12.23 Extensor tendon injuries in the hand and wrist

Extension of the wrist and fingers is vital to hand function. Although it is more obvious that flexion is required for pinch and grip, these functions can only be successfully accomplished if the extensor mechanism is intact. Extension allows the tactile surfaces of the hand and fingers to be exposed and brought into contact with objects being manipulated, and extension of the wrist both positions the fingers correctly for grasping and potentiates the long flexors of the fingers by passively increasing their tension, the tenodesis effect. Extension at the metacarpophalangeal (MCP) joints can only be produced by the long extensors of the fingers and thumb (the extrinsic system), but the interphalangeal (IP) joints are extended by both extrinsic and intrinsic systems, so that extensor tendon division proximal to the MCP joint does not eliminate all interphalangeal extension.

The extensor tendons transmit power from the muscle groups situated in the dorsal forearm compartments to the wrist, MCP, and IP joints, producing extension at four sequential joint levels across five rays. Contributions are received from the intrinsic muscles of the hand, entering the system distal to the MCP joints. This network of tendons can be injured at any point, by closed injury usually involving a traction force, or open penetrating, lacerating, or crushing injury. The consequences of such injury mainly affect joints directly controlled by the particular tendon(s) damaged, but effects may be seen at other joints, since the tendons in the system have to act across sequential joints which are inherently unstable without balanced control; they have complex interconnections, and the effects of unopposed antagonist muscles also have to be taken into account. The anatomy of the extensor tendons is shown in Figure 12.23.1.

Because of the exposed and vulnerable position of the extensor mechanism, injury to its tendons is common, occurring in all settings where the hand is at risk from injury, including the workplace, the home, especially the kitchen, and sports situations.

All tendons are vulnerable to sharp injury, and tendons weakened by age (as in mallet finger), trauma (as in extensor pollicis longus (EPL) rupture after distal radial fracture), and disease (as in rheumatoid arthritis) are more prone to closed rupture.

Figure 12.23.1 shows the zones into which the extensor tendons are divided for the purposes of classifying injuries and describing their treatment. In this chapter the zones of injury will be considered in sequence in all their aspects, starting with the most distal.

Injuries resulting in loss of extension power at the distal interphalangeal (DIP) joint are most commonly closed injuries, but open laceration dividing the tendon close to its distal insertion has a similar effect.

This common injury usually occurs in surprisingly innocuous circumstances, such as when the finger is stubbed or forced into sudden flexion while bed-making. Usually the patient is immediately aware of a flexion deformity but may not seek help straight away since the injury seems trivial. The injury either involves a stretching and softening disturbance of the tendon resulting in lengthening, or avulsion of a bone fragment at the tendon’s insertion. The clinical effect is the same. Patients with normal joint ranges simply show a DIP flexion deformity allowing passive extension. If the proximal interphalangeal (PIP) joint allows some natural hyperextension, a swan-neck deformity may be observed within a few days. This results from the modification in force distribution of the extensor mechanism as it tries to migrate proximally following distal detachment. This proximal movement is restrained by the central slip attachment at the PIP joint (Figure 12.23.2), and the increased tension there can cause hyperextension, or restriction of full flexion where hyperextension is not possible. An understanding of this dynamic change is important.

Investigation includes radiography, with a lateral view to demonstrate an avulsion fracture (Figure 12.23.3).

Treatment of closed mallet finger without fracture is by splintage. Repair of the tendon gives poor results because it is stretched and denatured. Various splints have been described, although the simplest is a padded malleable metal splint placed dorsally across the DIP joint, strapped to the middle and distal sections of the finger to maintain DIP extension. The splint should not be bent dorsally with the intention of forcing the joint into hyperextension because the pressure exerted directly over the joint dorsally can result in skin damage or loss. Splintage should be continuous, and if the patient wishes to remove it to wash the finger, DIP extension should be maintained throughout, since any drop into flexion recreates the injury. This form of splintage needs to be maintained for at least 6 weeks, during which time the patient should be seen regularly and the condition of the dorsal skin checked for pressure. If after 6 weeks there is any tendency for persistent deformity, splintage should be continued, and often this is necessary for up to 10 or 12 weeks.

It is helpful if the patient can learn the habit of allowing the finger to sit in flexion at the PIP joint as this reduces the tension at the sit of distal tendon rupture.

Occasionally a red and slightly oedematous appearance develops over the middle phalanx, usually after splintage has been completed. This is not usually infection, though antibiotic treatment is wise, but it seems to represent inflammation or possibly avascular changes in the disrupted tendon. It settles slowly.

Correctly applied splintage for mallet finger is effective in approximately 80% of cases, although 10–20 degrees of extension lag may persist without functional disturbance. More than 30 degrees of lag can be corrected after a delay of 6 months by Fowler’s release of the central slip at the PIP joint. This adjusts the imbalance between the tendon insertions at PIP and DIP levels, restoring tension distally, and can therefore only be done after complete healing of the disrupted tendon has occurred at its new length. Release can be performed under metacarpal block through a longitudinal incision on the side of the finger. The extensor mechanism is lifted intact by dissecting beneath the palmar edge of the lateral band, then the central slip is divided at its insertion without causing separation between lateral and central tendon components, or lateral migration of the lateral bands could cause a boutonnière deformity. This complication has to be protected against by splintage (see later) for 2–3 weeks after the operation. DIP extension is usually restored within days, the occasional failure being due to continued complete disruption of the distal extensor tendon. If the continued flexion deformity is severe enough, DIP fusion might be indicated.

A similar injury can affect the thumb, giving a flexion deformity of the IP joint, in contrast to loss of extension mainly at the MCP joint due to EPL rupture. Mallet thumb, like mallet finger, can be treated conservatively.

A very small chip fracture can be treated by splintage, but large fragments include a significant proportion of the joint surface, which should be restored. The fragment is wired or sutured back in place through drill-holes in the distal phalanx (Figure 12.23.3), supporting the joint in extension with a percutaneous K-wire crossing the joint and kept in place for 3–4 weeks. A brief period of dorsal splintage may be needed after wire removal.

The extensor hood over the shafts of the proximal and middle phalanges is broad and flat, and because of its superficial position it is often divided by sharp lacerations. Because it is broad, division may be incomplete and therefore not obvious on clinical examination. The divided tendon can be approximated by simple interrupted sutures. Untidy injuries may involve loss of tendon, but it is usually possible to restore continuity unless tendon is actually missing, in which case a small graft may be needed. Skin cover needs to be secure. Adhesions form easily, and tenolysis may be needed later. This is particularly likely when tendon injury in this area is associated with an underlying fracture. Rigid internal fixation helps by allowing earlier mobilization, and separation of the tendon from bare bone should be attempted by periosteal repair (Box 12.23.2).

This is caused by disruption of the central slip of the extensor mechanism at the PIP joint. It may be a closed injury due to forced flexion, or an open laceration at or proximal to the joint. Open laceration is not infrequently missed at the time of repair of a small laceration, because PIP extension can initially be produced by the lateral bands. However, propagation of the tear in the tendon between central and lateral components allows them to migrate palmar-wards round the joint, and they lose their extension force, becoming flexors. As they do so the pull at the DIP joint increases, causing hyperextension (Figure 12.23.4). The dysfunction is now obvious, and the patient seeks treatment, but delayed repair after this disturbance in the mechanism is often unsatisfactory.

When open tendon injury is identified primarily it should be repaired by direct suture with interrupted non-absorbable sutures (about 4/0), and the PIP joint supported in extension with a percutaneous K-wire for about 10 days. During this time, DIP flexion is encouraged, and after which active PIP movement is regained under the supervision of a physiotherapist. Some patients have difficulty in regaining movement.

Closed boutonnière deformity can also develop insidiously by the same mechanism, and patients frequently present 2–3 weeks later. Smith and Ross (1994) have described a test to detect the central slip rupture before it is clinically obvious. The wrist and MCP joint of the affected finger are passively flexed fully, and an intact central slip should produce full PIP extension. If it does not, there is laxity of the central slip, and early treatment is indicated.

The ability of dorsally placed lateral bands to extend the PIP joint is used in the method of closed treatment for this condition with a spring splint (the Capener splint) giving dynamic PIP extension while allowing active DIP flexion. This in turn helps to maintain the dorsal line of the lateral bands by tightening them. It is important that the splint selected is not tight, and the distal stems are short enough to allow DIP flexion (Figure 12.23.5). Splintage needs to be maintained for several weeks under the supervision of a therapist. Initially the joint is rested in extension in the splint, if necessary using a static volar splint until swelling has subsided to allow fitting of the dynamic splint. Then the patient is encouraged to start active flexion in the splint. Provided the treatment has been instituted early enough, migration of the lateral bands will be prevented and the torn tendon can heal without significant lengthening. If treatment is started too late, delayed reconstruction may become necessary. This is extremely difficult, and seldom gives entirely satisfactory results.

Various methods have been described, and involve either dorsal advancement and approximation of the lateral bands, use of a tendon graft, or a turnover procedure from the central extensor more proximally to secure reinsertion at the base of the middle phalanx. All methods should involve lengthening pf the extensor mechanism distal to the PIP joint. Support with a K-wire for 10 days is needed, and patients often experience stiffness, or recurrent deformity to some extent, or both. Physiotherapy and splintage may need to be continued for some time.

Skin loss associated with extensor tendon division presents a special problem, and soft-tissue repair, usually by local skin flaps, may be required as well as tendon repair.

There have been sporadic reports of closed sagittal band rupture causing extensor tendon subluxation at the MCP joint. This can happen at any age, but requires more force in the young, and can occur with very little force when tendons are weakened, as, for example, in rheumatoid arthritis. The mechanism is usually a blow on the dorsum of the hand, particularly the base of the finger, with a clenched fist. The sagittal band, usually on the radial side, gives way, allowing the extensor tendon to move in an ulnar direction (Figure 12.23.6). From the beginning there is loss of full power of extension at the MCP joint, and this tends to increase as the tendon slides further across. It may reach a point of equilibrium, or deterioration may continue until there is full loss of extension.

If the injury is recognized immediately, splintage may be enough to allow healing without extensor tendon subluxation. Later referral usually leads to the need for direct repair of the tear of the sagittal band.

Open laceration at this level can occur as the result of a sharp injury such as a knife, or contact with a tooth during a fight. A limited sharp injury may not initially cause much loss of extension because intact sagittal bands on either side can splint the ends together. However, they easily split, allowing the tendon ends to separate with extensor lag at the MCP joint. Lacerations in this area should be carefully explored for unexpected tendon injury. The tendon is repaired using a core stitch and running marginal stitch.

It is common for a tooth to penetrate the stretched skin over an MCP joint, usually of the middle finger, during a fight. Because all the tissues are stretched tight the tooth enters the joint, often causing delayed infection if appropriate action is not taken primarily. If the extensor tendon is in the path of the tooth it can also be divided. Because of the circumstances of the injury, the patient may not attend for treatment immediately. If he/she does, the wound should be explored, the joint irrigated and drained, and the central part of the tendon repaired if divided, under broad-spectrum antibiotic cover appropriate for oral flora. If treatment has been delayed and infection is developing, joint irrigation should be added to the regimen; tendon repair may be delayed if the infection is significant, and completed as a secondary procedure when infection has been eliminated.

The tendons are vulnerable to sharp injury throughout this area, but slightly less so at wrist joint level, being more deeply placed here, covered by the extensor retinaculum, and in the concavity of the joint in its neutral posture of slight extension. At the wrist, the tendons are more closely bunched together; therefore multiple tendon divisions are more likely than on the dorsum of the hand where they diverge.

The diagnosis is usually obvious from the posture of the fingers and the position of the laceration. Exploration usually requires extension of the original cut, and if that is oblique or transverse a zigzag design is best, taking into account the likely position of the divided tendon ends. When the injury is in the zone beneath the extensor retinaculum, it is necessary to reflect a section of the retinaculum to expose the appropriate compartment containing the injured tendons (see Figure 12.23.1). This is best done by lifting a flap based on one side or the other, rather than incising it longitudinally, which would allow bow-stringing. Extension is the usual posture of the wrist during contraction of the digital extensors, and so a pulley mechanism is needed.

When exploring multiple extensor tendon injuries it is important to identify and match individual tendons correctly, since slight differences of level of injury can create significant discrepancies in tension. Matching can be achieved by comparing the lengths of the tendons as they sit together, the direction and shape of each cut end, since they may vary in an identifiable way, and to some extent their position side by side, although this can be misleading as they can become transposed. Standard suture techniques are appropriate, such as the Kessler core stitch (4/0 non-absorbable braided polyester) and running 6/0 circumferential suture. Some extensor tendons are too flat to accommodate a three-dimensional suture such as this, and a simple mattress suture or continuous suture may be sufficient. Careful closure in layers of the surrounding gliding structures makes satisfactory excursion more likely. When treating more complex injuries, attention should be directed to the surface beneath the tendon as well as over it. Bone or fixation material must be separated from the repaired tendon, otherwise dense adhesion is very likely.

Wrist extensor tendons may be divided in deep lacerations in zone 7, always in association with division of more superficial tendons. Closed rupture occasionally occurs. Strong repair of the wrist extensors is essential for effective grip.

Following repair of a single extensor tendon, the hand and wrist are immobilized in extension. After 1 week the splint can be removed and the interphalangeal joints actively exercised under supervision. The splint is then replaced, but only extending to a point approximately 2.5cm distal to the MCP joint, so that some interphalangeal flexion is still possible. A further 3 weeks in this splint should allow tendon healing, and mobilization continues thereafter, under the care of a physiotherapist.

After primary repair of multiple extensor tendons, far superior results following early mobilization have been achieved with dynamic splintage (all excellent) as opposed to 40% excellent and 31% good following static splintage. Dynamic splintage can be started within days of repair.

It is not uncommon for EPL to rupture following Colles’ fracture, usually with little displacement. The EPL at the level of the distal radius is poorly vascularized, and vulnerable to disruption of what blood supply it has, perhaps combined with interference in synovial nutrition through haematoma. Tendon transfer is usually required, and either extensor indicis or a slip of abductor pollicis can be used.

Injuries to the dorsum of the hand involving extensive damage to or loss of soft tissue cover present additional problems. Usually when skin is lost, parts of the extensor tendons will be missing also, and injuries involving crushing may be associated with metacarpal fractures or even bone loss. Primary reconstruction is always the goal, and if it is not possible immediately should be accomplished within 5 days. Reconstruction is geared to the precise details of the injury, and after thorough debridement may involve skeletal fixation, tendon repair or grafting, and skin replacement usually by flap cover. If there is doubt about the extent of tissue damage or viability, or the patient is not fit, it may be reasonable to bring the patient back to the operating room for a second look and definitive reconstruction after 48h. Under most circumstances, however, primary reconstruction is generally thought to be preferable.

Tendon grafting is less commonly indicated in the extensor mechanism than in the flexor tendons. Loss of an individual extensor tendon can often be effectively treated by suture of the distal end to the side of a neighbouring tendon, since independent extensor tendon function is less important. Loss of multiple tendons may require grafting, however, and multiple tendon grafting material may be needed. Long extensor tendons of the toes can be used, with slight donor morbidity, or strips of fascia lata, with none. These can be threaded through subcutaneous fat of a flap at the time of skin replacement. A composite free flap of skin containing tendons and their gliding mechanisms can be used, the donor site being on the dorsum of the foot. The composite dorsalis pedis flap gives an excellent reconstruction, but some feel that the morbidity of this donor site is unacceptable. If it is carefully resurfaced with full-thickness skin and 100% take is achieved, donor morbidity is minimal.

If a skin defect combined with extensor tendon loss has been healed by free skin grafting, it may be possible to reinsert a tendon graft by creating a tunnel beneath or around the grafted area with a silicone rod. The rod is subsequently replaced by a tendon graft.

Under some circumstances loss of skin and extensor tendons with replacement by free skin grafting alone can result in some restoration of finger extension. This presumably occurs by a tenodesis effect, with some force transmitted through inelastic scar tissue. It cannot always be relied on, but if it fails, a more elaborate reconstructive procedure is available.

Adhesions following extensor tendon repair can be effectively treated by tenolysis. Before doing this, time should be allowed for full resolution of post-traumatic scar tissue, and maximum joint ranges should be achieved by the physiotherapist. Good skin cover is a requirement. The technique requires careful dissection of the tendons from their surrounding bed with preservation of some extensor retinaculum if possible. Early protected mobilization is essential.

Rupture of repaired extensor tendons is unusual, and should be treated by tendon transfer or grafting, according to the availability of reconstructive material.