Flexor Tenolysis 

Flexor tenolysis is a procedure used to remove adhesions from tendons and is designed to improve active digital flexion.

Despite attempts to develop surgical and rehabilitation techniques to maximize flexor tendon function following surgical repair, postoperative tendon adhesions remain a problem and a significant source of morbidity. In these cases, appropriately timed flexor tenolysis of nongliding adhesions can markedly improve function of the digit.

An image depicting flexor tendons can be seen below.

Precise digital function requires smooth gliding of flexor tendons within their sheath. Tendon adhesions following injury or repair limit gliding, thereby decreasing the active range of motion of the digit as compared to the passive range of motion.^[1]

Frequency

The occurrence of flexor tendon adhesions depends on the degree and location of soft tissue injury. Crush injuries and disruption in zone II are frequently complicated by tendon adhesions.

Violation of the tendon surface, whether traumatic disruption or from attempts at surgical treatment, results in production of adhesions through the normal inflammatory response.^{[2, 3]} The limited space between the profundus and superficialis tendons and the theca is a primary contributor to the problem. Once adhesions develop, tendon gliding within this confined space is affected and active digital motion is diminished.

The process by which flexor tendons heal is debatable. The conventional theory is that peripheral fibroblasts from the surrounding connective tissue invade the zone of injury and serve as a source of reparative cells. In this theory, the tendon itself is believed to have no intrinsic ability for repair. New evidence seems to indicate that the epitenon cells migrate into and across the zone of injury along a fibrin lattice and that collagen fibers, formed by the epitenon and endotenon fibroblasts, bridge the laceration site.^[4] Vascularization of the repair zone is from within the proximal end of the tendon by proliferation of vascular channels.^[5] These studies suggest that the tendon possesses the intrinsic ability to participate in the healing process.^{[6, 7]}

Peripheral adhesions attach to the repairing tendon, potentially limiting tendon excursion during flexion and extension. Although adhesions may add strength to the healing tendon, it is unlikely that adhesions are an essential component of the reparative process.

Patients present following tendon injury or repair with a complaint of decreased motion of the digit. On physical examination, a significant decrease of active range of motion compared to passive range of motion is demonstrated, especially in flexion.

Tenolysis is technically demanding and should not be entered into lightly. No absolute indications for tenolysis exist. Each case must be treated individually, taking into account the details of the initial injury, the initial surgical treatment, the postoperative therapy program, and patient-specific factors. Patient selection is paramount. Patient factors, such as motivation and the ability to follow an intensive postoperative rehabilitation program, age, occupational needs, neurovascular status of the digit, and the presence of joint contracture, help guide the decision-making process.

However, flexor tenolysis is recommended whenever active flexion of the digit is significantly less than passive flexion of the digit and all attempts at improvement through therapy have been exhausted.

Among orthopedic surgeons, no consensus exists regarding the exact timing of the procedure. Weeks et al demonstrated that 22 weeks following a tendon graft, most patients achieved maximum active motion of the digit.^[8] Therefore, they recommended operating at that time. Rank et al advocate waiting 6-9 months before considering flexor tenolysis.^[9] Green and Strickland support a minimum of 3 months prior to operative intervention.^[10] Significant improvement in active flexion after tenolysis can be confidently expected only in children older than 11 years.^[11]

Two flexor tendons exist within the theca (the enclosed tendon sheath) that participate in flexion of the digit. These tendons originate in the forearm and pass through the carpal canal at the wrist. The flexor digitorum superficialis (FDS) inserts into the base of the middle phalanx and flexes the metacarpophalangeal (MP) and proximal interphalangeal (PIP) joints. The flexor digitorum profundus (FDP), or deep flexor tendon, inserts into the base of the distal phalanx. It serves to flex all 3 joints in the finger. The deep flexor tendons, except for the FDP to the index digit, usually function as a unit due to proximal interconnections. This is in contrast to the independent function of the FDS tendons.

The flexor retinaculum is a fibrous sheath that surrounds the flexor tendons and provides mechanical advantage, preventing bowstring of the flexor tendons and aiding in flexion of the digit. Five annular (A) and 3 cruciate (C) bands make up the pulley system.

Moving from distal to proximal in the phalanx, the A5 pulley overlies the distal interphalangeal (DIP) joint. C3, A4, and C2 are over the middle phalanx. A3 covers the PIP joint. C1 and A2 are found over the proximal phalanx, and A1 is over the metacarpophalangeal joint. A4 and A2 pulleys arise from bone alone and, thus, are the strongest and most critical of the pulley. A1, A3, and A5 arise from the volar plate and bone. C3 often is an oblique band. It is just distal to the A4 pulley on the middle phalanx. A4 is a broad structure and lies over the middle one third of the middle phalanx. C2 originates at the base of the middle phalanx and is a thin band that crisscrosses. C1 also crisscrosses and overlies the distal portion of the proximal phalanx. A2 is the largest pulley, spanning the proximal half of the proximal phalanx.

Some disagreement exists regarding the exact vascular supply to the flexor tendons. From the forearm to the palm, blood supply is generally believed to be provided by segmental vessels from the paratenon, which give rise to longitudinal intratendinous vessels that travel with the tendons. At about the level of the midproximal phalanx, the vincula begin to contribute. A short vinculum and a long vinculum exist for each of the flexor tendons. These vincula enter the tendons on their dorsal surface. In addition, many investigators believe that the synovial fluid within the enclosed theca also contributes nourishment to the flexor tendons.

Tenolysis is absolutely contraindicated in patients with active infection, motor-tendon problems secondary to denervation, and unstable underlying fractures requiring fixation and immobilization. Relative contraindications include extensive adhesions, immature previous scars, and severe posttraumatic underlining arthrosis.