenberg P. Trigger finger and tendinosis. J Hand Surg (Eur). 2012;37:233–236.

13.  Miyamoto H, Miura T, Isayama H, Masuzaki R, Koike K, Ohe T. Stiffness of the first annular pulley in normal and trigger fingers. J Hand Surg (Am). September 2011; 36(9):1486-1491.

14.  Lyu SR. Close division of the flexor tendon sheath for trigger fingers. J Bone Joint Surg. 1992;74:418-420.

15.  Eastwood DM, Gupta MB, Johnson DP. Percutaneous release of the trigger fingers: an office procedure. J Hand Surg (Am). 1992;17:114-117.

16.  Bain GI, Turnbull J, Charles MN, Roth JH, Richards RS. Percutaneous A1 pulley release: a cadaveric study. J Hand Surg (Am). September 1995;20(5):781-784.

17.  Pope DF, Wolfe SW. Safety and efficacy of percutaneous trigger finger release. J Hand Surg (Am). March 1995;20(2):280-283.