Introduction

The concept of midcarpal instability (MCI) has evolved slowly since it was first described in 1934. Many investigators have contributed to our understanding of this condition over the years, which led to the consolidated classification by the senior author (DML) (Table 14.1).¹ It appears that MCI represents several distinct clinical entities differing in the cause and direction of subluxation but sharing the common characteristic of abnormal force transmission at the midcarpal joint. The following discussion centers on intrinsic MCI. Extrinsic MCI due to a dorsally mal-united distal radius fracture is treated by a distal radius osteotomy and hence falls outside the scope of this discussion.

Table 14.1 Classification of Midcarpal Instability

Pathomechanics

The mechanism of the clunk in palmar midcarpal instability (PMCI) has been described in detail by Lichtman et al.² The palmar arcuate ligament complex is comprised of a radial arm that is confluent with and distal to the radioscaphocapitate (RSC) ligament and an ulnar arm or the triquetrohamate-capitate ligament (TCL) (Figure 14.1). In the normal situation, the proximal carpal row moves smoothly from a flexed position when the wrist is in radial deviation to extension when the wrist is in ulnar deviation. This is due to the progressive tightening effect of the arcuate ligament as it stretches out to length (which incrementally pulls the midcarpal row into extension) and to the carpal bone geometry, which causes the triquetrum to translate dorsally along the helicoidal facet of the hamate. When the arcuate ligament is attenuated, this synchronous motion is lost.

FIGURE 14.1 (A) Line drawing of the volar ligaments. (B) Line drawing of the dorsal ligaments. Ligaments: TCL, triquetrohamate-capitate ligament; RSC, radioscaphoid ligament; LRL, long radiolunate ligament; SRL, short radiolunate ligament; UL, ulnolunate ligament; UC, ulnocapitate ligament; UT, ulnotriquetral ligament; SC, scaphocapitate ligament; STT, scaphotrapezial trapezoidal ligament; TH, triquetrohamate ligament; IC, intercarpal ligament Bones: R, radium; U, ulna; S, scaphoid; L, lunate; C, capitate; T, triquetrum;H, hamate; P, pisiform; Tm, trapezium; Td, trapezoid.

Studies by Trumble et al.³ and Viegas and coauthors⁴ have shown that sectioning either the TCL or the dorsal radiocarpal (i.e., dorsal radiotriquetral ligament) can produce a volar intercalated segmental instability (VISI) deformity and simulate PMCI. More recently, Lichtman showed in vivo that tightening the DRCL alone can stabilize the proximal carpal row and eliminate the clunk of PMCI—emphasizing the potential importance of dorsal ligament laxity in the pathogenesis of this disorder.⁵ The senior author now believes that PMCI is caused by laxity of both the TCL and the DRCL, which allows an excessive palmar sag of the heads of the capitate and hamate at the midcarpal joint. This produces a VISI pattern of the proximal row in the nonstressed wrist. This sag results in a loss of joint contact across the midcarpal joint, which manifests clinically as a loss of the smooth transition of the proximal row from flexion to extension as the wrist deviates ulnarward.

The proximal carpal row thus stays in a flexed position until the terminal extent of ulnar deviation, when the helicoidal shape of the hamate facet suddenly forces the triquetrum dorsally. This snaps the lunate and subsequently the scaphoid into extension, causing a sudden reversal of the VISI. This sudden proximal row extension is responsible for the painful and rapid catch-up clunk that occurs. As the wrist moves back to neutral, the triquetrum translates down the hamate facet—which allows the proximal row to drop back into VISI while the distal row again settles palmarly into its slightly subluxated starting point (Figure 14.2a and b).

FIGURE 14.2 Dorsal exposure of the midcarpal joint in a left wrist. (A) Triquetrohamate joint with the proximal row reduced. (B) Subluxed triquetrohamate joint with volar sag of the proximal row (T = triquetrum, H = hamate).

The dorsal pattern of MCI has not been studied as extensively. It appears that laxity of the radial arm of the palmar arcuate ligament permits the capitate and hamate to translate dorsally to an excessive degree, especially with ulnar deviation of the wrist.^6,7 It is of note that in both the palmar and dorsal patterns the proximal row always moves into extension and the distal row translates dorsally with ulnar deviation. It is the timing and force of this movement that differentiate the two patterns.

In PMCI, the distal carpal row starts out in palmar subluxation with the wrist in neutral. As the wrist moves into ulnar deviation, the subluxation suddenly corrects. In dorsal MCI, the wrist starts out in a reduced position in neutral. Dorsal subluxation of the distal row then occurs with ulnar deviation. In either case, the instability is caused primarily by laxity of the selected extrinsic carpal ligaments that support the proximal row—which prevents them from controlling the complex kinematic relationships between the articular surfaces across the midcarpal joint.

Diagnosis

Clinical Findings

In PMCI the patient presents with a history of clunking of the wrist. Patients can often reproduce the clunk on both sides because generalized ligamentous laxity frequently coexists. However, the patient may have a trivial injury that accentuates this normal laxity—resulting in a painful clunk. Upon physical examination, close inspection will reveal a sag of the midcarpal joint with the wrist in radial deviation—which is reduced with active or passive ulnar deviation (Figure 14.3a and b). The clunk may be reproduced by performing the midcarpal shift test.² This test is performed by placing the patient’s wrist in neutral with the forearm in pronation. A palmar force is then applied to the hand at the level of the distal capitate. The wrist is simultaneously loaded and deviated ulnarly. The test result is positive if a painful clunk occurs that reproduces the patient’s symptoms.

FIGURE 14.3 Palmer MCI. (A) Note the sag in the midcarpal joint with the wrist in radial deviation. (B) The carpus is reduced in ulnar deviation and the sag disappears.

In dorsal MCI, a history of an extension injury may be present. Patients complain of post-traumatic chronic pain, weakness, and wrist clicking. Tight grasping (especially in supination) aggravates the symptoms. A dorsal capitate displacement test is performed by applying dorsal pressure to the scaphoid tuberosity while longitudinal traction and flexion are applied to the wrist. There is an associated painful click as the lunate is abruptly shifted dorsally and ulnarly.

Imaging

Static X-rays are typically normal, but occasionally reveal a mild VISI pattern with the wrist in the neutral position. Arthrograms are normal, unless there are associated intracarpal or triangular fibrocartilage (TFC) tears. MRI findings are nonspecific. Videofluoroscopy provides the hallmarks for diagnosis of this condition. With normal wrist kinematics, the proximal carpal row rotates synchronously from flexion to extension as ulnar deviation of the wrist is achieved. With PMCI, the proximal row maintains a volar flexed position until terminal ulnar deviation is reached—at which point it suddenly snaps into extension.

In dynamic dorsal MCI, X-rays are usually normal. In chronic cases, X-rays often show a volar intercalated segmental instability (VISI) pattern (Figure 14.4a and b). The capitolunate displacement test shows dorsal subluxation of the proximal carpal row in addition to dorsal subluxation of the capitate from the lunate (Figure 14.5a and b).⁸ This led Louis and colleagues to coin the term capitolunate instability pattern (CLIP) wrist.⁹

FIGURE 14.4 Volar intercalated segmental instability. (A) Lateral X-ray demonstrating volar tilting of the lunate and extension of the scaphoid. (B) Same view with the lunate and scaphoid outlined for clarity.

FIGURE 14.5 Capitolunate displacement test. (A) Lateral X-ray demonstrating dorsal subluxation of the capitate on the lunate. (B) Same view with the lunate and capitate outlined for clarity.

Nonoperative Treatment

Nonsurgical treatment consists of activity modification, NSAIDs, and splinting.¹¹ Various pisiform support splints have been described. They work based on the observation that applying dorsally directed pressure under the pisiform reduces the carpal sag along with the VISI position of the carpal row. Applying this principle, a three-point dynamic splint may maintain the reduction while permitting wrist motion in milder cases (Figure 14.6). The splint may be worn full time for six to eight weeks to reduce the midcarpal synovitis, and then be worn as needed.

FIGURE 14.6 Three-point fixation with a dynamic splint.

The senior author has observed that active co-contraction of the extensor carpi ulnaris, flexor carpi ulnaris, and hypothenar muscles can reduce the sagging of the midcarpal joint. In fact, some patients can eliminate the catch-up clunk by contracting these muscles before ulnar deviation of the wrist. Patients are taught this isometric muscle contraction as part of the therapy program. Definitive treatment of this condition, however, ultimately requires surgical treatment.

Surgical Treatment

Initial efforts by the senior author were directed at soft-tissue reconstruction by rerouting of the extensor carpi ulnaris to stabilize the triquetrohamate joint.² The long-term results were disappointing. This evolved to a direct advancement and tightening of the arcuate ligament complex. Reefing of the DRCL is now preferred. This was based on the observation that temporarily reefing the DRCL by plicating it with a clamp significantly reduced the clunking during the midcarpal shift test. In severe cases, midcarpal arthrodesis is still preferred over soft-tissue procedures (Figure 14.7a and b).^12–14

FIGURE 14.7 (A) AP X-ray following a capitolunate fusion. (B) Lateral X-ray of the same patient.

Dorsal Reefing of the DRCL (DML)

The patient is positioned in the supine position, with the arm abducted and lying on an arm board. The procedure is performed under tourniquet control after limb exsanguination. An 8-cm dorsal longitudinal incision is made centered over Lister’s tubercle. The skin is elevated from the extensor retinaculum, and then the extensor pollicis longus is elevated from its groove and retracted radially. The fourth extensor compartment is elevated along with the finger extensor tendons and retracted ulnarward to expose the dorsal capsule. The DRCL is identified as it courses from its origin just ulnar to Lister’s tubercle to its insertion on the dorsal aspect of the triquetrum. The DRCL is divided by making a 3-cm transverse incision in the dorsal capsule approximately 1 cm distal to the end of the radius, with the wrist distracted (Figure 14.8a through d).

FIGURE 14.8 Reefing of the dorsal radiocarpal ligament. (A and B) Location of the incision in the dorsal capsule and dorsal radiocarpal ligament (DRCL). (C) Volar intercalary segmental instability deformity can be corrected by pulling proximal distal flap of capsule and DRCL. This rotates the proximal row around its axis. (D) Two rows of sutures (pants-over-vest) are placed to maintain capsular tightening.

The distal edge of the capsular flap is pulled proximally, which corrects the volar rotation of the lunate and the proximal carpal row. Fluoroscopy is used to check that there is a neutral alignment of the proximal row and that the capitate and lunate and radius are co-linear. A percutaneous 0.45-mm K-wire is then drilled from the triquetrum to the capitate to maintain this midcarpal alignment. Next, two rows of sutures are placed in a pants-over-vest fashion to shorten the dorsal capsule and maintain the tension on the proximal carpal row.

Results

In 1993, Lichtman et al. published a review of 13 patients who underwent 15 surgical procedures for MCI, at an average follow-up of 48 months.¹² Nine patients had one of several soft-tissue procedures. The first patient had a triquetrohamate ligament reconstruction using the extensor carpi ulnaris tendon, two patients had a palmar capsular reefing, one patient had a dorsal radiocarpal capsulodesis, and five patients underwent a distal advancement of the ulnar arm of the arcuate ligament. Two patients required repeat surgery due to failure. Six patients underwent a limited midcarpal arthrodesis. It was clear that midcarpal arthrodesis was the most reliable procedure. Only two of the patients with an arcuate ligament advancement and the patient with the dorsal capsulodesis had a satisfactory outcome compared to all six of the midcarpal fusions.

The results of dorsal capsular reefing are unpublished. Thus far, patients who have undergone this procedure have done well with no reported incidents to date of recurring clunk. It must be stressed that this procedure is only performed in mild to moderate cases, meaning that the clunk can be prevented with mild to moderate dorsally directed pressure on the pisiform. Should the clunk recur postoperatively, a midcarpal arthrodesis can be performed through the same incision.

In 2003, Culp et al. reported their experience of five patients who underwent an arthroscopic capsular shrinkage.⁵ Eight patients to date have now undergone this procedure. The average age was 33 (range 29 to 57) years. Follow-up has averaged 9 months (range 3 to 18) months. The midcarpal clunk has resolved in six of the eight patients with pain resolution. Range of motion has decreased 20% in the flexion/extension plane, and grip strengths have increased by an average of 15%. Long-term follow-up is still needed to assess the efficacy of this procedure.