Muscles

The extensor tendons originate from the finger extensor muscle bellies of the extensor digitorum communis (EDC), extensor indicis proprius (EIP), extensor pollicis longus (EPL), extensor digiti minimi (EDM), abductor pollicis longus (APL), and extensor pollicis brevis (EPB); the radial wrist extensor muscle bellies of the extensor carpi radialis longus and brevis (ECRL and ECRB); and the extensor carpi ulnaris (ECU). All of these muscles are innervated by branches from either the radial nerve or the posterior interosseous nerve.

Anatomic Variations of Extensor Muscles

Wrist Extensors.

The most common anatomic variations are accessory muscles and tendons associated with the wrist extensors. The extensor carpi radialis intermedius, reported to be found in 12% of limbs, may arise superficial and radial to or between the ECRL and ECRB. The significance of this accessory muscle is that it may be harvested for use as a tendon transfer in paralytic disorders when donor muscles are lacking. Anomalous tendons originating from the radial wrist extensors have been described inserting on the index or middle metacarpal base. These accessory tendons and interconnections may need to be released during tendon transfer procedures to achieve full excursion.

Finger Extensors.

The extensor medii proprius can be considered to be an EIP of the middle finger, found in 10% of hands, and has recently been used in reconstruction of chronic sagittal band injuries. The insertion is typically ulnar to the EDC insertion on the middle finger, as is the usual arrangement of the EIP with respect to the EDC index tendon and the EDM with respect to the small finger EDC tendon. The extensor indicis et medii communis is a variation of the EIP that inserts into the middle and index fingers.

The extensor digitorum brevis manus muscle (EDBM) is an anomalous muscle on the dorsum of the hand, found in 3% of hands, usually arising between the index and middle finger metacarpals and inserting on the extensor hood of the index or middle fingers with or without anomalies of the EIP. Ogura and associates described five types of EDBMs, depending on the insertion and relationship to the EIP. The clinical significance of the EDBM is that it can be mistaken for a dorsal wrist ganglion cyst; it becomes firm when the wrist is slightly flexed and the fingers are extended. It may also be a source of dorsal wrist pain and can be completely excised if needed ( Figure 5.1 ).

Extensor digitorum brevis manus (EDBM) muscle. Extension of the fingers increases the prominence of this anomalous muscle.

Tendons at the Wrist Level

The musculotendinous junction is usually approximately 4 cm proximal to the wrist joint, although muscle fibers of the EIP often continue to the wrist joint level. At the level of the wrist, the tendons course through six individual, synovial-lined, fibroosseous sheaths, known as the six extensor tendon compartments ( Figure 5.2, A ). The fifth extensor compartment is technically a fibrous tunnel only because it does not insert on bone. The sixth extensor tendon compartment, containing the ECU tendon, has a subsheath that maintains the relationship of the tendon to the underlying ulna, and rupture or injury of this subsheath may result in symptomatic ECU tendon subluxation ( Figure 5.3 andVideo 5.1 ). ( Case Study 5.1 ; also see Chapter 13 .)

A, Extensor tendons gain entrance into the hand from the forearm through a series of six canals, five fibroosseous canals and one fibrous canal (the fifth dorsal compartment, which contains the EDM). The first compartment contains the APL and EPB; the second, radial wrist extensors; the third, the EPL, which angles around the Lister tubercle; the fourth, the EDC to the fingers and EIP; the fifth, the EDM; and the sixth, the ECU. The communis tendons are joined distally near the MP joints by fibrous interconnections called juncturae tendinum. These juncturae are found only between the communis tendons and may aid in surgical recognition of the proprius tendon of the index finger. The proprius tendons are usually positioned to the ulnar side of the adjacent communis tendons, but variations may be present that alter this arrangement (see text discussion). Beneath the retinaculum, the extensor tendons are covered with a synovial sheath. B , Proprius tendons to the index and little fingers are capable of independent extension, and their function may be evaluated as depicted. With the middle and ring fingers flexed into the palm, the proprius tendons can extend the ring and little fingers. Independent extension of the index finger is not always lost after transfer of the indicis proprius, however, and is less likely to be lost if the extensor hood is not injured; and is probably never lost if the hood is preserved and the junctura tendinum between the index and middle fingers is excised. This figure represents the usual anatomic arrangement found over the wrist and hand, but variations are common, and the reader is referred to the section on anatomic variations.

(Copyright Elizabeth Martin.)

ECU lies in a separate fibroosseous tunnel, or subsheath. The extensor retinaculum lies superficial to and does not attach to the ulna but swings around and attaches to the pisiform and triquetrum.

(From Spinner M, Kaplan EB: Extensor carpi ulnaris: its relationship to the stability of the distal radio-ulnar joint, Clin Orthop Relat Res 68:124, 1970. Copyright Elizabeth Martin.)

Juncturae Tendinum

Proximal to the metacarpophalangeal (MP) joint level, stout interconnecting bands exist between the ring EDC and the small and middle fingers, and there is a less substantial band from the middle to the index finger. The importance of these juncturae tendinum is that finger extension can be preserved if the EDC is lacerated proximal to a junctura tendinum that connects that finger to an intact extensor tendon. The juncturae tendinum also restrict independent extension of the ring and middle fingers when the other digits are flexed at the MP joints. Varying morphologic views of juncturae tendinum have been described by Hirai and colleagues (see Figure 5.2 ).

Extensor Digitorum Communis Insertion

The mechanism by which extension of the MP joint is achieved by the pull of EDC tendons is not related to a direct insertion of the tendon on the base of the proximal phalanx. Van Sint Jan and colleagues showed that although there is a “central slip” on the base of the middle phalanx, there is no such structure on the base of the proximal phalanx. Instead, there is loose connective tissue between the EDC and the base of the proximal phalanx. Extension of the MP joint is transmitted by the pull of the EDC tendon through the sagittal bands ( Figure 5.4 ). When the sagittal band system is damaged, and the EDC tendon subluxates or dislocates off the central axis of the finger, MP joint extension is compromised.

A , EDC allows extension of MP joint via insertion onto the sagittal bands, which “lasso” around the base of the proximal phalanx. There is usually no tendinous insertion of EDC to the dorsal base of the proximal phalanx. When MP joint hyperextension is prevented, EDC is capable of extending MP, PIP, and DIP joints even in the absence of intrinsic muscle function. B , When MP joint hyperextension is allowed, as with intrinsic paralysis, “slack” develops in EDC system distal to the sagittal bands, in addition to increased tone in the flexor system, all producing a flexion posture at the PIP and DIP joints, or claw finger.

Anatomy of the Extensor Mechanism Over the Proximal Phalanx

The anatomy of the extensor mechanism is an intricate and layered system that changes geometry as the finger flexes and extends, allowing the lateral bands to displace volarly in flexion and return to the dorsum of the finger in extension. The intrinsic tendons from the lumbricals and interossei form the lateral bands, which join the extensor mechanism at the proximal third of the proximal phalanx. The lumbrical muscle functions both to flex the MP joint and to extend the IP joints owing to its insertion on the lateral band. The lumbrical also contracts during IP and MP extension in order to “relax” the profundus tendon by pulling it distally through its proximal origin from the FDP. The EDC trifurcates proximal to the proximal interphalangeal (PIP) joint, with the central component becoming the central slip and the lateral components joining up with the lateral bands. These conjoined lateral bands coalesce over the middle phalanx and continue distally to become the terminal tendon ( Figure 5.5 ).

A and B , Extensor tendon at MP joint level is held in place by the transverse lamina or sagittal band, which tethers and centers the extensor tendons over the joint. This sagittal band arises from the volar plate and the intermetacarpal ligaments at the neck of the metacarpals. Any injury to this extensor hood or expansion may result in subluxation or dislocation of the extensor tendon. Intrinsic tendons from lumbrical and interosseous muscles join the extensor mechanism at about the level of the proximal portion and midportion of the proximal phalanx and continue distally to the DIP joint of the finger. Extensor mechanism at PIP joint is best described as a trifurcation of the extensor tendon into the central slip, which attaches to the dorsal base of the middle phalanx, and the two lateral bands. These lateral bands continue distally to insert at the dorsal base of the distal phalanx. Extensor mechanism is maintained in place over PIP joint by transverse retinacular ligaments.

(Copyright Elizabeth Martin.)

Anatomy of the Extensor Mechanism Over the Middle Phalanx

The lateral bands are maintained in position by the triangular ligament, which unites them dorsal and distal to the PIP joint, and the transverse retinacular ligaments, which stabilize them to the flexor tendon sheath. The primary function of the triangular ligament is to prevent palmar subluxation of the lateral bands during PIP joint flexion, which can occur in the boutonnière deformity as a result of triangular ligament incompetence. The primary function of the transverse retinacular ligament is to prevent dorsal subluxation of the lateral bands during extension, as can occur in a swan neck deformity. There is a normal dorsal-palmar translation of the lateral bands with respect to the PIP joint axis of rotation during flexion and extension, which must be preserved to retain normal extensor function. The central slip insertion on the base of the middle phalanx helps to initiate extension of the PIP joint; however, PIP joint extension is possible even in the absence of the central slip, provided that the triangular ligament, lateral bands, and transverse retinacular ligaments are functioning normally ( Figures 5.6 and 5.7 ). Distal to the triangular ligament, the lateral bands converge to form the terminal tendon, which inserts onto the base of the distal phalanx. The germinal nail matrix, which creates the nail plate, arises approximately 1.2 mm distal to the terminal tendon insertion.

A , Illustration of extensor mechanism at PIP joint level. B , Cadaver finger dissection showing probe beneath transverse retinacular ligament at level of PIP joint.

( A , From Yu HL, Chase RA, Strauch B, editors: Atlas of Hand Anatomy and Clinical Implications, St Louis, 2004, Mosby, p 343. Redrawn by Elizabeth Martin.)

A , Triangular ligament. B , Cadaver triangular ligament.

( A , Copyright Elizabeth Martin.)

Extension of the Fingers

Extension of the fingers at the MP joint is exclusively a function of the extrinsic extensor tendons. Extension of the PIP joints, although primarily a function of the intrinsic interossei and lumbrical muscles, can also occur through the extrinsic tendon extensor system, provided that MP joint hyperextension is blocked. When intrinsic palsy allows the MP joint to hyperextend, the extrinsic extensor system becomes insufficient to extend the interphalangeal (IP) joints, and a “claw finger” results. This deformity occurs because of “slack” in the extensor mechanism distal to the sagittal bands and the increased flexor tone in this position (see Figure 5.4 ).

Extension at the MP joint is possible regardless of the position of flexion of the PIP and distal interphalangeal (DIP) joints, so the “intrinsic plus” and “hook grip” are both tenable positions. It is physically impossible, under normal circumstances, to extend or flex the PIP and DIP joints independent of one another (i.e., to extend the PIP joint without simultaneously extending the DIP joint). Only in individuals who can voluntarily or involuntarily lock their PIP joints in hyperextension or when the PIP joint is passively held in full extension, can DIP joint flexion be accomplished independently using the flexor digitorum profundus tendon.

Testing the Anatomic Integrity of the Central Slip: Elson Test

When the PIP joint is passively flexed completely, the central slip insertion is pulled distally along with its proximal attachments, and “slack” is created between the lateral band insertions on the terminal tendon and the lateral connections of the central slip to the lateral band. This slack can be easily appreciated by manually assessing the resistance to passive flexion of the DIP joint with the PIP joint fully extended versus fully flexed. This elegant mechanism permits full flexion of the DIP joint when the PIP joint is maximally flexed ( Figure 5.8, A and B ). A corollary is that active extension of the DIP joint becomes impossible when the PIP joint is fully flexed because of the slack in the lateral bands (see Figure 5.8, C and D ).

A , Maximal passive PIP joint extension prohibits full DIP joint flexion by normal tension in lateral bands. B , Full PIP joint flexion allows slack in the lateral bands, permitting full DIP joint flexion. C , Maximal passive flexion of PIP joint induces slack in the lateral bands via proximal interconnections, resulting in loss of power of active DIP joint extension and increased DIP joint flexion. D , Finger maximally flexed prohibits any ability to extend DIP joint actively. E , Injury to central slip eliminates the slack in the lateral bands produced by passive PIP joint flexion and allows extensor tension to be generated at DIP joint. This is the basis for the Elson test. F , With central slip injury, DIP joint can be actively extended with maximum PIP joint flexion.

When the central slip is injured or incompetent, it is possible to generate extensor force at the DIP joint with maximal passive PIP joint flexion, which is the basis of the Elson test for detecting acute central slip rupture. As described by Elson, the examiner passively flexes the PIP joint to 90 degrees over a tabletop and asks the patient to attempt active extension of the PIP joint while the examiner resists PIP joint extension. When acute rupture of the central slip occurs, no extension power is felt at the PIP joint but significant extension power, or hyperextension, is produced at the DIP joint. This test has been found to be the most sensitive physical examination test to detect acute central slip rupture.

In practice, I find that the Elson test is best performed under a digital block to eliminate any pain that may arise from a concomitant injury to the PIP joint. The hand is supinated, and the examiner passively maximally flexes the injured PIP joint with one hand and then asks the patient to attempt PIP joint extension as the examiner assesses extension force at the DIP joint by gently flexing the DIP joint with the other hand. If the examiner feels DIP joint extension with force compared with the adjacent or contralateral noninjured digits held in the same position, the central slip is incompetent. Boyes described another test for central slip integrity in 1970, in which the PIP joint is held in extension while the examiner assesses resistance to passive DIP joint flexion. This test is not helpful in acute situations, and it becomes positive only as a boutonnière deformity develops because of chronic retraction of the lateral bands.

Oblique Retinacular Ligament

Landsmeer described the oblique retinacular ligament (ORL) (also termed the Landsmeer ligament ) as originating from the flexor sheath at the volar aspect of the PIP joint and inserting dorsally into the terminal tendon (see Figure 5.5 ). The ORL theoretically tightens with extension of the PIP joint and extends the DIP joint during PIP joint extension. The existence and function of the ORL have been the subject of debate. Shrewsbury and Johnson showed that it is present less than 50% of the time except on the ulnar side of the ring finger, where it is found more than 90% of the time. Excision of the ORL has not been shown to cause an extensor deficit at the DIP joint.

An alternative explanation to Landsmeer’s theory is that the collateral ligaments of the DIP joint alone can account for the “spring back” tendency of the DIP joint in the absence of an ORL. Shrewsbury and Johnson noted that a complete extensor lag does not occur when the terminal tendon is intentionally sectioned, as in the treatment of the DIP joint hyperextension posture of a boutonnière deformity. In practice, identification and preservation of the ORL, if present, would be prudent. Shrewsbury and Johnson believed the presence of a functioning terminal tendon alone is sufficient to account for full extension of the DIP joint, and that the ORL was of no practical functional importance. Ueba and colleagues found the ORL present in 38 of 40 cadaver fingers in an anatomic and biomechanical study; the ORL contributed up to 30% of passive resistance to DIP joint flexion, with a maximum at 30 degrees of PIP joint flexion. Regardless of its presence or absence, the concept of the ORL is useful in surgically creating a passive tendon “checkrein” to enable simultaneous DIP and PIP joint extension in the setting of a chronic mallet finger.

Suture Repair Techniques

There are few published studies on the strength of various suture techniques for extensor tendon injuries compared with the plethora of studies concerning flexor tendon repair techniques. One problem concerns the variability in the thickness of the extensor tendon as it changes from proximal to distal. Proximally, at the forearm and wrist level, the tendons are thicker and more capable of holding core sutures, and at the finger level, the tendons become broader but quite thin, and are incapable of holding standard core sutures. Doyle measured the thickness of the extensor mechanism in the fingers to be within a range of 1.75 mm in zone 6 (dorsal hand) to 0.65 mm at zone 1. A similar range was found at the thumb level.

In 1992, Newport and Williams found the Kleinert modification of the Bunnell repair to be the strongest technique in a cadaver study of zone 6 extensor tendon repairs performed with 4-0 polypropylene (Prolene) suture material. In 1995, Newport and coworkers reported that the Kleinert-modified Bunnell technique and the modified Kessler techniques were the strongest techniques for zone 4 injuries, and were suitable for dynamic or active range of motion under controlled conditions and in short arcs.

In 1997, Howard and colleagues compared the MGH, modified Bunnell, and modified Krackow-Thomas repairs in cadaveric zone 6 extensor tendon lacerations and found the MGH technique to be superior. In a 2005 study of zone 4 extensor tendon repairs with 4-0 nonabsorbable, braided polyester (Ticron) suture, Woo and coworkers found the modified Becker technique to be the strongest repair, with a significantly greater resistance to a 1- and 2-mm gap and the greatest ultimate strength. Lee and colleagues compared the augmented Becker technique, the modified Bunnell technique, and a new, running interlocking horizontal mattress technique and found the newer technique to be stiffer, to produce less shortening, and to be faster to accomplish than the other techniques, without a significant difference in the ultimate load to failure. This newer technique, termed the corset suture, does not require the placement of core sutures and was found to have good to excellent clinical results in a study of zones 4 and 5 extensor tendon lacerations ( Figure 5.10 ).

A , Modified Bunnell suture was the strongest suture with the least loss of MP or PIP joint motion. B , Schematic representation of four-strand MGH, modified Bunnell, and modified Krackow-Thomas repairs. C , Starting running suture of corset suture. This suture configuration was evaluated in zone 6 but may be used in any zone. It does not employ any core sutures. D , Initiating the interlocking horizontal mattress suture. E , Completed running interlocking horizontal mattress suture.

( A, From Newport ML, Williams CD: Biomechanical characteristics of extensor tendon suture techniques. J Hand Surg Am 17:111 – 119, 1992, with permission from The American Society for Surgery of the Hand; B, From Howard RF, Ondrovic L, Greenwald DP: Biomechanical analysis of four-strand extensor tendon repair techniques. J Hand Surg Am 22:838–842, 1997, with permission from The American Society for Surgery of the Hand; C to E, From Lee SK, Dubey A, Kim BH, et al: A biomechanical study of extensor tendon repair methods: introduction to the running-interlocking horizontal mattress extensor tendon repair. J Hand Surg Am 35:19–23, 2010, with permission from The American Society for Surgery of the Hand.)

Doyle proposed the following techniques for extensor tendon repair:

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  Zone 1 (DIP joint): Running suture incorporating skin and tendon.

  
  
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  Zone 2 (middle phalanx): Running 5-0 stitch near cut edge of tendon, completed with a “basket-weave” or “Chinese finger trap” type of cross-stitch on the dorsal surface of the tendon ( Figure 5.11 ).

  
  

  
  

  
  

  

  
  

  
  

  Relatively thin extensor tendon just proximal to DIP joint can be repaired with this technique. A , Sharp laceration in zone 2 of the extensor tendon. B and C , Laceration repaired with a running suture ( B ) and oversewn with a Silfverskiöld cross-stitch ( C ).

  
  
  
  
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  Zones 3 through 5 in fingers, and zones 2 and 3 in thumb: Modified Kessler suture of 4-0 synthetic material in the thickest portion of the tendon. A 5-0 cross-stitch tied to itself at the beginning and end is run on the dorsal surface of the tendon ( Figures 5.12, 5.13, and 5.14 ).

  
  

  
  

  
  

  

  
  

  
  

  Doyle’s preferred technique for repair of zone 3 lacerations. A to C , Central slip laceration with sufficient tendon to repair with core suture and oversew with Silfverskiöld epitendinous stitch. D to F, Core stitch can be passed through trough in the base of the middle phalanx when the tendon laceration is distal, leaving a small stump of central slip.

  
  

  
  

  
  

  

  
  

  
  

  The author’s recommended technique for suture of zone 4 extensor tendon injuries. A , Modified Kessler suture is centered over the laceration and tied with suitable tension to avoid gapping or undue shortening of the tendon. The distance between longitudinal components of the suture is adjusted to avoid side-to-side “bunching” or shortening. Alternatively, two modified Kessler core sutures may be placed to avoid bunching of the repair. The relative increased thickness of lateral bands is used for placement of the longitudinal portions of the suture to obtain maximal holding power. B , The suture is “finished” with a cross-stitch to augment the repair further. This repair is well suited to the curvature of the extensor tendon over the proximal phalanx and the relative thinness of the tendon.

  
  

  (Copyright Elizabeth Martin.)

  
  

  
  

  
  

  

  
  

  
  

  Lacerations over MP joint (zone 5) are in a region of increased thickness and substance compared with the extensor tendon mechanism distally. A and B , The author’s preferred technique for repair of lacerations in this zone includes the modified Kessler ( A ), followed by the cross-stitch ( B ).

  
  

  (Copyright Elizabeth Martin.)

  
  
  
  
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  Zones 6 and 7: Same as for zones 3 through 5, except the cross-stitch is run around the entire circumference of the tendon, if feasible.

Author’s Preferred Treatment

I agree with Doyle’s recommendations except that I usually use two modified Kessler core suture repairs for zones 3 through 5 complete tendon lacerations, on either side of the tendon, to avoid “bunching up” of the tendon. For zone 1 injuries, I do a running suture of 5-0 polypropylene supplemented by a transarticular Kirschner wire in full extension for 6 weeks, instead of a “roll” suture incorporating skin and tendon; sometimes I will use several interrupted and buried figure-of-eight 5-0 polypropylene sutures to anatomically reapproximate the tendon in zones 1 to 4, if the tendon laceration is jagged.

Postoperative Management

The traditional postoperative program for extensor tendon repairs in zones 1 and 2 is 6 weeks of immobilization with either splint or Kirschner wire fixation of the DIP joint, and this generally remains the preferred regimen. Zones 3 through 5 repairs have historically been protected with the wrist in 40 degrees of extension, slight flexion at the MP joint, and extension at the PIP joints for 4 weeks. Zones 6 and 7 repairs have usually been managed with similar wrist and MP joint extension, allowing full active motion at the IP joints for 4 weeks. As in the rehabilitation of flexor tendon injuries, the main concern after repair is to maintain the integrity of the repair while limiting adhesion formation. The concept of early protected range of motion has been investigated for extensor tendon injuries, as it has been for flexor tendon injuries.

The ideal candidate for early range of motion (dynamic splinting) is a motivated patient with a complex injury involving more than one structure (e.g., tendon, bone, nerve). The concept of early passive motion for extensor tendon rehabilitation is that by moving joints through a controlled arc of motion, extensor tendon gliding of 3 to 5 mm may limit adhesion formation. Evans and Burkhalter found that 30 degrees of MP joint flexion created 5 mm of EDC glide in zones 5 through 7. The EPL glides approximately 5 mm at the Lister tubercle with 60 degrees of thumb IP joint flexion. The Evans and Burkhalter method of postoperative rehabilitation for extensor tendon repair in zones 5 through 7 starts with dynamic splinting 3 days postoperatively to allow MP joint flexion to about 30 degrees, keeping the wrist in 45 degrees of extension. Dynamic splinting involves passive joint extension with a dynamic outrigger device, with flexion limited by the confines of the palmar splint (see Figure 5.27 ). Controlled active mobilization involves active joint extension, limiting joint flexion with a palmar splint. Short arc motion protocol involves passive extension splinting with intermittent, splint-assisted passive flexion and active extension. Table 5.1 summarizes studies done on various postoperative splinting protocols.

Outcomes

In 1942, Miller suggested criteria for assessing extensor tendon repair outcomes, which were later endorsed by Newport and associates ( Table 5.2 ). This rating system takes into account extension lag and loss of flexion secondary to extensor adhesions and stiffness in terms of total active motion. In 1990, Newport and colleagues reported on the long-term results of extensor tendon repair treated with static splinting. Of patients without associated injury, 64% achieved good or excellent results, whereas only 45% of patients with associated injuries achieved good or excellent results. More fingers lost the ability to flex fully than lost the ability to extend. Injuries in zones 1 through 4 had a worse outcome than injuries in the more proximal zones. Fair or poor results were found in 7 of 12 zone 1 injuries, 6 of 6 zone 2 injuries, 10 of 14 zone 3 injuries, and 4 of 7 zone 4 injuries. These injury zones were associated with total extensor lags of the PIP and DIP joints of 11 to 45 degrees or more, and loss of flexion of 21 to 45 degrees or more. Zones 5 through 7 usually regained approximately 80% or more of normal motion. In a prospective randomized trial of dynamic versus static splinting for uncomplicated zones 5 and 6 lacerations, Mowlavi and coworkers found total active motion of 250 degrees for both groups at 6-month follow-up, with grip strength of 80% of normal in the dynamic group and 73% of normal in the static group. A systematic review of the literature in 2012 noted that both static and early motion protocols resulted in favorable results, but neither technique could be shown to be superior owing to variability in outcome measure reporting.

I employ dynamic splinting and controlled active motion for extensor tendon injuries in zones 4 through 7 in compliant patients, or when multiple structures are involved in certain patients with injuries in zones 2 and 3. There is no level I evidence that accelerated rehabilitation confers any long-term advantage in outcome over static splinting.

Complications After Extensor Tendon Repair

Adhesions are the most frequent complication of extensor tendon repair and can cause an extension lag and loss of flexion. An extensor tenolysis may be considered if, after 6 months, progress is considered to be unsatisfactory by the patient. Tenolysis of the extensor mechanism over the hand and finger may require concomitant joint releases and flexor tenolysis, either simultaneously or in a staged fashion. In the ideal situation, full passive motion should be present before tenolysis because this implies that there are no secondary capsular or ligamentous contractures. Lack of full passive motion after an appropriate course of therapy is not a contraindication to surgery, but the patient should be aware of the diminished expectations when joint release and mobilization are necessary. Creighton and Steichen reported the results of tenolysis after fracture and found only a 31% improvement in total active motion overall, 50% improvement in extensor lag if only a tenolysis was required, and 21% improvement in total active motion if a dorsal capsulotomy was required with no improvement of the active extensor lag.

Acute Mallet Finger Injury (Zone 1: Distal Interphalangeal Joint Level) ( Case Study 5.2 )

Case Study 5.2

A 45-year-old woman is kicked by a horse. Her left small finger DIP joint is subluxated volarly and deviated radially ( eFigure 5.1, A and B ).

The injury is not passively correctable. There is a “springy” feel when full extension of the joint is attempted.

Surgical exploration includes:

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  Ulnar collateral ligament of DIP joint torn and flipped into joint

  
  
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  Extensor mechanism torn 90% from ulnar to radial ( eFigure 5.2 )

  
  
  
  

  
  

  
  

  

  
  

Treatment:

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  Interposed ligament extracted and repaired

  
  
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  DIP joint pinned in neutral

  
  
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  Extensor mechanism repaired with interrupted 5-0 polypropylene sutures

  
  
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  Pins removed 6 weeks postoperatively ( eFigure 5.3 )

  
  
  
  

  
  

  
  

  

  
  

Outcome at 1 year postoperatively:

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  10-degree extensor lag

  
  
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  Full flexion

Mallet finger injury is characterized by discontinuity of the terminal extensor tendon resulting in an extensor lag at the DIP joint with or without compensatory hyperextension at the PIP joint ( swan neck deformity ). The injury has also been termed drop finger or baseball finger . Mallet fingers are classically described as “soft tissue” (tendon rupture) or “bony” (avulsed fragment of bone). For a seemingly simple injury, a lengthy, tedious treatment course is often required to obtain a satisfactory result. Poor outcomes are not unusual and can be a considerable source of frustration for the patient and the surgeon.

Classification

Doyle has classified mallet finger deformities as four types ( Table 5.3 ). The most common injury is type I. Patients presenting within 4 weeks of injury are considered to have acute injuries; patients presenting later than 4 weeks are considered to have chronic injuries. X-rays are always recommended for mallet injuries to assess for fractures.

TABLE 5.3

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