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Perspectives on Modern Orthopaedics

de Quervain Tenosynovitis of the Wrist

Ilyas, Asif M. MD; Ast, Michael MD; Schaffer, Alyssa A. MD; Thoder, Joseph MD

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Journal of the American Academy of Orthopaedic Surgeons: December 2007 - Volume 15 - Issue 12 - p 757-764
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de Quervain disease is a stenosing tenosynovitis of the first dorsal compartment of the wrist. It often presents with a gradual onset of pain that may be exacerbated by grasping, thumb abduction, and ulnar deviation of the wrist. The etiology is thought to be secondary to repetitive or sustained tension on the tendons of the first dorsal compartment. This tension produces a fibroblastic response, resulting in thickening and swelling of the compartment and discomfort with use of the hand and wrist.

Fritz de Quervain,1 a Swiss physician, is credited with describing the condition when he presented a case series in 1895. In 1930, Finkelstein2 presented 24 cases, provided a detailed review of the literature and results of animal studies, and described a physical examination test. Patterson3 first dubbed the condition de Quervain disease in 1936. Multiple names have been attributed to de Quervain disease, including stenosing tenosynovitis, stenosing tendinitis, peritendinitis, styloid tenovaginitis, and stenosing tendovaginitis (as used by de Quervain). These terms are misleading, however, because they imply merely inflammation of the tendon, whereas de Quervain disease represents an attritional and degenerative process of the compartment.4,5

No long-term epidemiologic study has been done of the prevalence of de Quervain disease, but it is known to be relatively common. Case series suggest that it affects women up to six times more often than men and is associated with the dominant hand during middle age.1–3,6–8 Historically, overexertion from household duties was the most common reported cause. Occupations requiring repetitive typing, lifting, and manipulation have been considered risk factors, as well. Ranney et al9 studied female workers in highly repetitive jobs and showed de Quervain disease to be the most prevalent tendon disorder of the wrist. Pregnant and lactating women represent an increasing cohort of patients with new-onset, self-limited de Quervain disease.10–13


Knowledge of the anatomy of the dorsal compartments of the wrist is central to understanding the pathophysiology of de Quervain disease. Many of the muscles that produce finger motion exist outside the hand (extrinsic muscles) and are opposed by muscles within the hand (intrinsic muscles). The extrinsic muscles exert their force by transmitting tension via tendons traveling through unyielding fibro-osseous tunnels on the radius. Six fibro-osseous tunnels representing the dorsal compartments on the distal radius surround the extensor tendons and function to prevent bowstringing of the extensor tendons. Each compartment is lined with a synovial sheath membrane.

The first dorsal compartment is approximately 2 cm long and is located over the radial styloid proximal to the radiocarpal joint. The abductor pollicis longus (APL) and the extensor pollicis brevis (EPB) tendons pass through this compartment (Figure 1). The APL originates on the distal third of the radius and has multiple slips (2 to 4), with variable insertions on the base of the thumb metacarpal and trapezium. The primary function of the APL is to abduct the thumb and assist with radial deviation of the wrist. The EPB originates on the dorsal surface of the radius and the interosseous membrane and inserts on the base of the proximal phalanx of the thumb. The EPB functions to extend the metacarpophalangeal joint and to weakly abduct the thumb.

Figure 1
Figure 1:
Anatomy of the first dorsal compartment demonstrating the insertion of the abductor pollicis longus (APL), extensor pollicis brevis (EPB), and extensor pollicis longus (EPL) tendons.


Stenosing tenosynovitis of the first dorsal compartment is caused by attritional forces secondary to friction; the attritional forces produce swelling and thickening of the extensor retinaculum covering the first dorsal compartment. The functional impairment is secondary to resisted gliding of the APL and the EPB within the narrowed fibro-osseous canal, resulting in pain and decreased motion.14

The histopathology of de Quervain disease generally does not involve inflammation but is related instead to thickening of the extensor tendons and surrounding extensor retinaculum. Clarke et al5 examined the microanatomic findings of the tendon sheaths and synovium of symptomatic patients; these authors found thickening of the tendon sheaths to be up to five times that of control subjects because of deposition of dense fibrous tissue, increased vascularity of the tendon sheaths, and accumulation of mucopolysaccharides, which are indicators of myxoid degeneration. Notably, the synovial linings were preserved and were histologically normal. The authors postulated that these changes, as opposed to the common histologic changes seen in chronic inflammation, may indicate that de Quervain disease is a result of an intrinsic degenerative mechanism rather than an inflammatory one, as is often described.5

Several theories exist regarding the cause of de Quervain disease. Possible etiologies include trauma, increased frictional forces, anatomic abnormality, biomechanical compression, repetitive microtrauma, inflammatory disease, and increased volume states, such as occurs during pregnancy.1–13,15,16 All of these processes have the ability to create the environment necessary to develop a stenosing tenosynovitis of the first dorsal compartment.

Several studies have identified anatomic variations of the first dorsal compartment.15–17 Variations include septation of the first dorsal compartment and the presence of multiple slips of the APL and, occasionally, of the EPB tendon. Bahm et al18 found division of the first dorsal compartment by an additional septum in 60% of patients with symptomatic de Quervain disease; the APL consisted of multiple tendons in 76%. In a cadaveric study, Shiraishi and Matsumura19 noted variation in the number of tendons, including up to seven slips of the APL and up to three of the EPB. Aktan et al20 examined the wrists of patients with de Quervain disease and found that the number of tendons present in the first compartment differed from the accepted standard in 82% of patients; 46% of the compartments were septated.

These anatomic variations may have an effect on the underlying pathophysiology of de Quervain tenosynovitis. Kutsumi et al14 examined 15 cadaveric wrists with and without septation of the first dorsal compartment and measured the gliding resistance of the APL and the EPB tendons in several wrist positions, including flexion, extension, abduction, and adduction. The authors found that the presence of septation and wrist position (eg, 30° of ulnar deviation, as in the Finkelstein test) affected the gliding resistance of the EPB tendon. These anatomic variations may predispose a patient to de Quervain disease. The patient with such a predisposition may respond poorly to nonsurgical treatment.


The clinical presentation of de Quervain tenosynovitis is fairly consistent. It most commonly presents with a gradual onset of pain localized along the radial side of the wrist, with an exacerbation of symptoms caused by grasping and raising objects with the wrist in neutral rotation. The differential diagnosis includes intersection syndrome, radial styloid fracture, scaphoid fracture, instability or basilar arthritis of the thumb, and radial neuritis.

Basilar arthritis of the thumb (arthritis of the trapeziometacarpal or scaphotrapezial joints) should be differentiated from de Quervain disease. Because of similar demographics, these two entities commonly coexist. Arthritic symptoms are elicited with palpation of the basal joint of the thumb and with painful axial compression and circumduction of the thumb. Intersection syndrome results from tendinopathy between the APL and common wrist extensor tendons. The patient presents with focal tenderness and crepitus 4 to 5 cm proximal to the wrist joint, centered dorsally over the second dorsal compartment. Although pain and crepitus are the most common presenting symptoms of intersection syndrome, some patients also report stiffness or neuralgia.

With de Quervain disease, the location of tenderness is more specific to the first extensor compartment over the radial styloid, with possible radiation of pain to the forearm and distally to the thumb. The patient also may report an increase in pain with repetitive motion of the thumb that is improved with rest or immobilization. In addition, uncommon but well-recognized presentations include extensor triggering or locking of the thumb as well as dorsal ganglion cyst formation.21–23

The Finkelstein test is the classic maneuver for diagnosis and is considered pathognomonic for de Quervain disease.2,24 It is performed by grasping the patient's thumb and quickly deviating the hand and wrist ulnarly. A positive test reproduces the pain. However, the examiner must be mindful that the patient may not be able to differentiate the pain of tenosynovitis focused at the radial styloid from that of basilar arthritis of the thumb.

An alternative to the Finkelstein test is the Eichoff maneuver. This test is performed by having the patient clench his or her thumb in a fist, followed by brisk deviation of the wrist ulnarly.24 The Eichoff maneuver has been confused with the Finkelstein test, which has led many to consider the Eichoff maneuver and Finkelstein test to be the same.25 Although sensitive, the specificity of the Finkelstein test may be called into question because of its propensity to provoke pain in asymptomatic patients and those with underlying arthritis.

Brunelli26 proposed a test involving strong abduction of the thumb with the wrist in radial deviation. The author proposed that his test was more effective than the Finkelstein test because it provoked tendon irritation of the first dorsal compartment against their pulleys.

Imaging Studies

de Quervain disease is diagnosed clinically; no imaging studies are required. Wrist imaging is required only in the presence of associated processes that may need to be evaluated, such as previous distal radius or scaphoid fracture, arthritis of the thumb, and instability of the wrist. Occasionally, radiographs may identify bony changes on the radial styloid, such as spurring or lesions that may directly irritate the first dorsal compartment.27 Several authors have recommended other imaging modalities, including magnetic resonance imaging, ultrasound, and bone scanning, and have demonstrated findings that may support the diagnosis of de Quervain disease.28–31 However, routine use of radiographs and advanced imaging is not required when the presentation is clear.



Nonsurgical treatment should be the first course of action for de Quervain disease. The patient presenting with mild to moderate pain that does not limit activities of daily living should be treated with rest, splinting, nonsteroidal anti-inflammatory drugs (NSAIDs) and/or corticosteroid injection of the first dorsal compartment. Splinting is an effective method for resting the APL and EPB tendons by immobilizing the thumb and wrist in a single position and reducing or preventing the friction that may exacerbate swelling and pain. Custom or prefabricated splints should be forearm-based; one such splint is a radial thumb spica extension that holds the wrist in neutral and the thumb in 30° of flexion and 30° of abduction. Although symptoms may improve with splinting, on removal of the splint, symptoms quickly return in some patients when the inciting activity is resumed.27

Corticosteroid injection into the first dorsal compartment is perhaps the most common and effective treatment of de Quervain disease. Many patients experience complete relief of symptoms with a single corticosteroid injection.7,8,32 Richie and Briner33 performed a pooled quantitative literature evaluation to determine the reported cure rate of corticosteroid injection for de Quervain disease; they reported that 83% of patients had complete relief with injection alone. Failure of response to corticosteroid injection has been attributed to poor technique and anatomic variations within the first dorsal compartment.

In their series of 63 patients, Harvey et al7 found that 82% had relief of pain after one or two corticosteroid injections. Of the 11 patients who did not have complete pain relief and went on to surgery, 10 had a separate compartment for the EPB. Zingas et al34 studied injection accuracy and found that the needle was accurately placed into the first dorsal compartment in 84% of patients. However, the EPB tunnel was missed in 68% of patients, either because it was too small or was in a separate compartment, thus compromising the overall outcome. Similarly, Witt et al35 found that 79% of patients who were resistant to corticosteroid injection had a separate compartment for the EPB tendon at the time of surgery.

Corticosteroid injection for de Quervain disease consists of 1 mL of corticosteroid with 0.5 to 1 mL of a local anesthetic. Success has been reported with a variety of corticosteroids (eg, betamethasone, triamcinolone, dexamethasone, methylprednisolone) combined with any of several local anesthetics (eg, bupivacaine, lidocaine).7,8,13,34–36 We prefer a water-soluble preparation; insoluble preparations have been associated with more local complications.37 As such, we administer 5 mg of dexamethasone and 1 mL of 1% lidocaine.

With the wrist in neutral radioulnar deviation, a rolled-up towel is placed under the wrist to position it in slight ulnar deviation (Figure 2). The injection site is prepped sterile. The course of the APL and EPB tendons along the radial styloid is palpated, and the borders of the first dorsal compartment are straddled with the examiner's opposite thumb and index finger. A 25-gauge needle is introduced into the tendon sheath at the level of the styloid, parallel to the tendons. Resistance indicates that the needle is likely in the tendon. The needle is carefully backed out while maintaining pressure on the plunger of the syringe. The injectable medication should flow smoothly and easily, with both visual and palpable inflation of the compartment.

Figure 2
Figure 2:
Injection of the first dorsal compartment with the wrist in neutral rotation and gentle ulnar deviation over a rolled-up towel. A 25-gauge needle is introduced into the tendon sheath at the level of the radial styloid and parallel to the tendons. The medication should flow smoothly and should both visually and palpably inflate the compartment.

Before injection, the patient must be informed that subdermal atrophy and hypopigmentation may occur at the injection site, particularly in the darker-skinned patient. Avoid injecting directly into the tendon. This carries the risk of weakening the tendon and causing tendon rupture. Adverse reactions to corticosteroid injection are generally minor and self-limited; they include pain, neuritis, fat necrosis, and postinjection flare.33,36–38 Additionally, local infection and tendon rupture, although unusual, may occur.

Richie and Briner33 performed a quantitative literature evaluation of studies of comparative treatment modalities for de Quervain disease. Of the 495 wrists studied, there was an 83% success rate for corticosteroid injection alone. Surprisingly, the success rate with injection and splinting together was just 61%. Splinting alone had a success rate of 14%. NSAIDs and rest yielded a 0% success rate. The efficacy of NSAIDs has been studied further; they were found to provide no benefit when used to supplement corticosteroid injection.38

Our initial preferred treatment is corticosteroid injection with dexamethasone and lidocaine. Subsequently, tendon gliding and stretching exercises are taught. We also prescribe a forearm-based thumb spica splint in the patient with persistent or severe symptoms. An additional injection may be offered after a 4- to 8-week interval for the patient who has experienced some improvement with the initial injection but who continues to report discomfort. When pain does not resolve after two corticosteroid injections and 6 months of nonsurgical management, and when other pathologies have been ruled out, then surgical release of the first dorsal compartment is recommended.


Surgical treatment is based on release of the fibro-osseous roof of the first dorsal compartment and decompressing the stenosed APL and EPB tendons. Fundamental to surgical intervention is protection of the radial sensory nerve and complete decompression of the first dorsal compartment, including release of additional tendinous slips and compartments. In several series, the reported incidence of separate compartments at surgery is higher than that seen in anatomic specimens.7,8,35,39 In particular, the potential for septation of the EPB compartment increases the chance that nonsurgical treatment will fail; surgical decompression may be compromised if the condition is not identified.7,34,35 Surgical treatment should be approached with the mindset that anatomic variations of the compartment are the rule rather than the exception. Injury to the radial sensory nerve and failure to recognize variations in the first dorsal compartment may result in continued pain and treatment failure.39–41

Our preferred technique is to perform the surgery under local anesthesia, with or without intravenous sedation, and tourniquet control. Although multiple incisions (eg, transverse, longitudinal, oblique) may be used to provide excellent exposure of the first dorsal compartment, we employ a chevron-style incision because we believe it aids in visualization of the radial sensory nerve, avoids tendon injury, and enhances wound healing (Figure 3, A). Once the skin incision is made, blunt dissection is used to identify and protect the radial sensory nerve. Sharp dissection with a scalpel through the subcutaneous tissue may injure branches of the nerve and should be avoided. One to three branches of the radial sensory nerve are identified and protected with blunt retractors (Figure 3, B).

Figure 3
Figure 3:
Surgical treatment of de Quervain disease. A, Oblique incision centered over the radial styloid. B, The skin is retracted. Careful blunt dissection will reveal branches of the radial sensory nerve in the subcutaneous tissue. C, The first dorsal compartment is released along its dorsal border, revealing the abductor pollicis longus (APL) and extensor pollicis brevis (EPB) tendons.

Dissection is then carried down to the first dorsal compartment. The retinaculum of the first dorsal compartment is completely incised with a scalpel in line with the APL and EPB tendons. Burton and Littler42 recommend releasing the sheath along its dorsal margin, thus leaving the volar flap intact to prevent subluxation of the tendons (Figure 3, C). The tendons are examined, and the compartment is diligently explored. The APL tendon is larger and is routinely composed of two or more distinct tendons. The EPB tendon is smaller, dorsal, and often lies in a separate compartment.7,34,35

Although complete excision of the extensor sheath is avoided, any intra-compartmental septae should be released and excised. Tendons may be carefully tensioned using atraumatic technique to simulate their function, aid in their identification, and confirm decompression. Active and free thumb abduction and extension then can be performed on the awake patient. Next, any loose tenosynovial tissue on the tendon is débrided. After confirming that the compartment is completely released, the tourniquet is released, and hemostasis is achieved.

We do not approximate the edges of the released extensor retinaculum. Step-cut lengthening is rarely required; we do not recommend a step-cut release with repair of the retinaculum. The skin incision is closed using single interrupted 4-0 nylon sutures. Postoperatively, a plaster thumb spica splint is applied to aid in pain control and wound healing. The splint and sutures are removed 10 to 14 days postoperatively, and the patient is allowed to resume normal activities as tolerated. Physical and occupational therapy is not routinely instituted unless specific patient circumstances indicate it.

Outcomes from surgical release of de Quervain disease have been uniformly excellent. The “cure rate,” as described by several investigators, represents resolution of symptoms without complications and has been reported to be ≥91%.2,43–46 Although most series have been unable to identify risk factors for long-term complications or patient satisfaction after surgical treatment, Ta et al44 found a positive correlation between duration of preoperative symptoms and postoperative satisfaction. Patients with preoperative symptoms lasting 9 months or longer were much more satisfied with their surgery than were patients who had been symptomatic for a much shorter period.


Corticosteroid injection has been associated with fat necrosis, subcutaneous atrophy, and skin depigmentation. 36,37,39,40 The patient should be counseled about the 5% to 10% risk of these complications.27

Other complications after surgery include radial sensory nerve injury, incomplete decompression, and volar subluxation of the tendons. 2,7,8,40,44,45,47,48 Injury to the radial sensory nerve may present with a spectrum of injury, from complete transection to neuroma in continuity to neurapraxia from overzealous retraction. Management of a lacerated radial sensory nerve is controversial; options vary from resection of the lacerated edge more proximally to primary repair using microsurgical techniques. Radial sensory nerve injury is a complication best avoided with careful surgical technique.

Persistent pain from inadequate decompression often represents failure to recognize and release an additional compartment, most commonly that of the EPB; reexploration is usually warranted. Volar subluxation of the APL and EPB tendons is an uncommon complication; it is often associated with a volar rather than dorsal release of the first dorsal compartment, or it may result from complete excision of the retinaculum. Reconstruction of the compartment with a slip of extensor retinaculum is effective in managing the subluxation.48,49

Additional reported complications include scar hypertrophy or tenderness, particularly with longitudinal incisions,47 reflex sympathetic dystrophy, and continued pain as a result of incorrect diagnosis. Associated missed diagnoses include basilar arthritis of the thumb, instability of the thumb, intersection syndrome, and radial neuritis. Wartenburg's syndrome (ie, superficial radial neuritis) has been shown to compromise the surgical outcome from de Quervain disease. Some patients require proximal neurolysis and repositioning of the nerve deep in the forearm to avoid painful neuropathy.50


de Quervain disease is a commonly encountered wrist pathology involving thickening of the first dorsal compartment of the wrist. Pain occurs during wrist and thumb motion from resisted gliding of the APL and EPB tendons in the narrowed fibroosseus canal. This condition is more common in women than in men. The diagnosis is clinical and is most closely correlated with a positive Finkelstein test or Eichoff maneuver. Radiographs may be indicated to rule out other wrist pathologies; however, they generally are not recommended in the evaluation of classically presented de Quervain disease. Nonsurgical management is the mainstay of treatment, consisting of rest, thumb spica splinting, and corticosteroid injection. When nonsurgical management fails to provide sustained relief, open surgical release of the first dorsal compartment, with identification of accessory compartments and protection of the radial sensory nerve, may be performed with excellent results.


Evidence-based Medicine: There are several level I (references 13, 34-36, and 38), level II (references 7, 8, 32, 44, and 45), level III (references 1-4, 6, 9, 11, 12, 23, 28-31, 40, 43, 46, 47, and 50), level IV (references 10, 21, 22, 41, and 48), and level V (references 25, 27, and 49) studies cited. The remaining references are anatomic, biomechanical, and meta-analysis studies, and review papers.

Citation numbers printed in bold type indicate references published within the past 5 years.

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33. Richie CA III, Briner WW Jr: Corticosteroid injection for treatment of de Quervain's tenosynovitis: A pooled quantitative literature evaluation. J Am Board Fam Pract 2003;16:102-106.
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38. Jirarattanaphochai K, Saengnipanthkul S, Vipulakorn K, Jianmongkol S, Chatuparisute P, Jung S: Treatment of de Quervain disease with triamcinolone injection with or without nimesulide: A randomized, double-blind, placebo-controlled trial. J Bone Joint Surg Am 2004;86:2700-2706.
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45. Zarin M, Ahmad I: Surgical treatment of de Quervain's disease. J Coll Physicians Surg Pak 2003;13:157-158.
46. Gundes H, Tosun B: Longitudinal incision in surgical release of De Quervain disease. Tech Hand Up Extrem Surg 2005;9:149-152.
47. Mellor SJ, Ferris BD: Complications of a simple procedure: de Quervain's disease revisited. Int J Clin Pract 2000; 54:76-77.
48. White GM, Weiland AJ: Symptomatic palmar tendon subluxation after surgical release for de Quervain's disease: A case report. J Hand Surg [Am] 1984;9:704-706.
49. McMahon M, Craig SM, Posner MA: Tendon subluxation after de Quervain's release: Treatment by brachioradialis tendon flap. J Hand Surg [Am] 1991;16:30-32.
50. Lanzetta M, Foucher G: Association of Wartenberg's syndrome and De Quervain's disease: A series of 26 cases. Plast Reconstr Surg 1995;96:408-412.
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