The role of arthroscopy in midcarpal instability

Relevant anatomy and biomechanics

Many investigators have contributed to the understanding of midcarpal instability (MCI), which Lichtman consolidated into classifications ( Table 9.1 ). 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 will center on intrinsic MCI. Extrinsic MCI due to a dorsally malunited distal radius fracture is treated by a distal radius osteotomy and hence falls outside the scope of this discussion.

The mechanism of the clunk in palmar midcarpal instability (PMCI) has been described in detail by Lichtman et al. 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) ( Fig. 9.1 A–B). Normally the proximal carpal row moves smoothly from a flexed position when the wrist is in radial deviation to an extended position 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 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.

Studies by Trumble et al. and Viegas et al. have shown that sectioning either the TCL or the dorsal radiocarpal ligament (DRCL) can produce a volar intercalated segmental instability (VISI) deformity and simulate PMCI. Lichtman showed in vivo that tightening the DRCL alone can stabilize the proximal carpal row and eliminate the clunk of PMCI, thus emphasizing the potential importance of dorsal ligament laxity in the pathogenesis of this disorder. He believed 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 ( Fig. 9.2 A–B). 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 ( Fig. 9.3 A–B).

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. ^, 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 differentiates 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 (DMCI), 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

Patients with PMCI present with a history of clunking of their wrist. Patients can often reproduce the clunk on both sides because generalized ligamentous laxity frequently coexists. Some patients may have a trivial injury that accentuates this normal laxity, resulting in a painful clunk. On 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 ( Fig. 9.4 A–B). The clunk may be reproduced by performing the midcarpal shift test. This test is performed by placing the patient’s wrist in neutral with the forearm pronated. 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.

In DMCI a history of an extension injury may be present. Patients complain of posttraumatic chronic pain, weakness, and wrist clicking. Tight grasping especially in supination aggravates the symptoms. The physical examination also reveals palmar sagging of the ulnar wrist. 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.