What Is Shrinkage?

Shrinkage is a physical phenomenon that occurs with heat modification of type I collagen in ligamentous tissue. When the collagen is heated to a critical temperature, the heat-labile intramolecular hydrogen bonds break.⁴ The protein undergoes a phase transition from a highly ordered crystalline structure to a random-coil state, which is similar to melting, and the tissue tensile properties change.⁵ Typically, this thermal denaturation of collagen type I occurs at approximately 60°C to 65°C. The heat in ligamentous tissues is generated by a RF pulse, which results in the oscillation of molecules as their polarity changes (i.e., ohmic resistance). The RF probe imparts a high-frequency (350 kHz to 1 MHz) alternating current from an electrical generator to the tissue. This current creates an ionic agitation in the tissue as the ions attempt to follow the changes in direction of the alternating current. This ionic agitation results in frictional heating within the tissue. The current passes either between the probe tip and a grounding pad (monopolar) or between two points on the probe tip (bipolar).

Molecular Effects of Thermal Shrinkage

Transmission electron microscopy shows significant alterations in the collagen architecture. These changes are characterized by the loss of the classic 67-nm periodicity of the type I collagen fibril that is evidenced by the loss of the periodical cross-striations in the collagen fibril. There also is an increase in the cross-sectional area of the collagen fibril. The margins of the fibrils begin to lose their distinct edge, while maintaining their circular shape. These ultrastructural effects are caused by unwinding of the collagen triple helix as a result of the temperature increase in the tissue.^6,7

Biological Response to Thermal Shrinkage

At time 0, after thermal shrinkage, under light microscopy there is evidence of diffuse hyalinization and fusion of the collagen fiber. By day 7, there is fibroblast proliferation around and within the hyalinized regions. By day 30, large fibroblasts have migrated into the region and produced new matrix. These newly arrived fibroblasts use the acellular “hyalinized” collagen as a scaffold for migration and matrix synthesis. At 3 months, active reparative changes are evident with an increase in vascularity. The fibroblasts have now regained a more normal appearance under transmission electron microscopy. At 7 months, the cell morphology and vascularity have returned to normal without evidence of any permanent tissue injury or severe inflammation.^8,9

Rationale for Shrinkage of Scapholunate Ligament Injuries

Our concept for the use of thermal shrinkage for the treatment of instability of the carpus with scapholunate ligament injuries arose from previous published work on the use of thermal shrinkage on other articulations and the favorable results that were achieved after mechanical débridement of partial scapholunate ligament tears.^11,12 We also were influenced by the biomechanical importance of the scapholunate ligament for stability of the carpus and the paucity of treatment methods for carpal instability, and the relative ease of performing an arthroscopic shrinkage of the scapholunate ligament. The scapholunate ligament (SL) is not a homogeneous structure. It is divided into three parts: dorsal, proximal, and palmar (Fig. W7-1). The dorsal part is the strongest subregion of the scapholunate ligament. It meets all the criteria for the definition of an articular ligament in that it is composed of collagen fascicles surrounded by connective tissue with intertwined neurovascular bundles.^13–15 It has a thickness of 2 to 3 mm and a length of 4 to 5 mm (Fig. W7-2) and merges with the dorsal capsule (Fig. W7-3).

Figure W7-1 The SL ligament is divided into three parts: dorsal, proximal, and palmar.

Figure W7-2 The SL ligament has a thickness of 2 to 3 mm and a length of 4 to 5 mm.

Figure W7-3 The SL ligament merges with the dorsal capsule. The dorsal part of the SL ligament is strictly connected with the articular capsule.

The proximal portion is grossly anisotropic. It is composed mainly of fibrocartilaginous tissue, which is weak owing to its avascularity. The transition zone between the proximal and palmar portions is marked by the radioscapholunate ligament, which inserts on the palmar aspect of the scapholunate ligament. The palmar portion is composed of thin collagen fascicles (1 mm thick) with a length of 4 to 5 mm. This portion is invisible through the standard dorsal arthroscopic portals in the face of an intact radioscapholunate ligament. The three parts do not have the same tensile strength. The dorsal part is most resistant to shear forces with an ultimate yield strength of 300N. The palmar part fails at a load of 150N, whereas the proximal portion can withstand only 25N to 50N of stress. The triquetrolunate ligament, which also is divided into three parts, has the exact reverse characteristics on loading to failure as those of the scapholunate ligament. Biomechanical studies also have shown that the dorsal subregion of the scapholunate ligament is responsible for controlling scaphoid flexion and the extension motion, whereas the palmar subregion controls rotational motion.^16–19

Based on this evidence, it was apparent to us that the use of thermal shrinkage of the scapholunate ligament was feasible and most appropriate for the dorsal part of the ligament. When considering the kinematics and the instability of the carpus in scapholunate ligament injuries, it is important to remember the role of the dorsal radiocarpal ligaments (Fig. W7-4) and the dorsal capsule (Fig. W7-5). They are intimately connected with the scapholunate ligament and must be included in the thermal shrinkage (Fig. W7-6).

Figure W7-4 The dorsal radiocarpal ligaments.

Figure W7-5 The dorsal capsule. ECRB, extensor carpi radialis brevis; ECRL, extensor carpi radialis longus.

Figure W7-6 The dorsal radiocarpal ligaments and the dorsal capsule are intimately connected with the SL ligament and must also be included in the thermal shrinkage.

The aim of thermal shrinkage of the scapholunate ligaments along with the dorsal ligaments and the dorsal capsule is to maintain the ligament and capsular shortening that is achieved during shrinkage, while awaiting the secondary fibroplasia and resultant thickening of the joint capsule and ligament. Another theoretical goal is the interruption of any painful afferent sensory pathways through the destruction of sensory receptors.^20–22

Technique

Wrist arthroscopy is performed using a standard technique. The arthroscopy is done by placing the affected extremity in a distraction tower with 3 to 5 kg of distraction. The correct amount and direction of the distraction force are monitored fluoroscopically, to avoid iatrogenic injury to the carpal ligaments, and to control the palmar flexion of the scaphoid. The joint is insufflated with 5 to 7 mL of normal saline followed by the establishment of the 3,4 and 4,5 portals as a viewing and working portal and a midcarpal portal. The wrist is examined from radial to ulnar, and the stability of the scapholunate interval stability is assessed by probing the transition zone between the dorsal portion of the scapholunate ligament, which is thick and taut, and the weaker proximal portion, which is identified by palpation. All patients undergo stress testing of the scapholunate ligament under direct visualization. Any ligamentous injury is classified according to the arthroscopic classification scheme described by Geissler.²³

The shrinkage of the scapholunate ligament is performed with a 2.3-mm monopolar RF probe that is dedicated for shrinkage (Micro-Tacs with an angled tip and a controlled temperature system). The shrinkage is performed on the entire dorsal section of the ligament (Fig. W7-7) extending up to its confluence with the dorsal capsule (Fig. W7-8). The palmar subregion of the scapholunate ligament is not included in the shrinkage. The scapholunate ligament and capsular tissue are treated with multiple single linear passes (grid pattern) to leave more viable tissue adjacent to the treated areas, which may result in faster cellular invasion and matrix formation. There is no objective way to measure the effect of RF probes, so the surgeon relies on the visual assessment of the morphological ligament tissue changes and capsular volume reduction to quantify the degree of tissue shrinkage.

Figure W7-7 The shrinkage of the SL ligament is performed with a 2.3-mm monopolar RF probe that is dedicated for shrinkage (Micro-Tacs with an angled tip and a controlled temperature system). The shrinkage is performed on the entire dorsal section of the ligament.

Figure W7-8 The shrinkage is performed extending up to its confluence with the dorsal capsule.

Using the Geissler classification of scapholunate ligament injuries (Table W7-1), symptomatic grade 1 lesions are treated with the standard technique for shrinkage as described. Grade 2 lesions that show dynamic instability (i.e., an increased scapholunate gap with loading) are treated with shrinkage as described in addition to Kirschner wire (K-wire) fixation of the scaphoid and lunate.^24,25 In grade 3 lesions, in which there is a complete scapholunate ligament perforation, the shrinkage is mainly performed on the dorsal capsule and radiocarpal ligaments with only marginal shrinkage of the torn dorsal ligament, combined with K-wire fixation of the scaphoid and lunate. Acute and subacute grade 3 lesions less than 4 months old that show a static scapholunate dissociation and rotational instability require an arthroscopic reduction and K-wire fixation.

The arthroscopic reduction is done with the “joystick” technique. One K-wire is drilled through the skin just radial to the extensor carpi radialis longus tendon into the proximal pole of the scaphoid toward the lunate, but not across the scapholunate interval; a second K-wire is drilled through the dorsal skin into the lunate, with the arthroscope in the midcarpal portal. The scaphoid and lunate are reduced and aligned using the scaphoid K-wire and lunate K-wire as joysticks. When the reduction is achieved, one or two additional scaphoid K-wires are drilled across the articulation into the lunate, under fluoroscopic control to ensure that the radiocarpal and midcarpal joints have not been violated. The K-wires are bent and left protruding through the skin. A thumb spica cast is worn. The cast and K-wires are removed 4 to 6 weeks postoperatively, and a cock-up splint is used intermittently between physiotherapy sessions for another 4 weeks.

Scientific Study

A prospective, randomized clinical study was done to determine the effectiveness of arthroscopic thermal shrinkage with RF for the treatment of symptomatic scapholunate ligament injuries. From 2001 to 2004, 120 patients with scapholunate ligament injuries were treated. Inclusion criteria consisted of patients with a Geissler grade 1, 2, or 3 scapholunate ligament injury that was associated with dorsoradial wrist pain that was unresponsive to 6 to 8 weeks of conservative treatment. Patients with dorsal intercalated segment instability deformities on plain x-rays were excluded. The patients were randomly assigned into four treatment groups as follows:

Clinical outcomes were evaluated at 3, 6, 12, and 24 months. Outcome instruments included preoperative and postoperative use of the modified Mayo wrist score; range of motion; a visual analog scale for pain at rest, during everyday activity, and during heavy manual work; grip strength as a percentage of the contralateral side; and standard and loading radiographs. Data from both groups were compared using the Student t-test for continuous variables, and the level of significance was set to P < .05.

Results

No complications were noted from the use of RF probes (Table W7-1). The scores for overall clinical outcome showed that patients in group A had better outcomes than patients in group B. Patients in group C also had better outcomes than patients in group D. No statistically significant changes were noted between the preoperative and postoperative x-rays for groups A and B. There was a statistically significant reduction, however, in the scapholunate interval seen on x-rays during loading for group C.

Based on these findings, we concluded that scapholunate ligament shrinkage in patients with symptomatic predynamic and dynamic instability is a safe technique and had a good success rate at a minimum 2 years of follow-up. The treatment of grade 1 scapholunate injuries with shrinkage is more effective than arthroscopic débridement alone in our hands. Similarly, scapholunate ligament shrinkage when combined with K-wire fixation is more effective than arthroscopic débridement and pinning for grade 2 and 3 lesions. In the short-term, arthroscopic shrinkage is a viable treatment option for scapholunate ligament tears. Long-term studies are still needed to evaluate this method fully.