Extensor tendon injuries in athletes.

REVIEW ARTICLE

Extensor Tendon Injuries in Athletes Aakash Chauhan, MD, MBA,* Bruce Jacobs, OTR/L,w Alexandra Andoga, BS,z and Mark E. Baratz, MDz

Abstract: Extensor tendon injuries of the hand and wrist in highlevel athletes can cause a delay in return to play and permanently affect their performance. Given the inherent demand for a speedy and complete recovery, orthopedic surgeons must have an understanding of how to best direct an athlete’s treatment for these injuries. The extensor anatomy is very intricate and a thorough understanding of the anatomy can help with both diagnosis and treatment. However, untreated or poorly managed injuries are at risk of leading to chronic deformities. We will discuss the diagnosis and management of the most common extensor tendon injuries and tendinopathies of the hand found in athletes: mallet fingers, swanneck deformities, boutonniere deformities, central slip ruptures, sagittal band ruptures, intersection syndrome, extensor carpi ulnaris tendinitis, and extensor carpi ulnaris subluxation. Key Words: extensor tendon injury, mallet finger, boutonniere deformity, swan-neck deformity, central slip rupture, sagittal band rupture, extensor tendinopathy, intersection syndrome, ECU tendon subluxation, ECU tendinitis

(Sports Med Arthrosc Rev 2014;22:45–55)

EXTENSOR TENDON ANATOMY OVERVIEW A complete understanding of the extensor anatomy of the hand and forearm can aid in the diagnosis and treatment of extensor tendon injuries. The extrinsic muscles originate from the elbow and forearm and the intrinsic muscles have their origins in the hand.

Extrinsic Muscles The extrinsic extensor muscles of the hand (Table 1) are innervated by the radial nerve proper and posterior interosseous nerve. As the extrinsic extensor tendons cross the wrist under the extensor retinaculum, they divide and travel into 6 fibroosseous dorsal compartments (Table 1). The extensor carpi radialis brevis can have variable innervation from the posterior interosseous nerve or the superficial branch of the radial nerve coming off from the radial nerve proper.1–3 The tendons of the fourth dorsal compartment (extensor digitorum communis and extensor indicis proprius) are interconnected by juncturae tendinum which allow simultaneous motion and help prevent tendon retraction in case of a traumatic laceration. As the tendons From the *Department of Orthopaedic Surgery, Allegheny General Hospital, Pittsburgh; wCenters for Rehab Services; and zHand and Upper Extremity Surgery, Orthopaedic Specialists at University of Pittsburgh Medical Center, Washington, PA. Disclosure: The authors declare no conflict of interest. Reprints: Mark E. Baratz, MD, Hand and Upper Extremity Surgery, Orthopaedic Specialists at University of Pittsburgh Medical Center, 125N. Franklin Dr. Suite 1, Washington, PA 15301 (e-mail: [email protected]). Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Website, www.sportsmedarthro.com. Copyright r 2014 by Lippincott Williams & Wilkins

Sports Med Arthrosc Rev

cross the metacarpophalangeal (MCP) joints of the hand, they are covered on top by the sagittal band which originates from the volar plate and deep intermetacarpal ligament (Fig. 1A). The sagittal bands stabilize the extensor tendon over the MCP joint and prevent ulnar subluxation during finger motion. At this point, the intrinsic muscles of the hand begin to contribute to the extensor function of the fingers.

Intrinsic Muscles Distal to the MCP joint, the extensor tendon anatomy becomes intricate and complex. The intrinsic muscles contribute to the extensor mechanism in various ways. The lumbricals which originate from the flexor digitorum profundus tendon contribute to the radial lateral band and the interossei contribute to the radial and ulnar lateral bands which coalesce with the lateral slips to form the lateral conjoint tendon. There is also small contribution from the interossei to the central slip. The lumbricals initiate flexion of the MCP joint due to their volar position with respect to the MCP joint. Distally, fibers from the lumbricals become the lateral band and rest dorsal to the proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints. In this position the intrinsics assist in extension of these joints (Fig. 1B). As the extensor tendon travels distally, it divides into a central slip which inserts into the base of middle phalanx and extends the PIP joint. Two lateral slips also come off at this level. The lateral conjoint tendons on the radial and ulnar side form the terminal tendon that inserts on the base of the distal phalanx (Fig. 1C). Other important stabilizers of the most distal aspect of the extensor mechanism are the triangular and transverse retinacular ligament, which if injured, can lead to boutonniere and swan-neck deformities, respectively. Specifically, the triangular ligament prevents volar subluxation of the lateral bands distal to the PIP; the transverse retinacular ligament prevents dorsal subluxation of the lateral bands at the level of the PIP joint. Extensor tendon injuries are divided into 9 zones (Fig. 1D). We will discuss the first 8 zones of injury as they are most relevant to extensor injuries seen in athletes. As a rule of thumb, odd zones are located over the joints and the even zones are located over the bone.

ZONES OF EXTENSOR TENDON INJURY Zone I (Mallet Finger) Mallet fingers are the most common closed tendon injury found in athletes5 and are the result of disruption of the terminal tendon on the distal phalanx. These injuries are commonly seen in athletes participating in baseball, football, basketball, and rugby. The mechanism of injury is usually caused by a forced flexion of an extended finger on a ball, the field, or direct contact with another player. Mallet fingers were classified by Doyle6 into 4 types: type I—closed, type II—open, type III—open with skin and tendon loss, and type IV—large fracture. Type IV is further

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TABLE 1. Extrinsic Extensor Anatomy of the Wrist and Hand

Innervation

Muscles

Radial nerve proper

Brachioradialis Extensor carpi radialis longus Extensor carpi radialis brevis* Extensor pollicis brevis Abductor pollicis longus Extensor pollicis longus Extensor digitorum communis Extensor indicis proprius Extensor digiti minimi Extensor carpi ulnaris

Posterior interosseous nerve

Dorsal Compartment — II II I I III IV IV V VI

*The extensor carpi radialis brevis has variable innervation.1–3

classified into 3 subtypes: A—transphyseal fracture in pediatric patients; B—damage involving 20% to 50% of the articular surface; and C—damage involving >50% of the articular surface with volar subluxation of the distal phalanx.6 Athletes with a mallet finger present with pain, swelling, and an extensor lag. Patients with hyperextensible PIP joints seem to be more prone to a compensatory swan-neck


deformity. The middle, ring, and small fingers are the most commonly involved digits.4 Plain radiographs of the finger are normal in the setting of soft-tissue injury. Mallet fractures with or without subluxation of the distal phalanx are best seen on a lateral radiograph (Figs. 2A, B).

Management of Mallet Fingers Management of acute bony or tendinous mallet fingers will depend on the athlete’s personal goals and the severity of the injury. Type I injuries are treated with extension splinting of the DIP joint with the PIP joint left free for 4 to 6 weeks, followed by night-time splinting for a similar duration of time.4 With regards to splinting type, a metaanalysis of 4 clinical studies showed no superiority between different types of splints (Stack, Perforated custom-made, Padded aluminum-malleable, Abouna, Pryor, and Howard splints) that were studied.7 A more recent blinded, prospective, randomized trial revealed no difference between volar padded, dorsal padded, or custom-splints for type I injuries.8 Type II and III injuries will need operative irrigation and debridement with appropriate soft-tissue coverage for type III injuries and Kirschner wire (K-wire) fixation if a bony injury is present. If the mallet finger exhibits volar subluxation with significant articular involvement such as a IV-C injury, surgical intervention has

FIGURE 1. Intrinsic extensor anatomy of the hand. A, The sagittal band is shown (ulnar side is being lifted by the forceps) over the extensor digitorum communis tendon (Copyright 2013 by Mark Baratz, MD. For permission to reuse contact [email protected]). B, Lateral dissection of a cadaveric digit demonstrating the contribution of the lumbrical muscle (arrow) to the lateral band (arrowhead). The extensor hood (bracket) is shown from a lateral view. Notice the transition of the lateral band from a volar to dorsal position when moving proximal (left) to distal (right) (Copyright 2013 by Mark Baratz, MD. For permission to reuse contact [email protected]). C, Extensor (dorsal) view of a dissected cadaveric digit. The terminal tendon (star), lateral band (arrow), and central slip (arrowhead) are labeled in this image (Copyright 2013 by Mark Baratz, MD. For permission to reuse contact [email protected]). D, For the extensor zones of injury in the hand, odd zones are located over the joints and the even zones are located over the bone. Image reproduced with permission from Baratz et al.4

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Extensor Tendon Injuries in Athletes

FIGURE 2. Mallet finger. Clinical (A) and lateral radiographic (B) view of an acute mallet finger are shown. Notice there is some hyperextension at the proximal interphalangeal (PIP) joint seen on the lateral x-ray view of the affected digit (Copyright 2013 by Mark Baratz, MD. For permission to reuse contact [email protected]). The clinical (C) and lateral radiographic (D) views of an an acute mallet finger after DIP extension splinting are shown. Notice the correction of the flexion deformity at the DIP joint and restoration of the PIP hyperextension seen compared with (A) and (B) (Copyright 2013 by Mark Baratz, MD. For permission to reuse contact [email protected]).

been recommended.9 However, it has been shown that even nonoperative treatment of mallet injuries involving greater than one third of the articular surface with or without subluxation showed satisfactory outcomes in a study of 22 mallet fingers at 2 years of follow-up.10 It is rare in our practice to offer surgical treatment for a mallet fracture, with or without subluxation of the DIP joint. We prefer nonoperative management with 4 to 6 weeks of splinting followed by 4 to 6 more weeks of night-time splinting using a DIP extension splint (Figs. 2C, D). Closed reduction percutaneous pinning with K-wires, so that the DIP is immobilized in full extension, or extension block pinning (modified Ishiguro technique) of the fragment and the DIP joint can be offered as surgical options (Figs. 3A–F).11 However, this would be under the rare circumstance where surgical treatment would be recommended or chosen by an elite athlete.

Management of Chronic Mallet Fingers Chronic mallet fingers (> 4 wk from injury) can be managed with splinting as far out as 3 months.12 Garberman et al13 showed similar restoration of active DIP extension (up to a limit of an extensor lag of 10 degrees) between splinting acute and chronic mallet fingers. Surgical intervention is considered for those patients who have developed a persistent deformity that affects their ability to play. However, in our experience, it is very unusual for an athlete to be sufficiently impaired by a mallet finger that they would consider surgical treatment as an option. See Supplemental Digital Content (http://links.lww. com/SMAR/A5) for rehabilitation for mallet finger injuries.

Swan-Neck Deformities Swan-neck deformities can result from failed treatment of mallet finger injuries. This results from proximal retraction r


and dorsal subluxation of the lateral bands. It more commonly occurs in athletes with hyperextensible PIP joints.

Management of Swan-Neck Deformities Splints are modified to place the DIP in extension and the PIP in flexion. Splinting is continued on a full-time basis for 4 to 6 weeks. If the deformity appears to be correcting itself, the patient is switched to night-time splinting. It may be necessary to have a radiograph of the patient’s finger while wearing the splint to ensure proper positioning. It is not uncommon for the patient to move the PIP into hyperextension even though the PIP block is molded at 0 degrees or slight flexion. A way to prevent PIP hyperextension in the splint is to fabricate the PIP block in 10 to 15 degrees of flexion. The finger and splint may then be radiographed again to evaluate the effectiveness of the splint. When the deformity corrects, but is not maintained, a schedule of part-time splinting (eg, 2 h on and 2 h off during the day) combined with night-time splinting may provide the necessary environment for healing. This may involve splinting of just the PIP joint, just the DIP joint, or both. The deformity is rarely completely eliminated. If nonoperative management fails, the deformity can be managed with a central slip tenotomy or a spiral oblique retinacular ligament (SORL) reconstruction.14,15 Central slip tenotomy seems to be effective for swanneck deformities when the extension lag at the DIP joint is 30 degrees is best treated with the SORL procedure. The swan-neck deformity can occur as the result a variety of causes. The most common are following volar plate rupture or mallet injury. Distinguishing between the 2 is important as treatment options obviously differ. Swanneck deformity treatment for volar plate rupture is volar plate repair or reconstruction as opposed to reconstruction www.sportsmedarthro.com |

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FIGURE 3. Extension block pinning technique for large, unstable mallet fingers. Above are steps of a modified Ishiguro technique for extension block pinning described by Hofmeister et al.11 A clinical example of a mallet finger (A) is shown. Intraoperatively, the DIP joint is maximally flexed to free the dorsal fracture fragment and viewed under flouroscopy (B). The DIP joint is then flexed to 45 degrees and a small K-wire (1.4 mm) is drilled proximal to the fracture fragment through the extensor tendon at an oblique angle through the distal aspect of the middle phalanx (C). To reduce the dorsal fragment, extend the DIP joint and manipulate the distal phalanx to acquire as anatomic reduction as possible (D), then drill another small K-wire (1.4 mm) longitudinally from the tip of the distal phalanx through the DIP joint and confirm pin position with fluoroscopy (E). A postoperative clinical view of the digit with the pins is shown (F). Images and technique reproduced with permission from Alex Shin, MD from Hofmeister et al.11

of the extensor mechanism following mallet injury. Placing the PIP in flexion and having the athlete attempt to extend the DIP will distinguish between the 2 conditions. If the athlete with a swan-neck deformity is unable to extend the DIP joint with the PIP flexed, the terminal tendon is incompetent. The SORL reconstruction (Figs. 4A–H) can be performed with a free tendon graft, typically the palmaris longus or second toe extensor. The graft is passed obliquely beneath the PIP joint between the neurovascular bundles and the flexor tendon sheath. The distal end of the graft is woven into the attenuated terminal tendon. The tendon is tensioned such that with PIP extension the graft will tighten, affecting DIP extension. With PIP flexion the graft becomes lax, allowing DIP flexion. This can be accomplished by pinning the DIP joint in extension and the PIP in slight flexion. The graft is then pulled tight and fixed to the shaft of the proximal phalanx. Pins are maintained in place for 3 weeks. At 3 weeks, active motion is permitted with splint immobilization of the DIP joint. At 6 weeks, full motion of the digit is initiated with night splinting of the


DIP for an additional 6 weeks. By 3 to 4 months patients will regain nearly full extension of the PIP joint, a slight lag at the DIP joint, and near-normal DIP flexion.

Zone II Zone II injuries are due to direct trauma. Surgical repair is recommended for complete tendon lacerations.4 Partial tendon lacerations are managed based on the residual function of the digit. If the athlete has full extension against resistance, then we permit unrestricted movement without resistance. The digit is monitored closely for signs of an extensor lag. The digit is taped with extension at the DIP joint for practice and competition. Unrestricted use is permitted at 3 to 4 weeks. If the athlete has full active extension, but is weak with resisted extension, we recommend 3 weeks of splinting in extension followed by active motion without resistance for an additional 3 weeks. If there is a partial extensor laceration with a loss of active extension we recommend repair. Repair is followed by 3 weeks of splinting in extension and 3 weeks of taping in extension for competition and static splinting at night. r





FIGURE 4. Spiral oblique retinacular ligament (SORL) reconstruction technique. In the SORL (eg, Thompson procedure) reconstruction, a palmaris longus or toe extensor tendon (eg, extensor digitorum longus) can be harvested (A) for the donor graft. After dorsal exposure of the digit, a tunnel is created in an oblique manner through the proximal aspect of the proximal phalanx and weaved under the proximal interphalangeal (PIP) joint (B). The graft is then brought from volar to dorsal to lie on top of where the terminal tendon inserts on the distal phalanx (C). The graft is then weaved into the attenuated terminal tendon (D). Next, the DIP is pinned with a K-wire in extension and the PIP is pinned in slight flexion (E). Finally the proximal aspect of the graft where the entry site is tensioned and secured to the proximal phalanx using a small suture anchor (F). At 4 months, the patient has a slight extensor lag of the DIP joint with no hyperextension of the PIP joint (G), with a closed grip, the patient demonstrates good PIP and DIP flexion (H). (Copyright 2013 by Mark Baratz, MD. For permission to reuse contact [email protected]).

The splint in all cases can be limited to the middle and distal phalanx.

Zone III (Boutonniere Deformity and Central Slip Ruptures) Central slip injuries can be a challenge in the elite athlete. Disruption of the central slip leads to flexion at the PIP joint and hyperextension at the DIP joint. The PIP flexion is accompanied by volar subluxation of the lateral bands secondary to attenuation of the triangular ligament. Boutonniere deformities usually develop over time and early recognition and intervention is important. Athletes are typically injured with forced hyperflexion at the PIP joint: a “jammed” finger. Disruption of the r


central slip can also occur with a laceration, crushing injury, volar dislocations, or fracture-dislocations at the PIP joint. The digit will be swollen and tender directly over the base of the middle phalanx. The Elson test is performed by flexing the PIP joint to 90 degrees and having the patient extend against resistance of the middle phalanx. A central slip rupture is confirmed if the DIP joint is able to extend during resistance. The lateral bands are recruited in a central slip deficient finger and therefore extend the DIP joint against resistance. A cadaveric study of fingers revealed that the Elson test was the most useful of 3 clinical examinations to assess the integrity of the central slip.16 Plain radiographs may show a dorsal fracture of the base of the middle phalanx with or without volar subluxation of the PIP joint. www.sportsmedarthro.com |

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Management of Central Slip Ruptures and Boutonniere Deformities Management of a closed central slip injury without significant bony involvement is treated with splinting the PIP joint in extension while leaving the DIP joint free to encourage the dorsal translation of the lateral bands that occurs with DIP flexion. Full-time splinting is recommended for 4 weeks followed by 4 weeks of night splinting. Taping may be required in the interim for work outs and competition.4 Chronic boutonniere injuries with fixed flexion of the PIP joint may require dynamic splint or serial casting to regain passive extension. Surgery is recommended for open injuries, volar dislocations, or fracture-dislocations of the PIP joint, lacerations over the central slip, failed splinting, and large displaced avulsion fractures (Figs. 5A–G). Multiple surgical techniques for central slip injuries and chronic boutonniere deformities have been reported in the literature including central slip repair or reconstruction, extensor tenotomy, and lateral band mobilization or reconstruction.17–25 See Supplemental Digital Content (http://links. lww.com/SMAR/A5) for rehabilitation for central slip/ boutonniere (zone III) injuries.

Zone IV Zone IV injuries are typically lacerated tendons. The management is identical to that described for zone II injuries.

Zone V (Sagittal Band Rupture and Fight Bites) Zone V injuries are located over the MCP joint. The 2 most common injuries are sagittal band injuries and the “fight bite.”

Fight Bite The fight bite presents with small laceration over the MCP joint. The injury may be more apparent when the athlete is making a fist. Fight bites have a high risk of developing infection secondary to the polymicrobial flora from the human mouth. Depending on the time of presentation, signs of infection such as erythema, swelling, limited range of motion at the MCP joint, and gross pus may be present. Radiographs including oblique views centered on the metacarpal head may show a fracture or impaction injury. Unless the laceration is clearly superficial, the prudent move is to explore the joint.

Management of Fight Bites Arthroscopic inspection and irrigation offers an excellent view of the joint and easy irrigation without taking down the sagittal band. This allows immediate mobilization if procedure is carried out before there is an established infection. A septic joint with surrounding cellulitis seems to respond best to a period of immobilization until the infection abates; usually 5 to 7 days. Routine antibiotics should be initiated prophylactically and postoperatively. Broad-spectrum IV antibiotics should cover the most commons organisms (eg, Streptococcus viridans, Eikenella corrodens, Staphylococcus aureus, gram-negatives, and anaerobic flora). Treatment should include ampicillin/sulbactam (Unasyn), or if penicillin allergic, a combination of clindamycin and a fluoroquinolone. Vancomycin can be added if there is clinical concern for a methicillin resistant Staphylococcus aureus (MRSA) infection. Oral antibiotic therapy can be initiated postoperatively and should include amoxicillin/clavulanate (Augmentin), or if penicillin




allergic, trimethoprim-sulfamethoxazole (Bactrim) for 5 to 7 days. Although rare, transmission of viral pathogens such as hepatitic B and C should be considered. Regular tetanus prophylaxis should also be given during treatment.

Sagittal Band Ruptures Sagittal band ruptures can be caused by blunt injury over the MCP joint, laceration or direct injury to the sagittal band, and resisted extension or flexion across the MCP joint. These can be seen in athletes involved in direct contact (eg, boxing, football, and rugby) with the term “boxer’s knuckle” also coined for this injury complex. Rayan and Murray26 classified sagittal band injuries into 3 types: type I—injury without instability; type II—tendon subluxation; and type III—tendon dislocation into the webspace. In the same study, they found that the middle finger was the common location, followed by the small, index, and ring fingers.26 Also, chronic attritional injuries to the extensor hood of the MCP joint can be found in boxers that have repetitive blunt trauma to the MCP joint. Patients present with swelling, tenderness, and a snap or extension deficit during attempts at straightening the finger from a flexed position. Type II and III injuries will demonstrate ulnar subluxation or dislocation of the tendon with an inability to initiate extension. An anatomic study by Young and Rayan27 revealed that even partial sectioning of the proximal portion of the radial side of the sagittal band caused tendon subluxation but sectioning of the ulnar side did not. Koniuch et al28 also demonstrated similar findings in their cadaveric dissections, and contributed this to juncturae tendinum attached to the ulnar side of the tendon and the tendency toward ulnar deviation of the MCP joint. Imaging is rarely necessary to make this diagnosis or plan appropriate treatment.

Management of Sagittal Band Ruptures There is no good evidence to guide us in deciding between nonoperative and surgical treatment for this injury. A study of 8 professional athletes (6 boxers and 2 hockey players) who underwent open repair of 11 sagittal band injuries demonstrated good results, with a return to play in 5 months with no reported complications.29 The authors did note that a capsular repair was not performed secondary to concerns of overtightening and thereby reducing MCP joint motion.29 Athletes in this study were immobilized for 6 weeks, not significantly different from what would occur with nonoperative treatment. We offer athletes both the option of immobilization with the caveat that there is the possibility of requiring surgery in the event that immobilization is unsuccessful. Closed treatment involves splinting the injured and adjacent digit in a hand-based splint for 3 to 4 weeks with the MP joint flexed 30 degrees and the IP joints free. Surgical repair is performed under local anesthesia through a dorsal longitudinal approach. The 2 leaflets of the sagittal band are elevated off the dorsal capsule. Repair is performed with a braided 3-0 nonabsorbable suture. When the repair is secure the athlete is asked to flex and extend the digit. The tendon should track over the center of the metacarpal head. The ulnar sagittal band can be released if the tendon continues to track to the ulnar side of the head. If the substance of the tissue on the radial sagittal band is insufficient, juncturae on the ulnar aspect of the extensor can be released proximally and brought across the r





FIGURE 5. Zone III injury with boutonniere deformity. Clinical view of an acute boutonniere deformity (A) secondary to a displaced and rotated avulsion fracture at the dorsal base of the middle phalanx (B). Intraoperative view of the central slip attached to the avulsion fracture (C) and placement of a suture anchor in the base of the middle phalanx (D) to repair the central slip after excision of the fracture fragment. The reapproximation of the disrupted central slip is shown (E). The patient 6 months after surgery demonstrates some persistent loss of proximal interphalangeal (PIP) extension with no hyperextension of the DIP joint (F), but has good flexion of the PIP and DIP joints (G) with a fully closed grip. (Copyright 2013 by Mark Baratz, MD. For permission to reuse contact [email protected]).

head to reconstitute the radial sagittal band and centralize the tendon (Figs. 6A, B). See Supplemental Digital Content (http://links. lww.com/SMAR/A5) for rehabilitation for sagittal band ruptures and fight bites.

Zone VI Zone VI injuries in an athlete can occur with laceration from a penetrating object or from the sharp edge of a r


displaced metacarpal shaft fracture (Figs. 7A, B). These are injuries that are managed with direct surgical repair of the tendon using a core stitch and an epitendinous stitch. The injured tendons are usually repaired with local anesthesia. Following repair, the athlete is asked to flex and extend the digit. The repair is inspected for gapping and a sense is derived as to the degree of flexion that is possible without undue tension on the repair. With a strong repair active extension with a flexion block based on intraoperative www.sportsmedarthro.com |

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FIGURE 7. Zone VI Injury (Lacerated Extensor Digiti Minimi [EDM]) Secondary to a Displaced Metacarpal Shaft Fracture Anteroposterior view of the hand showing a displaced 5th metacarpal shaft fracture (A). Intra-operative view of a lacerated EDM (adjacent to forceps) secondary to the fracture (B). (Copyright 2013 by Mark Baratz, MD. For permission to reuse contact [email protected]).

Zone VII

FIGURE 6. Sagittal band repair. Intraoperative view of an acute sagittal band rupture (A) with ulnar dislocation of middle finger extensor digitorum communis. The repair of the radial side of the sagittal band is shown (B). Postoperative buddy taping (C) of the sagittal band repair of the middle finger to the adjacent radial digit during the strengthening phase. (Copyright 2013 by Mark Baratz, MD. For permission to reuse contact [email protected]).

findings is begun immediately. Unprotected motion is permitted at 3 to 4 weeks and strengthening is commenced at 6 weeks.


Zone VII injuries are located over the extensor retinaculum and result from penetrating trauma. In acute injuries, we attempt to perform direct repair of the tendon with release of only part of the retinaculum. Repaired is performed with a 3-0 braided, nonabsorbable core stitch using a taper needle supplemented with a 6-0 monofilament nonabsorbable suture on a taper needle. Repair of the retinaculum is suggested as this will prevent bowstringing and subluxation of the tendons.4 Performing this repair under local anesthesia is particularly useful as it is possible to watch for gapping of the repair or catching of the repair site against the edge of the retinaculum. We would not hesitate to leave a portion of the retinaculum open to permit full excursion of the repaired tendon.

Zone VIII Zone VIII injuries are injuries at the musculotendinous junction of the extensor compartment of the forearm. These injuries typically arise from traumatic lacerations or a forceful flexion with or without pronation of the forearm secondary to a high-energy fall (as would be seen from a fall from height while jumping in gymnastics, basketball, etc.). Repair is difficult given the thin overlying fascia. Operative r




techniques that can supplement primary repair include side to side repair, tendon transfers, or a weaved autograft.30,31 Takami et al31 described a case series of 10 patients including 5 athletes with zone VIII injuries that were either treated with direct repair (side to side repair) or extensor tendon transfer. Five of the patients were described as having “excellent” outcomes (no extension lag and no lack of flexion) and 4 of the patients had “good” outcomes (up to 15 degrees of an extensor lag with no lack of flexion).31 We recommend that these injuries must be immobilized following surgery for at least 3 to 4 weeks. See Supplemental Digital Content (http://links. lww.com/SMAR/A5) for rehabilitation protocol for zones VII and VIII injuries.

Extensor Tendinopathies Intersection Syndrome Intersection syndrome is an overuse condition characterized by inflammation at the crossing point of the first and second dorsal compartments. This condition is commonly seen in rowing, skiing, and racquet sports. Patients will present with vague distal dorsal-radial forearm pain that is tender to palpation and located approximately 4 to 8 cm proximal to the radial styloid.32 Pain associated with intersection syndrome can be recreated with resisted wrist extension and thumb extension or abduction. In more severe cases, crepitus can be palpated over the area of discomfort. Nonoperative treatment typically begins with immobilization, anti-inflammatory medications, and activity modification. Refractory cases are treated with steroid injections beneath the distal and proximal edges of the abductor pollicis longus and extensor pollicis brevis as they cross the radial wrist extensors. Release of the extensor retinaculum over the radial wrist extensors has been described but is not part of our treatment algorithm.

Extensor Carpi Ulnaris (ECU) Tendinitis, Subluxation, and Rupture ECU disorders are commonly seen in baseball, golf, hockey, and racquet sports. Varying degrees of injury have been described including tenosynovitis, subluxation, and even frank dislocation of the tendon from the bony groove of the ulna.33–36 The mechanism of injury is thought to include: forced wrist supination and flexion with ulnar deviation. Examples of this include an elite tennis player who torques the wrist in this position to maximize topspin or the nondominant hand of a double-handed backhand. It also could occur during a check swing or during transition of ball contact to the follow through phase while swinging a bat or golf club. The ECU tendon originates from the common extensor origin and during pronation angulates approximately 30 degrees towards its insertion at the base of the fifth metacarpal.35,37,38 As the tendon approaches the wrist, it is surrounded by a subsheath that stabilizes the tendon within the ulnar groove creating a “fibroosseous” tunnel.38 The extensor retinaculum over the sixth dorsal compartment is separate from the subsheath but provides stability to the ulnar side of the wrist. The subsheath forms from the deep antebrachial fascia, stabilizes the tendon within the tunnel during wrist motion, and has ulnar and radial attachments vulnerable to disruption.37–39 The ulnar attachment of the r



subsheath is reinforced by longitudinal fibers of the linea jugata.38 Inoue and Tamura described a classification system for ECU subsheath injuries based on location of failure and direction of sheath displacement. Type A involves a disruption of the ulnar side of the sheath with the sheath lying on the tendon; type B is a disruption of the radial side of the sheath with the sheath lying under the tendon; type C is a delamination of the sheath in an ulnar and volar direction, however, the tendon remains in the sheath.35,40 The athlete with ECU tendinitis will have pain localized over the ulnar aspect of the wrist with tenderness on palpation of the ECU tendon in the groove. There may be associated synovitis and pain is often more pronounced with resisted ulnar deviation or resisted finger abduction. A complete examination for ulnar-sided wrist pain may help exclude concurrent diagnoses. Plain radiographs are useful to identify confounding variables such as ulnocarpal abutment, acute or nonunited ulnar styloid fracture, and calcification in the triangular fibrocartilage complex that can be seen in pseudogout and arthritis of the distal radio-ulnar joint. In the elite athlete, an MR arthrogram may show delamination in the tendon, early subluxation of the tendon, and synovitis. A peripheral tear of the triangular fibrocartilage complex with disruption of the ECU subsheath can create ECU tendonitis. A lunotriquetral ligament tear or signal change in the lunate from ulnocarpal abutment may influence optimum care.

Management of ECU Injuries If the patients fail a period of activity modification, rest, immobilization, and anti-inflammatory agents, then consideration can be given to a steroid injection. The need for surgical debridement is uncommon in the absence of synovitis and delamination of the tendon. In the face of failed nonoperative treatment and associated tendinosis, the tendon can be debrided and oversewn. At the time of surgery the ECU subsheath is inspected for evidence of a peripheral tear. The repaired retinaculum is protected for 3 to 4 weeks in a long-arm cast with the forearm in neutral and an additional 2 weeks in a short-arm cast. The athlete with subluxation of the ECU tendon will be tender over the sixth dorsal compartment and can complain of “snapping” with supination and ulnar deviation. Acute ECU subluxation can be managed with a 3 to 4 weeks of long-arm immobilization with the understanding that the inciting injury may have been acute on chronic exacerbation. If that is the case, there is the risk of persistent symptoms. With surgical treatment the ECU tendon is approached via a dorsoulnar incision. The sheath is inspected for a rent on the ulnar or radial margin (types A and B, respectively) versus an attenuated sheath with a volarly subluxed tendon. Relatively acute tears can be managed with repair. A patulous sheath can be taken down and reapplied to the volar margin of the ulnar grove with microsuture anchors (Figs. 8A, B). In the absence of quality tissue, the sheath can be reconstructed with a strip of extensor retinaculum or a free tendon graft. Following surgery, the wrist and forearm are immobilized in neutral in a long-arm cast for 4 weeks, followed by a short-arm cast for 2 weeks. Therapy for motion and grip are begun at 6 weeks. Resisted forearm rotation is not begun until 10 to 12 weeks based on tenderness in the region of the repair or reconstruction. Return to play can www.sportsmedarthro.com |

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motivation in returning to play are necessary to create a comprehensive treatment plan. Conservative treatments are preferred in many circumstances, but surgical interventions may be necessary for both acute and chronic injuries. REFERENCES

FIGURE 8. Extensor carpi ulnaris (ECU) sheath repair. Cadaveric view of an ECU subsheath rupture (A) with reapproximation of the disrupted sheath (B). (Copyright 2013 by Mark Baratz, MD. For permission to reuse contact [email protected]).

occur as early as 3 to 4 months, but can be managed on a case by case basis.33 MacLennan et al41 performed ECU reconstruction on 21 patients and found a significant improvement in wrist flexion-extension, radial-ulnar deviation, and pronationsupination following surgery. In addition, they observed an improvement in grip strength. Self-reported pain scores significantly decreased postoperatively. MacLennan and colleagues stated that all 21 of their patients were able to return to some form of employment. Twenty of those 21 patients were able to return to the job, sport, or activity in which they had sustained their injury. There were no instances of recurrent ECU subluxation.41 Inoue and Tamura performed ECU repair or reconstruction on 12 patients. Reconstruction was performed using a portion of the extensor retinaculum. At follow-up, all patients demonstrated normal range motion and no patients reported a recurrent dislocation.40

CONCLUSIONS Extensor tendon injuries in athletes can be disabling and have long-term effects if not diagnosed and treated appropriately. When evaluating athletes who present with these injuries, a structured physical examination, appropriate imaging, and discussion with the athlete of their


1. Abrams RA, Zieta RJ, Lieber RL, et al. Anatomy of the radial nerve motor branches in the forearm. J Hand Surg (Am). 1997; 22:232–237. 2. Branovacki G, Hanson M, Cash R, et al. The innervation pattern of the radial nerve at the elbow and in the forearm. J Hand Surg. 1998;23B:167–169. 3. Cricenti S, DeAngelis M, DiDio L, et al. Innervation of the extensor carpi radialis brevis and supinator muscles: levels of origin and penetration of these muscular branches from the posterior interosseous nerve. J Shoulder Elbow Surg. 1994;3: 390–394. 4. Baratz ME, Schmidt CC, Hughes TB. Extensor tendon injuries. In: Green DP, Hotchkiss RN, Pederson WC, et al, eds. Green’s Operative Hand Surgery. 5th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:187–217. 5. Posner MA. Injuries to the hand and wrist in athletes. Orthop Clin North Am. 1977;8:593–618. 6. Doyle JR. Extensor tendons-acute injuries. In: Green DP, Hotchkiss RN, Pderson WC, eds. Green’s Operative Hand Surgery, ed 4. New York (NY): Churchill Livingstone; 1999:1962–1987. 7. Handoll HH, Vaghela MV. Interventions for treating mallet finger injuries. Cochrane Database Syst Rev. 2004;3: CD004574. 8. Pike J, Mulpuri K, Metzger M, et al. Blinded, prospective, randomized clinical trial comparing volar, dorsal, and custom thermoplastic splinting in treatment of acute mallet finger. J Hand Surg Am. 2010;35:580–588. 9. Niechajev IA. Conservative and operative treatment of mallet finger. Plast Reconstr Surg. 2005;76:580–585. 10. Kalainov DM, Hoepfner PE, Hartigan BJ, et al. Nonsurgical treatment of closed mallet finger fractures. J Hand Surg. 2005; 30A:580–586. 11. Hofmeister EP, Mazurek MT, Shin AY, et al. Extension block pinning for large mallet fractures. J Hand Surg Am. 2003;28: 453–459. 12. Patel MR, Desai SS, Bassini-Lipson L. Conservative management of chronic mallet finger. J Hand Surg Am. 1986;11: 570–573. 13. Garberman SF, Diao E, Peimer CA. Mallet finger: results of early versus delayed closed treatment. J Hand Surg. 1994;19: 850–852. 14. Kleinman WB, Petersen DP. Oblique retinacular ligament reconstruction for chronic mallet finger deformity. J Hand Surg. 1984;9:399–404. 15. Kanaya K, Wada T, Yamashita T. Thompson procedure for chronic mallet finger deformity. J Hand Surg. 2013;38:1295–1299. 16. Rubin J, Bozentka DJ, Bora FW. Diagnosis of closed central slip injuries. A cadaveric analysis of non-invasive tests. J Hand Surg. 1996;21B:614–616. 17. Matev L. Transposition of the lateral slips of the aponeurosis in treatment of long-standing “boutonniere deformity” of the fingers. Br J Plast Surg. 1964;17:281–286. 18. Urbaniak JR, Hayes MG. Chronic boutonniere deformity—an anatomic reconstruction. J Hand Surg. 1981;6:379–383. 19. Dolphin JA. Extensor tenotomy for chronic boutonniere deformity of the finger: report of two cases. J Bone Joint Surg Am. 1965;47:161–164. 20. Curtis RM, Reid RL, Provost JM. A staged technique for the repair of the traumatic boutonniere deformity. J Hand Surg. 1983;8:167–171. 21. Stern PJ. Extensor tenotomy: a technique for correction of posttraumatic distal interphalangeal joint hyperextension deformity. J Hand Surg Am. 1989;14:546–549. r




22. Meadows SE, Schneider LH, Sherwyn JH. Treatment of chronic boutonniere deformity by extensor tenotomy. Hand Clin. 1995;11:441–447. 23. Aiache A, Barsky AJ, Weiner DL. Prevention of the boutonniere deformity. Plast Reconstr Surg. 1970;46:164–167. 24. Snow JW. A method for reconstruction of the central slip of the extensor tendon of a finger. Plast Reconstr Surg. 1976; 57:455–459. 25. Ahmad F, Pickford M. Reconstruction of the extensor central slip using a distally based flexor digitorum superficialis slip. J Hand Surg. 2009;34A:930–932. 26. Rayan GM, Murray D. Classification and treatment of closed sagittal band injuries. J Hand Surg. 1994;19:590–594. 27. Young CM, Rayan GM. The sagittal band: anatomic and biomechanical study. J Hand Surg. 2000;25:1107–1113. 28. Koniuch MP, Peimer CA, VanGorder T, et al. Closed crush injury of the metacarpophalangeal joint. J Hand Surg. 1987; 12(5 pt 1):750–757. 29. Hame SL, Melone CP. Boxer’s knuckle in the professional athlete. Am J Sports Med. 2000;28:879–882. 30. Botte MJ, Gelberman RH, Smith DG, et al. Repair of severe muscle belly lacerations using a tendon graft. J Hand Surg [Am]. 1987;12:406–412. 31. Takami H, Takahashi S, Ando M. Traumatic rupture of the extensor tendons at the musculotendinous junction. J. Hand Surg. 1995;20A:474–477. 32. Budoff JE. Tendinopathies of the hand, wrist, and elbow. In: Trumble TE, Rayan GM, Budoff JE, Baratz ME, eds.

r



33.

34.

35. 36.

37.

38. 39.

40.

41.

Principles of Hand Surgery and Therapy. 2nd ed. Philadelphia: Saunders Elsevier; 2010:343. Montalvan B, Parier J, Brasseur JL, et al. Extensor carpi ulnaris injuries in tennis players: a study of 28 cases. Br J Sports Med. 2006;40:424–429. Allende C, Le Viet D. Extensor carpi ulnaris problems at the wrist-classification, surgical treatment, and results. J Hand Surg Br. 2005;30B:265–272. Inoue G, Tamura Y. Recurrent dislocation of the extensor carpi ulnaris tendon. Br J Sports Med. 1998;32:172–174. Burkhart SS, Wood MB, Linscheid RL. Posttraumatic recurrent subluxation of the extensor carpi ulnaris tendon. J Hand Surg. 1982;7:1–3. Palmer AK, Skahen JR, Werner FW, et al. The extensor retinaculum of the wrist: an anatomical and biomechanical study. J Hand Surg. 1985;10B:11–16. Taleisinik J, Gelberman RH, Miller BW, et al. The extensor retinaculum of the wrist. J Hand Surg Am. 1984;9:495–501. Spinner M, Kaplan EB. Extensor carpi ulnaris. Its relationship to the stability of the distal radio-ulnar joint. Clin Orthop Relat Res. 1970;68:124–129. Inoue G, Tamura Y. Surgical treatment for recurrent dislocation of the extensor carpi ulnaris tendon. J Hand Surg Br. 2001;26B:556–559. MacLennan AJ, Nemechek NM, Waitayawinyu T, et al. Diagnosis and anatomic reconstruction of extensor carpi ulnaris subluxation. J Hand Surg. 2008;33A:59–64.

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Flexor tendon injuries in athletes.

Repair of extensor tendon injuries of the hand.

Extensor tendon injury due to repetitive wrist dorsiflexion: morphological study of extensor retinaculum and extensor tendon.

Early controlled active mobilization with dynamic splintage for treatment of extensor tendon injuries.

A brief review of extensor tendon injuries specific to the pediatric patient.

Traumatic Extensor Tendon Injuries to the Hand: Clinical Anatomy, Biomechanics, and Surgical Procedure Review.

Results of acute zone III extensor tendon injuries treated with dynamic extension splinting.

Achilles tendon injuries in elite athletes: lessons in pathophysiology from their equine counterparts.

MUSCLE INJURIES IN ATHLETES.

Different distributions of operative diagnoses for Achilles tendon overuse injuries in Italian and Finnish athletes.

[Distal biceps tendon injuries -- injuries of the distal biceps tendon].

Long-term results of extensor tendon repair.

Biomechanical characteristics of extensor tendon suture techniques.

Exertion injuries in adolescent athletes.

Overuse injuries in adolescent athletes.

Pediatric elbow injuries in athletes.

Elbow injuries in athletes. Preface.

Achilles tendon injuries.

Two-staged extensor tendon reconstruction for zone 6 extensor tendon loss of the fingers: indications, technique and results.

Missed tendon injuries.

Allograft reconstruction for extensor mechanism injuries.

Bilateral spontaneous extensor tendon ruptures in Madelung's deformity.

Behavior of the extensor pollicis longus tendon in experiment.

Injuries to elite wheelchair athletes.