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INTRODUCTION

A variety of distinct clinical entities characterize midcarpal instability (MCI). As yet, there is no universally accepted classification system for MCI, nor are the pathomechanics of the disorder completely understood. At a most basic level of understanding, there is known to be an abnormal force transmission across the midcarpal joint.

To consolidate the known varieties of MCI, we have proposed a classification scheme based on whether the pathology is extrinsic or intrinsic to the wrist. Patients with MCI associated with bony pathology of the radius or ulna, including negative ulnar variance or those with distal radius malunions, are grouped into the extrinsic category. The intrinsic forms are characterized by wrist laxity and are further subdivided into purely dorsal or palmar instability or a combination of both, depending on the direction of subluxation. The dorsal type is characterized by the findings of Louis and associates, in which they used a dynamic dorsal displacement test with the addition of videofluoroscopy to establish a diagnosis. They termed this presentation capitolunate instability pattern (CLIP) wrist. Another example of dorsal intrinsic MCI was described by Johnson and Carrera. They termed this chronic capitolunate instability (CCI), describing a series of patients with pain, weakness, and wrist clicking, which was also provoked by a dorsal capitate displacement stress test under fluoroscopy. It is likely that these are both the same condition.

Lichtman and associates have described a palmar intrinsic type in which videofluoroscopy showed that the proximal row maintained a volar-flexed position (in neutral), which snapped into extension as the wrist went from neutral into ulnar deviation. This along with a midcarpal shift test, which reproduced the clunk, was diagnostic of palmar midcarpal instability (PMCI). Caputo and associates classified MCI into four subtypes based on pathology occurring on the radial or ulnar side of the wrist. Types I and II were similar to those described by Lichtman. Types III and IV referred to rotatory subluxation of the scaphoid and were attributed to the scaphotrapezoid ligament laxity. These patients presented with scaphoid tenderness, a catch-up clunk, a positive midcarpal shift test, a positive resisted finger extension test, and/or a positive scaphoid shift test. Carpal instability nondissociative (CIND) was described by Wright and associates in a series of patients who presented with an array of symptoms and directions of instability. These could have possibly been grouped along with those reported by Louis and associates, Lichtman and associates, Johnson and Carrera, and others. They felt that the pathology could be contributed to by intrinsic ligamentous insufficiency, extrinsic bony pathology, or both. Table 50-1 represents the authors’ recommended classification of these patterns of MCI.

PATHOMECHANICS

A brief look at normal wrist physiology is required to understand the pathology and mechanics involved in MCI. The ring model is a useful representation of the dynamic motion of the carpus. Normally, the proximal and distal rows move smoothly in concert during flexion/extension and radial/ulnar deviation. At maximal radial deviation, the entire proximal row is flexed and translated dorsally, and the distal row is translated palmarward. This is best identified by observing the position and angulation of the lunate on a true lateral image (using scaphopisocapitate referencing). In neutral, the lunate is centered in the lunate fossa and is collinear with the long axis of the radius and capitate. On ulnar deviation, the entire proximal row smoothly shifts into an extended position. With intact wrist ligaments, the physiologic joint reaction forces generated at the radial and lunar carpal links (i.e., the scaphotrapeziotrapezoid (STT) and triquetrohamate joints, respectively) are the principal drivers of this elegantly executed mechanism.

In PMCI, there is the laxity of the triquetrohamatocapitate ligament, the dorsal radiotriquetral ligament, and possibly the periscaphoid ligaments. As a consequence of this ligamentous insufficiency, a palmar sag at the midcarpal joint (as represented by a volar-flexed lunate and palmar-translated capitate) is present in neutral deviation when the midcarpal joint reactive forces are relaxed. This in turn leads to abnormal force transition across the midcarpal joint, in contrast to the smooth physiologic transition of the proximal row from flexion to extension as the wrist moves ulnarly. Instead, the proximal row remains flexed until the wrist is ulnarly deviated and the helicoid triquetrohamate joint becomes engaged, forcing the entire proximal row into extension. This corresponds to the sudden painful “catch-up” clunk that patients experience. To recapitulate, in PMCI the wrist begins in a subluxed state in neutral and suddenly corrects when the wrist is ulnarly deviated. Dorsal MCI (and possibly extrinsic MCI) differs in that the wrist is reduced in neutral and subluxes dorsally in ulnar deviation.

However, in both the palmar and dorsal presentations, the proximal row always rotates into extension, and the distal row translates dorsally as the wrist ulnarly deviates.

CLINICAL EXAMINATION

Patients with PMCI typically present with a history of a painful clunking of the wrist while moving into ulnar deviation and often are able to voluntarily reproduce the clunk. There may or may not be a history of a precipitating injury. MCI is particularly common in patients with generalized ligamentous laxity, including adolescent females. It also has been described in acquired laxity secondary to chronic wrist ligament stress (as in paraplegics and their prolonged dependence on crutches).

On clinical examination, a palmar sag of the wrist resembling a dorsal distal radioulnar joint (DRUJ) dislocation is often noted with the wrist in neutral ( Fig. 50-1 ). At maximum ulnar deviation, the palmar sag disappears suddenly as the “catch-up” clunk occurs. Tenderness over the triquetrohamate joint corresponds to the presence of localized synovitis and/or cartilage degeneration.

Volar sag .

In instances in which the patient cannot reproduce the clunk, the midcarpal shift test can be diagnostic ( Fig. 50-2 A and B). This is done by stabilizing the forearm in pronated position at 15 degrees of ulnar deviation and by directing pressure palmarly over the distal capitate to reproduce the palmar translation. Next, the wrist is axially loaded and ulnarly deviated. A positive test is one that reproduces the patient’s clunk and pain. Reproduction of the palmar translation and production of a clunk without pain are not diagnostic in that patients with ligamentous laxity (without PMCI) may have this finding. Passive dorsal translation (reduction) of the subluxed midcarpal joint, performed by pushing dorsally on the triquetrum with the wrist in neutral, corrects the sag, which is due to a volar intercalated segmental instability (VISI) posture, and eliminates the clunk as long as the dorsally applied pressure is maintained. The midcarpal shift test should be performed on the contralateral wrist for comparison. Many patients with generalized ligamentous laxity demonstrate bilateral midcarpal laxity as well.

Midcarpal shift test . Steps 1 ( A ) and 2 ( B ) are shown.

Patients with dorsal MCI usually have a history of an extension injury and complain of wrist clicking and weakness, which is most noticeable in supination, and chronic post-traumatic pain. The dorsal capitate displacement test is done by placing dorsal pressure on the scaphoid tuberosity while longitudinal traction and flexion to the wrist are applied.

Plain radiographs are useful in ruling out dissociative abnormalities or extrinsic causes of symptoms such as a distal radius malunion or a negative ulnar variant. Usually, radiographs of PMCI demonstrate a mild volar angulation or volar intercalated segmental instability posture of the lunate. Arthrograms are usually normal, since the process is characteristically due to ligamentous attenuation and not disruption. Magnetic resonance imaging (MRI) studies do not add value to the plain radiographs (except to rule out extraneous bony pathology). Videofluoroscopy is the imaging gold standard in MCI. The pathologic sudden snap from flexion to extension can be dynamically visualized while the wrist is ulnarly deviated. In addition, videofluoroscopy is helpful in ruling out an associated dissociative lesion, especially on the posteroanterior view.

Arthroscopy cannot be used to make the diagnosis of MCI. It may be used to evaluate erosive lesions between the triquetrum and the hamate, or it can be used to discern other abnormalities such as triangular fibrocartilage complex (TFCC) tears, ulnar impaction syndrome, and dissociative lesions.