Tendon transfer is most often the treatment of choice for tendon ruptures in the rheumatoid hand.
The goal for a tendon transfer is to redistribute power to improve function.
Tendon transfers do not restore normal motion but result in improved function.
In the patient with rheumatoid arthritis, tendon ruptures are relatively common in the hand and wrist. They are caused by tendon abrasion by roughened or sharp spikes of bone; ingrowth of proliferative synovium into the substance of the tendon tissue, resulting in tendon weakening; and tendon ischemia.
Rupture of the flexor or extensor tendons in the rheumatoid wrist usually occurs insidiously and is rarely associated with pain.
Rehabilitation after tendon transfers includes edema control, protective orthotic positioning, tendon transfer training, functional electrical stimulation, and functional retraining.
Close communication between the therapist and the surgeon is critical to the successful outcome of tendon transfer procedures.
Tendon rupture in rheumatoid arthritis is relatively common, particularly in uncontrolled, advanced disease. The cause may be proliferative tenosynovitis on the dorsal or volar surfaces of the hand, where proteolytic enzymes, such as collagenase, attack the tendon directly and cause attenuation and eventual rupture. Tendon rupture may also occur as a result of secondary joint instability and subluxation, as seen in the distal radioulnar joint, where the ulna subluxes dorsally secondary to similar effects of the same proteolytic enzymes. However, here, their destructive power is directed at the dorsal and palmar ligaments and the triangular fibrocartilage complex of the distal radioulnar joint, with resultant ligamentous laxity and joint instability. The erosive changes on the bone and cartilage cause a rough surface that potentiates erosion of the distal ulna through the soft tissues stabilizing the joint and may also lead to attrition of the tendons of the fourth, fifth, and sixth extensor compartments when the bone comes in contact with the tendon directly. Although advances in the medical treatment of rheumatoid arthritis control the disease better than ever, not all of the newer anti-tumor necrosis drugs are well tolerated by all patients, and in these patients, the arthritis has the potential to progress in a relentless, destructive fashion. Therefore, surgeons and therapists still must be alert to the potential for tendon rupture in patients with rheumatoid arthritis. For patients who have tendon rupture, direct tendon repair is rarely possible because of frequent delays in treatment and the condition of the tendon after rupture. Tendon transfer, therefore, becomes the treatment of choice, and the general principles of tendon transfer are applicable to patients with rheumatoid arthritis. For example, the joint to be motored must have a full passive range of motion, a donor muscle–tendon unit must be both available and expendable, and the muscle–tendon unit must have sufficient power to replace the ruptured tendon. The soft tissues through which the tendon transfer must pass should be relatively free of disease. Perivascular inflammation, boggy synovium, and intrinsic muscle contractures are all relative contraindications to tendon transfer in the hand, as would be skin ulceration or paper-thin skin caused by vasculitis or chronic glucocorticoid and other immunosuppressive therapy.
Despite this relatively grim-sounding scenario, tendon transfers to restore finger extension and flexion or to increase thumb mobility may significantly improve function. Moreover, tendon transfers may improve the appearance of the hand and yield a high degree of patient satisfaction.
As with joint replacement arthroplasty, tendon transfer may prove more palliative than curative; however, the opportunity to improve function in a patient with rheumatoid arthritis is not an opportunity to be squandered, and patients with successful outcomes are often satisfied.
In the patient with rheumatoid arthritis, tendon ruptures are relatively common in the upper extremity, particularly in the hand and wrist. Tendon rupture often is the result of the tendon being abraded by rough bone or a sharp spike of bone. This may occur on the dorsum of the wrist secondary to dorsal dislocation or subluxation of the distal radioulnar joint, rupturing the tendons of the fourth, fifth, and, occasionally, sixth extensor compartment. This often is referred to as caput ulnae or Vaughan-Jackson syndrome ( Fig. 108-1 ). On the palmar surface of the wrist, the flexor pollicis longus (FPL) and flexor digitorum profundus (FDP) to the index and long fingers may be abraded by a spur on the scaphoid or by spur formation at the level of the scaphotrapezial joint. The eponym for tendon ruptures at this level is Mannerfelt’s syndrome ( Fig. 108-2 ). This must be differentiated clinically from anterior interosseous nerve palsy, which also can be seen with rheumatoid arthritis ( Fig. 108-3 ). Rheumatoid cyst formation from the elbow joint may cause compression of the anterior interosseous nerve and secondary loss of interphalangeal (IP) joint flexion in the thumb, as well as distal IP joint flexion in the index finger. These are the same digits affected by tendon rupture in Mannerfelt’s syndrome.
Proliferative synovium may actually grow into the substance of the tendon tissue, destroying it locally to the extent that the tendon weakens and eventually ruptures. Commonly seen in the finger proximal to the level of the A1 pulley, tenosynovial ingrowth may occur anywhere tenosynovium is found, such as the dorsum of the wrist proximal or distal to the extensor retinaculum. Although this has the potential to cause rupture, this synovial ingrowth more often results in limited tendon excursion as the tendon swells and no longer passes beneath the annular or retinacular pulley system on the flexor surface of the finger. If aggressive medical treatment that includes corticosteroid injections is unsuccessful, tenosynovectomy with reduction tenoplasty is the treatment of choice, with reasonable long-term results, particularly at the A1 pulley level in the finger. Release of the A1 pulley should be avoided because it increases the moment of force of the profundus tendon at the metacarpophalangeal (MCP) joint level in an ulnar direction and therefore may lead to increased premature ulnar deviation in the involved digits. Finally, tendon ruptures may occur as the result of ischemia to the tendon. This is similar to what occurs to the extensor pollicis longus (EPL) tendon in patients with minimally displaced to nondisplaced Colles’ fractures. Rupture is the result of a nonviable tendon passing back and forth beneath a pulley, leading to attrition and failure of the tendon.
Rupture of flexor or extensor tendons in the rheumatoid wrist usually occurs insidiously and is rarely associated with pain. Initially, the patient may note inability to extend the small finger or perhaps the small and ring fingers. The differential diagnosis may be difficult initially because the extensor tendons at the level of the MCP joint may have subluxed ulnarward secondary to attenuation of the sagittal fibers on the radial side of the dorsal apparatus of the extensor mechanism between the central tendon and the palmar plate. In the presence of a flexible wrist, close observation of the tenodesis effect should aid the clinician in diagnosis (see Fig. 108-1 ). Palmar flexion of the wrist will result in relative finger extension if the extensor tendons are intact. If the tendons have ruptured at the wrist or more proximally, the IP joints should remain in a relatively flexed position, regardless of wrist motion. In patients with limited wrist motion, this tenodesis effect may be more difficult to demonstrate. In patients with previous surgical arthrodesis of the wrist, the tenodesis effect is impossible to demonstrate. Therefore, a high index of suspicion, combined with a careful history of sudden, painless loss of finger motion, is helpful in making the diagnosis. Ideally, arthrodesis has been performed with dorsal synovectomy, Darrach’s procedure, and coverage of the distal ulna with a flap of retinaculum to protect the extensor tendons from further damage. Tendon rupture should then occur only rarely.
In the patient presenting with lack of extension of one or all fingers, the clinician also should carefully examine the elbow. Rheumatoid cysts of the radiocapitellar joint may compress the posterior interosseous nerve, resulting in paralysis and loss of finger extension. When this occurs, the wrist usually is deviated radially as a result of lack of extensor carpi ulnaris function. However, the extensor carpi radialis longus (ECRL) inserts in the base of the index and functions normally. The extensor carpi radialis brevis (ECRB) may or may not be involved as a result of local effects of the cyst or arthritic changes at the elbow. This presentation should alert the clinician that posterior interosseous nerve palsy rather than tendon rupture may be responsible for the loss of finger extension. On the palmar surface of the wrist, the clinician must be equally astute and recognize that lack of thumb and index finger flexion may be secondary to rupture of either of these tendons, usually at the level of the scaphotrapezial joint, or paralysis of the anterior interosseous nerve. Wrist extension, if clinically possible and not limited by wrist arthritis, should show IP joint flexion through the tenodesis effect and confirm the diagnosis of nerve palsy rather than tendon rupture. If wrist extension does not affect the position of the IP joint of the thumb or the DIP joint of the index finger, tendon rupture is the more likely diagnosis. Direct pressure over the muscle belly of the FPL is an effective way to test whether the distal tendon is intact. Direct pressure should result in flexion of the IP joint of the thumb through a reflex contraction of the muscle, much like the Thomas test used to examine a patient for potential rupture of the Achilles tendon. If direct pressure, usually applied by the examiner’s thumb, over the muscle belly of the FPL does not result in involuntary contraction of the muscle and flexion of the IP joint of the thumb, the examiner should suspect rupture of the FPL as opposed to palsy of the anterior interosseous nerve ( Fig. 108-4 ). In addition to Mannerfelt’s syndrome (discussed earlier) as a potential cause of rupture of the FPL or FDP of the index finger, rupture of these tendons has been reported as a complication of volar plate fixation of distal radius fractures and after malposition of a Hamas total wrist.
Flexor Tendons and Thumb
Many authors have described principles of tendon transfer, but none more succinctly or eloquently than Richard Smith. The surgeon must be certain that the muscle considered for transfer is available, expendable, and strong enough to perform the desired function. The more closely the donor tendon resembles the recipient tendon in amplitude, excursion, and direction of pull, the better the expected functional result. The force that a muscle can exert is proportional to its cross-sectional area, and muscle strength is greatest at its resting length. If a muscle is stretched or contracted, it loses strength.
Careful clinical and radiologic examination of the MCP and IP joints also is required in planning surgical reconstruction. Restoration of IP joint motion is particularly important in cases of previous MCP joint fusion.
In the case of rupture of the FPL or FDP to the index or long finger, interposition tendon graft to the FPL may be the best option to restore thumb flexion. The palmaris longus or one of the usual two slips of the extensor digiti quinti (EDQ) may be used for interposition tendon grafting ( Fig. 108-5 ). Tendon transfer should be considered when the patient is seen more than 6 months after the rupture and the proximal muscle of the FPL or FDP has become contracted and is no longer capable of serving as a motor unit. Transfer options include the flexor digitorum superficialis (FDS) of the long or ring finger to the stump of the distal FPL. If enough distal tendon is present, the brachioradialis is an excellent muscle to restore flexion power to the thumb. The combination of transfer of the brachioradialis to the FPL with transfer of the ECRL or ECRB to the FDP of the index and long fingers, as used for high median nerve palsy, may be a good choice for tendon rupture as well.