The causes of persistent wrist pain following carpal tunnel release include scar tenderness and pillar pain. The goal of this study was to evaluate latent pisotriquetral arthrosis as a source of ulnar-sided wrist pain following open carpal tunnel release.
Seven hundred consecutive carpal tunnel releases were reviewed, looking for postoperative presentation of pisotriquetral arthrosis, as well as management and outcome. Fourteen patients with long-standing postoperative pain at the base of the hypothenar eminence had clinical and radiographic signs of pisotriquetral degenerative arthrosis, which conceivably had existed preoperatively and been unmasked thereafter. In 6 patients with persistent symptoms despite conservative measures, excision of pisiform was curative. Altered isometric stresses over the pisotriquetral articulation as a result of releasing the transverse ligament, which constitutes a major radial static stabilizer of this joint, seems to cause articular maltracking, and consequently aggravates a preexisting asymptomatic pisotriquetral arthrosis. Long-standing discomfort is characteristically associated with loss of grip strength and dexterity.
Pisotriquetral dysfunction and arthrosis should always be considered in the differential diagnosis of persistent wrist pain following either open or endoscopic carpal tunnel release that does not respond to nonoperative measures. Clinical scrutiny, adequate clinical inspection, and radiographic evaluation readily establish the diagnosis. Conservative treatment includes immobilization, nonsteroidal anti-inflammatory drugs, and intra-articular injection of corticosteroids under fluoroscopic control. The corticosteroid injection combined with a local anesthetic also serves as a diagnostic test. Excision of the pisiform is indicated where conservative treatment has failed.
Scar tenderness and pillar pain are common, well-known complications in the recovery phase following open carpal tunnel release that delay hand use and return to work.1-5 The former is often attributed to intraoperative severance of cutaneous branches of the median nerve, while the latter is defined as pain and tenderness on both sides of the incisional scar and is usually ascribed to an inflammatory reaction at the prominences of the trapezial ridge and the hook of the hamatum where the divided transverse ligament attaches.
Few patients localize the tenderness to the base of the hypothenar area. A plausible explanation for this distinct postoperative pain is the altered isometric stresses over the pisotriquetral articulation as a result of releasing the transverse ligament, which constitutes a major radial static stabilizer of this joint,5 causing articular maltracking and occasionally setting off a consequent degenerative process or aggravating a preexisting asymptomatic pisotriquetral arthrosis. In the majority of patients, this discomfort resolves gradually within few weeks. Long-standing discomfort is characteristically associated with loss of grip strength and dexterity, and may ultimately end as an established pisotriquetral arthrosis.
Materials and Methods
Between 1994 to 2004, 700 consecutive patients underwent open carpal tunnel release. Two hundred thirty-eight patients (34%) were men and 462 (66%) were women. Average patient age was 50 years (range, 25-82 years). The medical charts of the patients were reviewed. Age at presentation, sex, presenting symptoms and signs, modality of treatment, surgical outcome, and postoperative residual and persistent complaints were recorded, looking particularly for patients reporting ulnar-sided postoperative pain.
Carpal tunnel release was performed through a slightly ulnarward interthenar incision. A protective splint was applied postoperatively for 7 days, and an exercise program was initiated thereafter.
At 6-week follow-up, 57 patients reported pain on either or both sides of the incisional scar. At 6-month follow-up, 14 patients (9 women and 5 men) with an average age of 48 years (range, 42-69 years) had persistent pain and discomfort localized to the base of the hypothenar area on use of the hand, which was exacerbated when applying a full hand grip or during activities such as pushing up from a chair or pushing objects with a flat palm. Ten were right-handed, and 4 were left-handed, and in 12 patients the involved hand was their dominant one. None of the 14 patients had preoperative clinical signs of pisotriquetral dysfunction. Five reported an antecedent wrist trauma. Ten were able to localize the pain directly at the pisiform, while 4 described poorly localized pain. Seven patients subjectively described their pain as mild, 5 as moderate, and 2 as severe (quantifying the pain upon the visual analog pain scale as 1-3, 4-7, and 8-10, respectively).
Clinical examination revealed a well-localized tenderness to direct pressure over the pisiform, evinced by opposed flexion and ulnar deviation of the wrist, and side-to-side passive motion of the pisiform about its articulation with the triquetrium (grinding test). Crepitus was elicited while performing this maneuver.
None of these 10 patients showed any clinical signs of an ulnar nerve lesion, distal ulnar impingement, ulnar styloid nonunion, tear of the triangular fibrocartilage, injury to the ulnar carpal collateral ligament, or synovitis of the flexor carpi ulnaris or extensor carpi ulnaris tendons. Radiographic examination of the pisotriquetral articulation in all 14 patients showed joint incongruity, diminished joint space, and spur formation (Figures 1-3).
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|Figure 1: Radiograph of a left wrist showing degenerative changes at the pisotriquetral joint in a patient with local tenderness following carpal tunnel release. Note the narrow joint space and subchondral sclerosis of the pisiform articular surface with osteophyte formation (proximal pole). Figure 2: Sagittal CT reconstruction of the wrist showing an incongruent pisotriquetral joint with marginal spur and subchondral bone cyst formation. Figure 3: Technetium-99m planar bone scan performed as a part of the workup of persistent left wrist pain following carpal tunnel release. Note the bilateral focally increased uptake at the pisotriquetral joint. The scintigraphic finding at the right wrist was subclinical, while being unmasked at the left wrist following the release of the transverse carpal ligament. |
Initial conservative treatment included immobilization, nonsteroidal anti-inflammatory drugs (NSAIDs), and intra-articular injection of corticosteroids under fluoroscopic control. The corticosteroid injection combined with a local anesthetic served also as a diagnostic test: pain was temporarily relieved and thus proved to originate from the pisotriquetral joint. Eight patients had complete but temporary relief of symptoms after corticosteroid instillation. Five experienced partial and temporary resolution of pain, and therefore received a second injection. One had a partial relief for few hours.
In 5 patients, complete resolution of symptoms was achieved following conservative treatment, while the remaining 9 patients who reported a temporary relief were offered excision of the pisiform 1 to 3.5 years after carpal tunnel release. Three of them declined surgery despite persistent symptoms.
The 6 patients who underwent excision of pisiform were followed for 8 to 24 months. All 6 experienced uniformly good clinical results with complete pain relief without loss of dexterity, range of motion (ROM), or dysfunction of the flexor carpi ulnaris tendon. Five patients returned to work within 8 weeks. One patient had some residual local discomfort, which resolved 1 year later. No complications were noted.
All 6 cases had varying degrees of chondromalacia of the pisiform and marginal osteophytes (Figure 4). Five patients had chondromalacia of the triquetral articular surface. Erosive changes were more accentuated on the ulnar peripheral rim of the pisiform articular surface.
|Figure 4: Macroscopic arthritic changes in an excised pisiform, including chondromalacia and peripheral erosions. |
Surgical Technique for Excision of Pisiform
A skin incision was placed through the interthenar former scar, extended and curved toward the hypothenar eminence and proximal to wrist crease. The ulnar neurovascular bundle was identified, retracted gently radialward, and protected. The pisohamate ligament was divided. Formal neurolysis was not performed. The pisiform was enucleated through a midline incision along the flexor carpi ulnaris tendon, and shelling out the bone subperiosteally in a radial to ulnar direction. The tendon was repaired and the skin sutured. The wrist was splinted for 7 days, and protected ROM was encouraged thereafter.
The pisiform is the only carpal bone to have a tendon insertion from a forearm muscle.6 It is completely covered by the abductor digiti minimi and the tendonous insertion of the flexor carpi ulnaris. The transverse carpal ligament, which acts as a stabilizer of the carpal arch,7 attaches to its radial aspect, the extensor retinaculum to its ulnar side, and the pisohamate and pisometacarpal ligaments to its distal aspect.6 The pisiform articulates with the triquetrum on an ovoid, flat surface,8 and therefore lacks inherent articular stability.
The pisiform ligament complex is a group of ligaments attached to the pisiform that contribute to its stability in different planes9 and regulates pisiform tracking (Figure 5).
|Figure 5: Illustration of the pisotriquetral complex. Abbreviations: FCU, flexor carpi ulnaris; P, pisiform; PHL, pisohamate ligament; PML, pisometacarpal ligament; TCL, transverse carpal ligament (providing radial anchor point to the pisotriquetral joint). |
Stability is also maintained by the delicate balance between dynamic ulnarly directed forces applied by the flexor carpi ulnaris and the abductor digiti quitni muscles5 and the radial pisotransverse carpal ligament tension.
In a radiographic study, Vasilas et al10 described the tracking of the pisiform and found a proximal overriding of the pisiform on the triquetrum of 5% to 10% in neutral and 10% to 90% in full flexion, and a distal overriding of 0% to 50% in extension. They also described parallelism of the articular surfaces between the pisiform and the triquetrum.
Division of the transverse carpal ligament has been shown to allow up to 20% displacement of the ends of the carpal arch5 and may induce ulnar translation of the pisiform accompanied by ulnar tilt of the articular surface of the pisiform, resulting in pisotriquetral instability and maltracking. The manifestation of this kinematic derangement ranges from discomfort and pain at the base of the hypothenar eminence and clicking sensation, through chondromalacia and established degenerative arthrosis with completely exposed subchondral bone.
Carroll and Coyle11 reported on 3 patients with pisotriquetral dysfunction following release of the carpal tunnel. Seradge and Seradge5 reported on 5 patients with pisotriquetral pain syndrome after carpal tunnel release. Excision of the pisiform was curative.
Rayan et al9 classified the radiographic instability of the pisotriquetral joint into mild without findings, moderate with altered normal parameters, and severe manifested as dislocation.
Although an uncommon cause of ulnar wrist pain, pisotriquetral degenerative arthrosis is probably underdiagnosed, as the symptoms are not distinctive and the signs are not unique for this entity, but rather overlap with those of other causes for ulnar-sided wrist pain. Pain caused by pisotriquetral arthrosis is often vaguely localized to the base of the hypothenar eminence and is aggravated by contraction of flexor carpi ulnaris.12 Palpation reveals joint tenderness and painful crepitus aggravated by grinding the pisiform with side-to-side movements or dorsally against the triquetrum.13
As routine radiographic views usually fail to reveal the pisotriquetral joint, various radiographic studies have been suggested for satisfactory visualization of this joint. Adequate demonstration of the joint can be attained by acquisition of anteroposterior and oblique views as proposed by Jameson et al,14 by positioning the forearm in 30° of supination from neutral for neutral and wrist extension and in 45° of supination for wrist flexion. Both computed tomography (CT) and scintigraphy are helpful in questionable cases. While CT can better define and characterize the bony geometry and degenerative articular changes, technetium-99m bone scan may point toward the arthritic location.
Relief of symptoms following injection of a local anesthetic agent into the pisotriquetral joint space, preferably under fluoroscopic control, assists in substantiating the diagnosis.
Primary osteoarthritis is the main cause of pisotriquetral joint osteoarthritis,15,16 which usually affects patients older than 50 years, especially women.8 Secondary osteoarthritis is usually a sequela of a misdiagnosed fracture of the pisiform or triquetrum or subluxation of the pisiform bone. Pisotriquetral complex failure may lead to pisiform bone dislocation or instability, as well as to secondary osteoarthritis.14,17 Pisotriquetral arthrosis secondary to ligamentous disruption, including incision of transverse carpal ligament, may be by kindling a de novo process, aggravation of a preexisting degenerative state, or unmasking a previously asymptomatic arthrosis.
Nonoperative management of pisotriquetral arthrosis includes NSAIDs, resting splints, and local corticosteroid instillation. Operative management for persistent cases entails excision of the pisiform, occasionally coupled with decompression of Guyons canal.
In the current study, only 5 patients benefited completely from nonoperative management, while excision of the pisiform was curative in all 6 operated hands.
Yamaguchi et al6 characterized the degenerative changes observed at the pisotriquetral joint and classified their location into 5 types: type 1, central; type 2, peripheral; type 3, fan shaped; type 4, mixed; and type 5, total. The location was also noted as distal, proximal, radial, or ulnar. Degenerative changes were most commonly of a type 2 pattern (peripheral), with change located most commonly in the distal, distal-radial, and radial aspects. In our study, the erosive changes were more accentuated on the ulnar peripheral rim of the pisiform articular surface. This may be attributed to the compressive forces applied through the ulnar rim of the pisiform upon its reciprocal surface of the triquetrum, due to probable ulnarward tilt of the pisiform articular facet resulting from the loss of the radialward directed tethering.
Pisotriquetral dysfunction and arthrosis should always be considered in the differential diagnosis of persistent wrist pain following either open or endoscopic carpal tunnel release that does not respond to nonoperative measurements. Clinical scrutiny, adequate clinical inspection, and radiographic evaluation readily establish the diagnosis. Excision of the pisiform is indicated where conservative treatment has failed.
- Cseuz KA, Thomas JE, Lambert EH, Love JG, Lipscomb PR. Long-term results of operation for carpal tunnel syndrome. Mayo Clin Proc. 1966; 41(4):232-241.
- Kulick MI, Gordillo G, Javidi T, Kilgore ES Jr, Newmayer WL III. Long-term analysis of patients having surgical treatment for carpal tunnel syndrome. J Hand Surg Am. 1986; 11(1):59-66.
- Kuschner SH, Brien WW, Johnson D, Gellman H. Complications associated with carpal tunnel release. Orthop Rev. 1991; 20(4):346-352.
- MacDonald RI, Lichtman DM, Hanlon JJ, Wilson JN. Complications of surgical release for carpal tunnel syndrome. J Hand Surg Am. 1978; 3(1):70-76.
- Seradge H, Seradge E. Piso-triquetral pain syndrome after carpal tunnel release. J Hand Surg Am. 1989; 14(5):858-862.
- Yamaguchi S, Viegas SF, Patterson RM. Anatomic study of the pisotriquetral joint: ligament anatomy and cartilagenous change. J Hand Surg Am. 1998; 23(4):600-606.
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- Blum AG, Zabel JP, Kohlmann R, et al. Pathologic conditions of the hypothenar eminence: evaluation with multidetector CT and MR imaging. Radiographics. 2006; 26(4):1021-1044.
- Rayan GM, Jameson BH, Chung KW. The pisotriquetral joint: anatomic, biomechanical, and radiographic analysis. J Hand Surg Am. 2005; 30(3):596-602.
- Vasilas A, Grieco RV, Bartone NF. Roentgen aspects of injuries to the pisiform bone and pisotriquetral joint. J Bone Joint Surg Am. 1960; 42 (8):1317-1328.
- Carroll RE, Coyle MP Jr. Dysfunction of the pisotriquetral joint: treatment by excision of the pisiform. J Hand Surg Am. 1985; 10(5):703-707.
- Green DP. Pisotriquetral arthritis: a case report. J Hand Surg Am. 1979; 4(5):465-467.
- Johnston GH, Tonkin MA. Excision of pisiform in pisotriquetral arthritis. Clin Orthop Relat Res. 1986; (210):137-142.
- Jameson BH, Rayan GM, Acker RE. Radiographic analysis of pisotriquetral joint and pisiform motion. J Hand Surg Am. 2002; 27(5):863-869.
- Paley D, McMurtry RY, Cruickshank B. Pathologic conditions of the pisiform and pisotriquetral joint. J Hand Surg Am. 1987; 12(1):110-119.
- Lam KS, Woodbridge S, Burke FD. Wrist function after excision of the pisiform. J Hand Surg Br. 2003; 28(1):69-72.
- Moojen TM, Snel JG, Ritt MJ, Venema HW, den Heeten GJ, Bos KE. Pisiform kinematics in vivo. J Hand Surg Am. 2001; 26(5):901-907.
Drs Stahl (Shalom), Stahl (Shy), and Calif are from the Department of Hand Surgery, Rambam Medical Center, Haifa, Israel.
Drs Stahl (Shalom), Stahl (Shy), and Calif have no relevant financial relationships to disclose.
Correspondence should be addressed to: Edward Calif, MD, Department of Hand Surgery, Rambam Medical Center, PO Box 9602, Haifa 31096, Israel (email@example.com).