An athlete’s hands are susceptible to a variety of acute and cumulative traumas depending on their chosen sport. Depending on the timing of the injury, the immediate requirements of the athlete, and future aspirations, treatment strategies may need individual customization. This article offers a brief review of the anatomy and complex function of the extensor mechanism, discusses the etiologies of various extensor injuries, and outlines the multiple treatment options and expected outcomes.
Extensor tendon injuries can be difficult to treat given the high demands and expectations of the athlete.
Delaying treatment until completion of a season is a viable option in certain circumstances.
Neglected mallet injuries in patients with hyperlax joints can lead to a swan neck deformity.
Boutonniere injuries and tendon lacerations should be definitively treated without delay whenever possible.
Tendinitis and overuse syndromes can often be treated conservatively.
Athletes are not only prone to sport-specific hand and wrist injuries but often have unique short- and long-term goals that often necessitate tailored treatment plans. The specific sport, position played, competition level, and future expectations and aspirations must all be considered as the consulting physician guides the athlete toward realistic and mutually acceptable treatment strategies. Definitive treatment postponement until after the current season or return to play with protective devices may be reasonable in certain circumstances. This approach should be applied in a more guarded manor in the skeletally immature athlete and avoided if long-term outcomes could be unacceptably compromised.
Muscles of the extensor system
The extensor tendons of the fingers and thumb are comprised of the extensor digitorum communis (EDC), extensor indicis proprius, extensor digiti minimi, extensor pollicis longs, and extensor pollicis brevis. Wrist extension is produced through functions of the extensor carpi radialis longus, extensor carpi radialis brevis, and extensor carpi ulnaris (ECU).
Dorsal wrist compartments
The musculotendinous junctions of the wrist and finger extensors lie several centimeters proximal to the wrist with the exception of the extensor indicis proprius, whose muscle belly frequently continues to the level of the wrist joint. At the level of the radial metaphysis, the tendons are separated into 6 synovial lined fibro-osseous sheaths ( Fig. 1 ), save the fifth, which has no osseous connections. The sixth extensor compartment is also unique as its subsheath is intimately involved with the dorsal aspect of the triangular fibrocartilage complex.
Juncturae tendinum and sagittal bands
Proximal to the metacarpophalangeal (MCP) joint are stout interconnections between the tendons of the EDC. These connections limit independent ring and middle finger extension when the other digits remained flexed. The sagittal bands are expansions over the extensor tendons at the level of the MCP, which originate from the volar plate and insert onto the extensor hood. The sagittal bands maintain the centralized position of the extensor tendons throughout the arc of motion and facilitate MCP extension by a lasso effect transmitted via the volar plate connections.
Anatomy of the extensor hood: Metacarpophalangeal to fingertip
The anatomy of the extensor system distal to the MCP joint is a complex system of converging and separating components that change position and geometry during flexion and extension of the digit, resulting in synergistic and balanced movement. The tendons of the lumbricals lie on the volar radial aspect of the proper digits and flex the MCP and extend the interphalangeal joints when activated. The interossei produce digital adduction/abduction and coalesce with the lumbricals to form the lateral bands. The lateral bands bifurcate and join the extrinsic extensor system at the level of the proximal phalanx. The EDC trifurcates just proximal to the proximal interphalangeal (PIP) joint. The central branch terminates as the central slip, which inserts on the base of the middle phalanx, and the lateral components join the lateral bands to form the conjoined lateral bands, which continue distally, eventually becoming the terminal tendon and inserting at the base of the distal phalanx ( Fig. 2 ).
The lateral bands exhibit some physiologic translation, but are maintained in their appropriate position by the balance of tension between the triangular ligament and the transverse retinacular ligament. The triangular ligament unites the lateral bands together on the distal dorsal aspect of the middle phalanx and prevents volar subluxation during PIP flexion, and the transverse retinacular ligaments constrain the lateral bands via their connections to the flexor tendon sheath to prevent excessive dorsal translocation.
The oblique retinacular ligament (ORL) originates from the volar sheath of the flexor system at the PIP joint and inserts dorsally into the terminal tendon. The ORL tightens during PIP extension, leading to concomitant extension of the distal interphalangeal (DIP). The importance and consistency of this structure has been debated in the literature.
Zones of injury
Extensor tendon injuries are classified from distal to proximal. Injuries overlying joints are given odd numbers: zone 1 over the DIP joint, 3 over the PIP joint, 5 over the MCP joint, and 7 over the wrist. The thumb is labeled differently so the interphalangeal joint is zone 1 and the MCP joint is zone 3. Injuries over nonarticulating segments are labeled with even numbers: zone 2 over the middle phalanx, 4 the proximal phalanx, 6 the metacarpals, and 8 in the forearm ( Fig. 3 ).
Zone One Mallet Finger Injury
The mallet, baseball, or droop finger indicates terminal tendon discontinuity and resultant extensor lag at the DIP joint. The mechanism of injury is most often forced flexion of an extended finger and failure can occur through the tendon itself or the distal phalanx. Offering a similar clinical presentation, forced hyperextension through the DIP joint can impact and fracture the dorsal articular surface resulting in a more severe fracture/dislocation injury pattern. Baseball/softball players are particularly susceptible to this injury when sliding into base with an outstretched hand. Similarly, being struck on the end of the finger by any ball (basketball, football, dodge ball, etc) can inflict the same injury.
Mallet injuries are easily identified based on the history of jamming the finger and the obvious inability to actively extend the DIP joint. Dorsal swelling, contusion, and pain with preserved passive motion are the hallmarks of the physical examination, although a much more benign presentation is not uncommon in the absence of bony involvement. Recognition of a hyperextensible corresponding PIP joint ( Fig. 4 ) may identify those patients prone to the more functionally significant compensatory swan neck deformity. Plain radiographs of the finger will be normal in the setting of isolated soft tissue injury. Attention should be focused on the amount of articular disruption and the presence of volar subluxation on those with bony involvement.
Acute mallet finger injury
Depending on the desires of the athlete and perhaps the point in the season in which the injury occurs, 3 treatment options include temporary benign neglect, full-time extension splinting, or temporary percutaneous DIP pinning (with or without continued play).
Late presentation soft tissue mallet injuries can still be treated successfully. Splinting acute and chronic mallet fingers within 3 to 4 months achieved restoration of DIP extension and a residual extensor lag of less than 10° noted in 1 study. An athlete could reasonably opt to complete their season without the hindrance of a restrictive splint or invasive surgery, although they should be made aware that, intuitively, the greater the delay in treatment, the less likely a full restoration of function. Particularly in athletes with hyperlaxity, the development of a swan neck deformity resulting from focused tension at the central slip insertion is a real possibility. Swan neck posturing may be substantially more debilitating than a mallet finger with painful snapping as the PIP moves from the hyperextended to flexed position, loss of dexterity, and loss of grip strength. Additionally, surgical correction of both the DIP extensor lag and PIP hyperextension may be necessary if this sequelae of mallet undertreatment develops.
Extension splinting is the preferred treatment in nonathletes and compliant athletes, which offers predictable outcomes without the inherent risks of surgery. The DIP joint is held in full extension with the PIP joint left free of immobilization unless substantial laxity is noted. Bony involvement of 30% to 40% of the articular surface can still be effectively treated in a similar manner with satisfactory results at 2 years. Athletes can return to sport immediately if the splint wear can be tolerated during competition. Of the many different methods of immobilization described, none have shown superiority, so splint choice should be based on comfort and compatibility with return to play. , Alternating between 2 different style splints can alleviate dorsal skin maceration from perspiration. One useful technique is the use of a combination of kinesiotape in association with the orthosis to assist in maintaining the DIP in extension. After 6 to 8 weeks of full-time splinting, the patient is weaned to 6 weeks of night splinting. PIP hyperextension addressed by extending the splint proximally to maintain the PIP joint in slight flexion could further hinder athletic participation. A slight post-treatment residual extension lag is not uncommon or unexpected, considering that as little as 0.5 mm lengthening can lead to a 10° extension lag. Despite this, with proper compliance, a more substantial deficit is rare, , and return to previous levels of competition can be anticipated. For less compliant patients, Crawford noted a 20% incidence of a potentially bothersome deformity greater than 10°.
Surgical indications for the treatment of an acute mallet finger in an athlete include fracture fragments of greater than 40% of the articular surface with volar subluxation of the distal phalanx, or inability to adhere to full-time splinting therapy despite a desire for acute treatment and rapid return to play.
Simple mallet finger injuries, soft tissue or bony without subluxation, can be treated with transarticular Kirschner wire placement yielding expected postoperative mobility ranging from approximately 5° from full extension to 65° to 80° of flexion. The wire, typically a 0.062-inch Kirshner wire (if continued athletic participation is planned), is placed in a retrograde fashion, obliquely across the DIP joint and cut beneath the skin for removal in 6 to 8 weeks, followed by 6 additional weeks of night splinting. Continued splint wear is recommended during competition for fear of hardware failure. By placing the wire in an oblique manner, should it break, it can be readily retrieved.
Bony mallet injuries with volar subluxation generally require surgical treatment by one of several different options, including extension block pinning. Some authors believe that these large fragments can be treated in an analogous fashion to simpler mallet injuries with no increased morbidity other than a dorsal bump. Postoperatively, however, the exposed dorsal Kirschner wire’s susceptibility to infection (around 14% incidence ) or migration complicates immediate return to sport, a minimal extension lag of less than 5° and near normal flexion can be expected.
Chronic mallet finger injury
A chronic mallet finger or secondary swan neck deformity may result from a neglected or underappreciated injury. Although defined as an injury more than 4 weeks old, the guidelines for acute treatment can be applied for up to 4 months after injury. , Older injuries affecting only the DIP joint are often well-tolerated and surgical intervention is often not desired. Secondary swan neck deformity from proximal tendon retraction and dorsal subluxation of the lateral bands, in contrast, is poorly tolerated during competition.
ORL reconstruction , or central slip (Fowler) tenotomy are the 2 primary reconstructive surgeries. Central slip tenotomy is the simpler of the 2 procedures, but is only effective with mild deformities involving less than 30° extension lag at the DIP joint and less than 20° hyperextension at the PIP joint. The central slip is released just proximal to the PIP joint allowing proximal migration of the extensor mechanism and reestablishment of tension at the attenuated terminal slip assuming that the healed pseudotendon has matured and is stable—typically around 6 months. ORL reconstruction, in contrast, can reliably correct swan neck deformities with more severe PIP hyperextension and an average of 42° of DIP extensor lag.
Oblique retinacular ligament reconstruction technique
A curvilinear incision is made on the dorsum of the finger extending from the MCP to the insertion of the terminal tendon. The ulnar lateral band is chosen to preserve the radially based lumbrical. The lateral band is isolated and divided at the level of the MCP joint. A plane is developed at the level of the PIP joint deep to the neurovascular bundle but volar to the flexor tendon sheath and the isolated lateral band is shuttled from an ulnar to radial direction. A 2-mm unicortical hole is drilled in the proximal phalanx shaft and diverging Keith needles are driven across the far cortex and used to pull the tendon into the bone ( Fig. 5 ). While securing the tendon in place, tension should be pulled until a position of 30° of flexion across the PIP joint and extension across the DIP is obtained. Sutures through the tendon stump can now be secured down over the far cortex bony bridge. A retrograde 0.045 Kirschner wire is then placed across the DIP joint. Postoperatively, gentle range of motion of the PIP joint from 30° to 60° of flexion can be initiated at 3 weeks, and the Kirschner wire across the DIP joint is left in place for 6 weeks ( Fig. 6 ).
Zones 2, 4, and 6 Extensor Tendon Injuries
Zones 2, 4, and 6 injuries are due to open trauma involving 1 or both lateral bands and/or the triangular ligament, central slip, or EDC tendon, respectively. In the athletic population these are uncommon injuries but still occur from cleats or skates that could potentially lacerate the hand.
Clinical evaluation and treatment
The initial evaluation should always assess contamination and risk of infection and include formal debridement as indicated. For zones 2 and 4 injuries if full extension against resistance is preserved or if the injury involves less than 50% of the tendon, the athlete can return to activity with buddy taping for 3 to 4 weeks, although the digit should be monitored for delayed extensor lag. ,
A zone 2 partial laceration with loss of active extension, complete laceration, or developing extensor lag can be directly repaired with equivalent results of an acute mallet finger. If immediate repair is undertaken, protection with DIP pinning will allow early return to play if an extended DIP position can be tolerated during competition.
For zone 6 injuries, partial active extension may still be possible via the junctura and the examiner should maintain a high index of suspicion. A complete zone 4 or 6 injury should be treated with immediate direct surgical repair. Our preferred technique is a running interlocking horizontal mattress repair with a 4-0 nonabsorbable braided stich as described by Lee and colleagues ( Fig. 7 ). This technique is easy and quick and has been shown to be stiffer while minimizing tendon shortening compared with other more complex patterns. Unfortunately, delayed presentation or treatment is not amenable to direct repair and will require more complex reconstructive options.