Virtually all orthopaedic surgeons encounter athletes with hand or wrist injuries during their careers. Although not every team physician needs to be a “hand surgeon,” the frequency of these injuries caused by sporting activity ensures that we will all be called on to provide at least an initial evaluation. Because most sports require intensive use of the hands, athletes recognize that a hand or wrist injury will have an immediate impact on their performance. Whether it is a minor league catcher or an elite professional wide receiver, an athlete with a hand injury intuitively appreciates the interplay between upper extremity function and competitive ability. The injuries often sustained in each individual sport generally have distinguishing characteristics, because most sports place specific demands on an athlete’s hands in a consistently reproducible manner. Accordingly, certain types of athletes are more prone to certain diagnoses and conditions.
The desire to participate and the drive for optimal performance that characterizes most athletes make them special patients. Caring for this unique population requires an understanding of their wishes for an expedient and complete recovery. As treating physicians, we need to grasp not only the pathoanatomy of the athlete’s injury but also the financial, social, and psychological consequences. Surgical expertise must be coupled with intelligent decision making to expedite the athlete’s short- and long-term recovery. Restoring the elite athlete’s unique skill set after these injuries provides professional challenges that often require consultation with a hand and upper extremity specialist.
Four mechanisms responsible for athletic hand injuries have been proposed by Mirabello and colleagues : throwing, weight bearing, twisting, and impact. Often a combination of factors is responsible for the injury. Werner and Plancher categorized the potential for injury based on the type of sport exposure. Mechanisms included were impact with a ball or competitor; contact with a racquet, stick, or club; and external contact, as is seen in gymnastics, rock climbing, and weight lifting. Although almost any injury can be seen in any athlete, certain sport-specific patterns of injury have been recognized. Interphalangeal (IP) fracture/dislocations are frequent in high-intensity ball sports such as volleyball and basketball. Hamate fractures are often diagnosed in golfers and tennis players. Skiers are vulnerable to acute injury of the thumb ulnar collateral ligament (UCL). Some injuries are notoriously easy to miss, such as a flexor digitorum profundus (FDP) tendon avulsion in a football or rugby player. Because of the small margin for diagnostic error and the temporal nature of most recommended interventions, neglect and/or misguided treatment algorithms are certain to lead to a poor outcome. Maintaining a high index of suspicion for the worst-case scenario may be the first step in evaluating the injured hand of an athlete.
In general, providing care for an athlete can be difficult and charged with emotion, especially as he or she reaches elite or professional status and the stakes get larger. Coaches, managers, agents, and parents may all have various levels of knowledge about injuries and disparate agendas for return to play. Too often these agendas are not complementary and are unproductive. Our initial goals are to diagnose accurately, present options comprehensively, and communicate effectively. The patient management questions set forth by Green and Strickland create a solid framework for treatment algorithms:
Is the method of treatment expected to provide the best long-term result?
Would we manage this injury in a similar manner in a nonathlete?
Are the potential complications of my treatment significantly greater than might be expected from a more conservative approach?
Will the treatment allow the athlete to return to competition with little risk for reinjury?
Would reinjury unfavorably influence the prognosis for a satisfactory recovery?
The complexities of hand biomechanics are beyond the scope of this chapter (this information is covered in Chapter 70 , “Wrist and Hand Anatomy and Biomechanics”). Because of the anatomic intricacies of the hand and its vulnerability to a multitude of distinct conditions across virtually all sports, this chapter focuses only on the osseous and soft tissue injuries most commonly encountered by the general orthopaedic surgeon or sports medicine specialist who is acting as first responder. Consequently, only the most pertinent elements of the history and physical examination, followed by key imaging findings and treatment options, are presented here. Clinical pearls, decision-making principles, and our preferred surgical techniques are interspersed in keeping with the format of this textbook.
Osseous and Soft Tissue Injuries of the Digits
Ligamentous Injuries and Dislocations
A dislocation of the carpometacarpal (CMC), metacarpophalangeal (MCP), or IP joint is a frequently encountered sports injury. With regard to dislocations, a recent epidemiologic study showed that the hand was the second most common site of injury, after the shoulder. Awkward falls, contact with other competitors, or entanglement with equipment explain many of these incidents. Dislocations may occur from either hyperextension or hyperflexion forces, often combined with torsional and/or axial stress, the result of which dictates the direction of maximal displacement. Most IP dislocations are effectively treated by immediate closed reduction, whereas some MCP and CMC dislocations require surgical treatment. Recognition of the irreducible complex MCP dislocation, which is often perpetrated by misinformed responders who exert excessive longitudinal traction on the affected digit on the field or sideline, allows for timely surgical intervention that eliminates further damage to articular cartilage surfaces from repetitive futile attempts at relocation. When forces fail to exceed the threshold for dislocation, isolated ligamentous injuries may arise with a spectrum of possible severity.
Collateral ligament injuries of the digit are much less common than those that occur at the thumb MCP joint (see the section on Thumb Injuries later in this chapter). Hyperabduction injuries usually occur in an ulnar direction when the finger is flexed and the ligament is taut, and hence the radial collateral ligaments of the three ulnar-most digits are most at risk. Most hyperabduction injuries are partial injuries (grade I or II sprains) that may be treated with early active range of motion and “buddy taping” to the adjacent finger. A radiograph should be obtained for all suspected collateral ligament injuries. In a complete (grade III) tear, avulsion fractures may be evident, and the joint is often unstable in the coronal plane. Testing of the affected collateral ligament is performed in flexion. If the joint is grossly unstable or if an avulsion fragment is displaced, an open repair is preferred. If the ligament is avulsed from bone, a suture anchor works well for fixation. If the fracture fragment is large enough, we prefer to use tension band or mini fragment screw fixation. Immobilization of the joint in flexion (intrinsic plus or “safe” position) prevents the development of an extension contracture. For chronic tears presenting in a delayed fashion with pain and instability, temporary pinning of the MCP joint in flexion may be indicated for 2 to 3 weeks, with active motion begun thereafter.
Although MCP dislocations may occur in any digit, the index and small fingers are most vulnerable because of their relatively unprotected location. Volar MCP dislocations are relatively rare. Dorsal MCP dislocations are classified as simple (easily reduced) or complex (irreducible), depending on the effectiveness of closed manipulation. Simple dislocations present with the MCP hyperextended between 70 and 90 degrees ( Fig. 77-1 ). The reduction maneuver combines gentle flexion, slight traction, and a volarly directed pressure at the base of the proximal phalanx ( Fig. 77-2 ). Complex dislocations are often characterized by interposition of the volar plate between the articular surfaces, rendering them irreducible by closed means ( Fig. 77-3 ). The lumbrical muscle is wrapped around the radial side of the metacarpal head, and the flexor tendons loop around its ulnar side. Simple traction will only tighten this noose and prevent reduction. The metacarpal head often dimples the skin of the distal palm. Posteroanterior radiographs may show joint space widening or even bayonet apposition. Sesamoid interposition is possible when the index or small fingers are involved. A Brewerton view, taken with the forearm supinated and the MCP joints against the x-ray plate, may show an associated metacarpal head fracture.
Every athlete deserves an attempt at closed reduction for a dislocated MCP joint. Although performing immediate reduction “on the field” is tempting, this procedure is best performed with adequate anesthesia and patient comfort. Attempts at longitudinal distraction or exaggeration of the hyperextension deformity will convert a reducible subluxation into an irreducible dislocation by permitting the volar plate to fall dorsally between the metacarpal head and the base of the proximal phalanx. If the joint is successfully reduced with digit flexion and volarly directed pressure at the base of the proximal phalanx, a dorsal blocking splint may be applied, preventing hyperextension beyond neutral. Early active motion is started under the supervision of a therapist within 1 week.
When an attempt to perform a closed reduction is unsuccessful, we prefer to use a dorsal approach to perform an open reduction. In this approach, the dorsal capsule is opened and the interposed volar plate is manually extricated or split in the midline to achieve reduction. The dorsal approach also provides excellent access for fixation of the occasional osteochondral shear fracture of the metacarpal head. Volar approaches theoretically risk injury to malpositioned digital nerves. In particular, the radial digital nerve is displaced centrally and superficially by index MCP dislocations, and the ulnar digital nerve is displaced by small MCP dislocations. Care must be taken immediately after skin incision if this approach is chosen. Alternatively, a percutaneous approach to reducing complex dislocations has been reported. Return to sports is guided by return of range of motion and comfort level, because chronic instability of this joint is not typically recognized. An early return to sports (within 1 to 2 weeks) is possible with buddy taping and use of a protective customized splint for athletes who participate in contact sports.
Proximal Interphalangeal Joint
Virtually all athletes are subject to injuries of the soft tissue stabilizers of the proximal interphalangeal (PIP) joint over the course of their careers. Pure hyperextension forces produce volar plate injuries, whereas hyperflexion forces may disrupt the central slip. The collateral ligaments are susceptible to torsional and angular stresses ( Fig. 77-4 ). Frequently the athlete relates a history of “jamming” the finger. These injuries are very familiar to athletes whose sport involves the use of a ball. Picture a high-velocity overhead spike at the volleyball net that is blocked with a fingertip instead of the palm or a late reaction to a point-blank basketball pass in the paint. When additional energy is imparted to the digit(s), simple sprains may escalate to disabling complex fractures/dislocations.
The athlete’s account of the injury may provide verbal or even visual clues as to “which way the finger went.” If stated without hesitation, the pathoanatomy is almost instantly determined. When the patient cannot recall the sequence of events leading to the injury, the physical examination is paramount. After radiographic evaluation, the examiner must try to discern the area of maximal tenderness—dorsal, volar, radial, or ulnar—which is easiest for injuries of the mildest form. As the severity increases, it becomes more difficult to characterize the injury, especially in the acute phase when swelling and sensitivity to manipulation are heightened. Any deformity in the resting position is noted. Reproduction of the mechanism of injury will be uncomfortable. Range of motion is often limited by pain at first presentation and is not predictive of a certain pathology.
A central slip injury or avulsion should be suspected in all PIP injuries for which the athlete has mainly dorsal tenderness. Three tests can be performed to ensure that the central slip is still attached to the dorsal base of the middle phalanx. First, “tenodesis extension” of the PIP joint is checked with the MCP joint in full flexion. The PIP joint should passively extend to within 15 degrees of full extension. Next, passively extend the PIP joint and ask the patient to flex the distal interphalangeal (DIP) joint. Inability to flex this joint implies retraction of a ruptured central slip, with extension forces concentrated at the DIP joint through the lateral bands. Finally, perform the Elson test by flexing the PIP joint to 90 degrees. If the DIP joint becomes rigid to passive flexion as the digit is actively extended, then the central slip is ruptured and extension is occurring through the lateral bands.
Mild PIP joint hyperextension injuries produce partial injury to the volar plate and on examination are stable with both active and passive extension. Treatment involves buddy taping for 3 to 4 weeks, with Coban elastic wrap used carefully at night to decrease edema. Isolated collateral ligament sprains are treated similarly. Flexion contractures notoriously develop after small volar plate bony avulsions from the base of the middle phalanx, which are seen best on perfect lateral radiographs of the digit. These contractures may be pronounced enough to create a “pseudoboutonnière” deformity, where the presenting flexion deformity at the PIP joint is mistaken for the resultant posture after a central slip injury. However, careful inspection fails to reveal true accompanying DIP hyperextension, and the Elson test is negative. Aggressive early motion recovery is the mainstay of treatment of volar plate sprains at the PIP joint. Static progressive or dynamic extension splinting may be necessary in recalcitrant cases of flexion contracture. Patients should be counseled on the persistent discomfort and swelling that can last for months with these seemingly innocuous injuries. Residual loss of motion is common.
Obvious PIP dislocations are often self-diagnosed and self-treated. Delayed presentation is frequent when self-relocation is successful, because many athletes do not question the persistent pain and swelling of the joint until sometimes weeks or even months after the incident. Most PIP dislocations are closed injuries, but open dislocations are not uncommon and require appropriate respect and urgent operative treatment. Open PIP dislocations have occurred in soccer goalkeepers, softball players, and martial arts experts.
When a dorsal PIP dislocation occurs, the volar plate and collaterals are injured, but the articular surfaces of the joint are still in congruent contact upon reduction. Stable reductions are treated with buddy taping and early range of motion. When the joint has a tendency to hyperextend, possibly as a result of baseline PIP volar plate laxity, a splint is fashioned to sit dorsally and keep the joint partially flexed (i.e., a dorsal block splint). Even simple dislocations are quite painful, and the athlete will need to work arduously with his or her trainer or occupational therapist to regain full flexion within the first 3 weeks after injury. At 3 weeks, active extension is emphasized to combat the development of flexion contractures, with use of a resting/nighttime splint in full PIP extension. If a flexion contracture remains 5 weeks after injury, dynamic PIP extension splinting should be prescribed. An accelerated return to certain sports is possible within 7 to 14 days, depending on the degree of pain, swelling, and improvement in digital motion.
Complex PIP dislocations may present with displaced articular surfaces and bayonet positioning of the phalanges ( Fig. 77-5 ). Rupture of the volar skin can occur from an inside-to-outside mechanism, and residual stiffness is more common after treatment. In the absence of a large accompanying fracture, a closed reduction with anesthesia produced by a digital block is attempted by gently pushing the middle phalanx (P-2) over the articular surface of the proximal phalanx (P-1). Soft tissues occasionally may become entrapped, necessitating an open reduction through a dorsal approach. The dorsal surgical approach splits the interval between the central slip and the lateral band on one side. The volar plate is cut in the midline, and the joint is reduced. Stability is checked after the reduction is performed, and a dorsal splint that blocks terminal extension is fabricated for use in the first 2 to 3 weeks, with the PIP joint in approximately 20 to 30 degrees of flexion. Again, residual flexion contracture is a concern, and active extension is emphasized by 3 weeks. Return to sports, especially if contact is anticipated, is delayed for 3 to 4 weeks with these more severe injuries. Buddy taping during the respective sporting activity is recommended until 6 weeks after injury or until nearly full motion is achieved.
Dislocations associated with significant volar fracture fragments at the base of P-2 are almost uniformly challenging to treat. Various authors have classified these injuries, and a variety of fracture configurations may exist, from simple large volar fragments to complex comminuted pilon injuries involving the entire articular surface of P-2 ( Fig. 77-6 ). It may be helpful initially to categorize these injuries by the percentage of the articular surface involved. Fractures with up to 30% involvement are usually stable after reduction and can be treated with dorsal block splinting or a dorsal K wire inserted into the head of P-1, under fluoroscopic guidance, to block the last 30 degrees of extension. The pin is removed at 3 weeks, but active flexion is encouraged during this time. Injuries involving the “gray zone” of 30% to 50% of the joint surface are potentially unstable, and care is dictated by the degree of instability. Fractures with involvement of more than 50% of the joint surface are consistently unstable and require surgical care virtually every time. Generally speaking, if a stable closed reduction cannot be obtained without unrealistic positioning of the joint, operative fixation is indicated.
If the volar fragments are large, direct fixation may be attempted with mini screws ( Fig. 77-7 ) or K wires ( Fig. 77-8 ) through a formal volar approach. For the open approach, a Bruner or curvilinear incision is made and the flexor tendon sheath is opened between the A-2 and A-4 pulleys to retract the tendons for exposure to the joint. The volar fragments are reduced and held with 1.0- or 1.5-mm screws ( Fig. 77-9 ). This procedure is technically demanding, and loss of motion is the unfortunate rule in most cases. A percutaneous technique has been described recently in a small case series. If the volar fragments are comminuted, open reduction may need to be combined with spanning external fixation, either statically or with dynamic traction. Badia and associates described a modification of a traction technique that was originally reported by Gaul and Rosenberg ( Fig. 77-10 ). Once the fixator is applied, a limited open reduction can be effected through a midaxial approach to elevate any articular fragments not reduced by the traction device.
It is surprising how many athletes ignore an injured, stiff PIP joint. When a PIP fracture/subluxation or fracture/dislocation is chronic (i.e., older than 4 weeks), a reconstructive procedure may be the only remaining option to improve PIP function. Although a detailed description is beyond the scope of this chapter, both volar plate arthroplasty and the newer technique of hemihamate arthroplasty for reconstruction of the base of P-2 are effective options. The hemihamate reconstruction is preferred in young active patients with a neglected PIP fracture/dislocation because it comes closest to restoring normal anatomy ( Fig. 77-11 ).
Volar dislocations of the PIP joint are rare but must not be missed, because treating them after a delayed presentation results in suboptimal function. An avulsion of the central slip occurs with volar dislocations. Closed reduction of most acute volar dislocations is successful, and the central slip avulsion is allowed to heal with the PIP joint splinted in full extension for approximately 6 weeks. The DIP joint is kept free for maintenance of active flexion during this phase. After 6 weeks, active PIP flexion is initiated and a nighttime static PIP extension splint and/or daytime dynamic extension splint is used for an additional 6 weeks.
An open dorsal approach is used for repair of volar PIP dislocations with avulsion fractures of the central slip attachment or central slip avulsion. A tension band technique is used with 26-gauge wire, a mini fragment (1.0- or 1.3-mm) screw, or a suture anchor ( Fig. 77-12 ). Rehabilitation entails protecting the dorsal central slip insertion for at least 6 weeks. Return to sports is delayed until approximately 3 months after surgical fixation of this injury.
DIP Joint or Thumb IP Joint
Dislocations of the DIP joints of the fingers and the IP joint of the thumb are less common than PIP joint dislocations. This phenomenon is explained by the short lever arm of the distal bony segment, highly congruous articular surfaces, and tight-fitting collaterals inserting at the lateral tubercles of the distal phalanx base (P-3 of the digit, and technically P-2 of the thumb). Dislocations of the terminal phalanx occur dorsally or laterally and are often associated with open wounds. Concomitant fractures and injuries to the flexor and extensor tendon insertions must be considered.
Once radiographs are performed to assess for an accompanying fracture, a closed dislocation is readily reduced with use of digital block anesthesia. The reduction is performed with traction and pressure exerted at the dorsal aspect of P-3 (or P-2 of the thumb). Stability is checked after the reduction is performed, and the digit initially is splinted in slight flexion. Active motion can begin after 5 to 7 days, with a block to terminal extension at about 20 degrees. Dorsal block splinting can be removed altogether by 3 weeks. Open injuries require irrigation and debridement in a sterile setting. Irreducible dislocations have been reported but are rare. Also seldom reported are simultaneous dislocations of both IP joints in the same digit. Checking flexor and extensor tendon function after a successful closed reduction is critical. Low-profile splinting and/or buddy taping may allow for an early return to sports.
CMC Dislocations of the Fingers
CMC injuries occur less frequently than their distal small joint counterparts in the digits. Anatomically, the ring and small finger metacarpal bases are more mobile and less constrained than the index and long metacarpal bases. The ring and small metacarpal bases articulate with two separate facets of the hamate. The base of the small metacarpal is convex from dorsal to palmar. This relationship and the insertion of the extensor carpi ulnaris tendon on the dorsal base of the metacarpal make the fifth CMC joint more unstable in a dorsal direction. The index base articulates with the trapezoid and also has facets that contact the trapezium, capitate, and long finger metacarpal. The long finger metacarpal base articulates primarily with the capitate and less so with the index and ring metacarpal bases. The index and long metacarpals have strong interosseous ligaments and are inherently more stable. The extensor carpi radialis longus and brevis tendons insert into the base of the index and long metacarpals, respectively.
Significant force is usually necessary to cause a digit CMC dislocation, and such force can occur with several sports-related mechanisms. Clenched-fist injuries come to mind first, in which the more mobile fourth and fifth metacarpal-hamate articulations are at risk from poorly executed “punches.” High-energy crush injuries of various causes may disrupt even the most stable columns of the index trapezoid (second CMC) and long capitate (third CMC) joints.
A history of ulnar-sided hand pain and deformity is typical, with crushing or axial force mechanisms of injury reported. Although volar dislocations have been reported, dorsal dislocations and fracture/dislocations make up the majority of injuries at the CMC level and usually involve axial and shear forces across the articular surfaces.
Radiographic evaluation is mandatory, and posteroanterior, lateral, and 30-degree pronated lateral radiographs of the hand depict the site of injury ( Fig. 77-13 ). Concomitant fractures at the bases of the metacarpals and/or the dorsal aspect of the hamate are probable. If the extent of fracture associated with the CMC dislocation is unclear, computed tomography is the advanced imaging modality of choice to better characterize the injury pattern.
Closed reduction of acute dislocations at the CMC level can usually be achieved with an adequate level of anesthesia, although irreducible dislocations have been reported. Persistent instability after an initial closed reduction is often evident, and supplemental percutaneous K wire fixation is recommended for most simple dislocations without a fracture. When a simultaneous fourth and fifth CMC dorsal dislocation is encountered, fixation may traverse the individual CMC articulations. Alternatively, parallel or slightly divergent wires may be oriented across the fourth and fifth metacarpal bases and into the stable third metacarpal base without crossing any articular cartilage. If a dorsal coronal fracture of the hamate is present, open reduction with internal fixation (ORIF) is performed using 2.0- or 2.4-mm screws, and the ring and small finger metacarpal bases are reduced and pinned to the volar part of the hamate. During dorsal open approaches to fracture fixation, care is taken to preserve crossing branches of the dorsal ulnar sensory nerve. Not uncommonly, the ring and small finger metacarpal bases are fractured and comminuted. In this situation, separate fragment-specific fixation may be attempted after applying longitudinal traction with the fingertraps.
The uncommon central CMC dislocations (index and long fingers) may be more reliably treated with the ORIF approach. Spanning joint fixation is not entirely inappropriate in some circumstances, given the paucity of motion at these articulations. Neglected dislocations of any CMC may warrant an attempt at ORIF once a diagnosis is made, with removal of abundant fibrous tissue at the site of a developing pseudoarthrosis. For chronic cases presenting months to years after injury, resection arthroplasty or arthrodesis are the remaining available salvage procedures, given the inevitable destruction of articular cartilage in these circumstances. Boxers and martial artists are prone to degenerative arthritis at these locations, with the arthritis attributed either to repetitive axial loading over a career or missed traumatic instability from a specific incident.
After successful reduction and pinning of acute CMC dislocations, the hand is protected for the first 4 to 5 weeks until pins are removed. MCP motion may begin early, and many surgeons advocate burying the pins to reduce complications relating to pin tract infection. After the pins are removed, a low-profile hand-based thermoplastic splint is fabricated, and emphasis is placed on MCP joint flexion arc of motion and gradual strengthening. Return to sports may be accelerated to soon after pin removal if the athlete can demonstrate adequate comfort, mobility, and strength. Delayed complications after appropriate treatment of these injuries are exceptionally rare.
Because most sports involve intensive use of the hands, both open and closed injuries to the flexor and extensor tendons happen routinely. For open injuries, examination, exploration, and repair of damaged structures are performed expediently. Closed tendon injuries in the hand may be subtle and overlooked, but they can cause sufficient morbidity that they deserve special attention for the purposes of this chapter. Extensor mechanism injuries are possible at the DIP, PIP, and MCP joint levels, with each producing consistent findings that must be mastered by the evaluating physician. At the opposite side of the finger, FDP avulsion, or “jersey finger,” is a serious and often neglected injury that will compromise composite digital flexion if it is not treated.
The anatomy of the dorsal apparatus of the finger is complex and has generated intricate descriptions. Its delicate balance allows the integration of intrinsic and extrinsic muscle function to coordinate fine digital motion. Disruption of the attachment of the terminal extensor tendon into the dorsal base of the distal phalanx has been termed mallet finger . Synonyms for this injury are baseball finger and drop finger , and “jamming” or “stoving” injuries in ball sports occur commonly. Axial load and forced flexion of the DIP joint can stretch the terminal tendon, avulse the tendon attachment, or cause an avulsion of bone from the dorsal epiphyseal ridge of the distal phalanx. Warren and associates described an area of terminal tendon hypovascularity as the site of vulnerability. The physical examination demonstrates the drooped posture of the DIP joint and the inability to completely extend the joint actively. The degree of dorsal swelling and tenderness is variable. Often players who present with an inability to extend the DIP joint after an injury also have PIP volar plate laxity with obvious hyperextension and a resulting swan neck deformity. Radiographs are obtained to define any bony injuries, with close attention paid to large avulsion fractures associated with volar subluxation of the DIP joint. It is more common to see a smaller avulsion fracture with variable displacement but without significant joint malalignment.
Splinting is the treatment of choice for virtually all mallet finger injuries. A comfortable DIP extension splint is placed; hyperextension is avoided because it may lead to dorsal skin necrosis, and the PIP joint is left free to avoid unnecessary proximal joint stiffness. Splints are worn full time for 6 to 8 weeks, followed by nighttime splinting only for an additional 4 to 6 weeks. Interestingly, as long as the joint is passively supple to full extension, nonoperative treatment may be commenced up to 3 months after the injury was sustained. Open treatment can result in unnecessary complications, and the surgeon should resist the temptation to “make good better” by overzealously performing surgery for these injuries. This clinical entity is one of the few for which the overwhelming evidence favors nonoperative treatment, even if slight volar subluxation of the DIP joint is seen on the initial lateral radiograph. In this regard, soft tissue and bony mallet injuries are treated identically.
We collectively treat all but a few select mallet finger injuries nonoperatively. Use of a comfortable volar-based thermoplastic DIP extension splint is preferred. The splint may be further secured with use of 0.5-inch adhesive tape or Coban wrap. A second splint might be provided for wear during showering and should be exchanged on a hard surface that supports the joint in full extension. Splinting is continued for a minimum of 6 weeks. In neglected cases with a late presentation, splinting can be prescribed for a longer period until satisfactory clinical results are achieved. Athletes who either remove the splint prematurely or inadvertently dislodge it essentially must “start the clock over.” Compliance is paramount, and good results are expected in virtually every case. Persons with PIP volar laxity are fitted with a figure-of-eight–type splint to block PIP hyperextension. Simultaneous volar and dorsal splinting can be provided to athletes in contact sports who want to play during the period of immobilization. A rare unstable fracture/dislocation of the DIP joint is the only acute scenario in which operative treatment warrants consideration. Chronic mallet injuries may lead to swan neck deformity, and chronic rigid deformities are referred to hand specialists for consideration of tenodermodesis or DIP fusion.
Closed Boutonnière (Central Slip Rupture)
The communis extensor tendon divides into three parts over the PIP joint of the digit. The central slip inserts into the dorsal base of the middle phalanx at the epiphysis. Two lateral slips of the extrinsic extensor tendon separate from the central slip just proximal to the PIP joint and accept a tendinous contribution from the intrinsic musculature to become the conjoined lateral bands at the level of the middle phalanx. These conjoined lateral bands are joined by the oblique retinacular ligament, which arguably facilitates conjugate extension of the PIP and DIP joints. In a closed injury, with forced flexion of the PIP joint, the central slip can rupture from its insertion. Concurrent injury to the tenuous triangular ligament allows volar subluxation of the lateral bands relative to the PIP joint axis of rotation. The boutonnière posture is defined by the resulting flexion moment at the PIP joint and hyperextension moment on the DIP joint from the malpositioned lateral bands ( Fig. 77-14 ). Avulsion fractures at the central slip attachment site can also cause this deformity. Boutonnière deformities may be classified as either acute or chronic and as either supple or rigid.
The Elson test has been shown to diagnose central slip ruptures most accurately. The affected digit is flexed 90 degrees over the edge of a table, and the patient is asked to actively extend the PIP joint against resistance. If the central slip is intact, the DIP joint remains supple. If the central slip is ruptured, the DIP joint remains rigid. This test will not diagnose a partial injury to the central tendon and may be inhibited by pain or lack of patient cooperation. As a confirmatory test, the PIP joint is held passively extended and the athlete is asked to flex the DIP joint. The inability to flex the DIP joint indicates a tear of the central slip.
Acute open lacerations of the central slip are repaired openly, and the repair is protected with a dynamic extension splint, such as the Capener or Bunnell splint, for 6 weeks. Although operative repair of a closed boutonnière deformity has been reported, most of these deformities can be treated with PIP extension splinting, leaving the DIP joint free ( Fig. 77-15 ). DIP flexion is encouraged because it pulls the lateral bands distally and expedites healing of the central slip. Extension splinting requires strict attention and must be uninterrupted. If compliance is an issue, percutaneous pinning of the PIP joint is an option, with pin removal at no later than 3 weeks and protected mobilization with a Capener splint for an additional 2 to 4 weeks. Return to sports in the nonprofessional athlete at 6 weeks is possible with buddy taping of the finger. In the elite athlete, many factors need to be weighed to arrive at the best treatment for the individual. Some players in certain sports will opt to accept the cosmetic deformity and return to active play without splinting once the pain subsides.
For the athlete who presents with severe DIP hyperextension (indicating significant retraction of the central slip), O’Dwyer and Quinton describe operative repair of the central slip with a suture anchor ( Fig. 77-16 ) and joint pinning for 2 to 3 weeks. With a neglected or chronic boutonnière deformity, the PIP contracture can be supple or fixed. If passive PIP extension is full, splinting can be tried, unless the athlete refuses to devote the 6 to 8 weeks necessary for successful closed treatment. If the PIP contracture is fixed, aggressive active splinting or serial casting is performed to effect full PIP extension. Once full passive extension is attained, static PIP splinting is maintained for 6 weeks. Rarely, a contracture release is performed by cutting the check rein ligaments located proximal to the volar plate, which is sometimes combined with open reconstruction of the central slip and mobilization of the lateral bands.
It should be reinforced that a “pseudoboutonnière” follows a ligamentous injury as a result of a hyperextension mechanism, with resultant scarring and contracture of the volar plate. This mechanism postures the PIP joint in flexion, mimicking a boutonnière position. However, the hyperextension mechanism of injury and subsequent examination can readily distinguish a true boutonnière from a pseudoboutonnière. In the latter, a chip avulsion fracture fragment is often seen near the volar lip of the middle phalanx where the injury occurred. In addition, with a pseudoboutonnière, the tenderness is almost exclusively at the volar side of the PIP joint, and the DIP motion is almost always normal. In the true boutonnière deformity, active and passive flexion of the DIP joint is impaired because of excessive tension on the terminal tendon as a result of proximally migrated lateral bands. Treatment of pseudoboutonnière is directed at progressive stretching of the PIP volar plate, with the introduction of dynamic splinting if necessary.
Sagittal Band Rupture
The extensor digitorum communis tendons are maintained over the dorsal apex of the MCP joints by a dorsal sling of adjacent transverse fibers, termed the sagittal bands . The sagittal bands act as a tether to prevent either radial or ulnar subluxation of the communis tendon at the level of the MCP joint. The sagittal band invests the extensor mechanism, crossing both volar and dorsal to it, ultimately blending into the volar plate. Radial sagittal band rupture can occur from forceful finger extension (a “flea-flicker” injury), a direct blow, or an ulnarly directed force. The radial sagittal band of the long finger ruptures most commonly, although ulnar sagittal band ruptures have been reported. Pain and snapping may occur, and a careful examination will document the tendon subluxation or dislocation. Clinically, the patient presents with an extensor lag at the involved MCP joint. Passive extension of the MCP joint is possible, however, and the patient can then usually maintain the finger in an extended position with the extensor tendon centralized. Tendon subluxation is promptly reproduced upon active MCP flexion.
Acute sagittal band ruptures can be treated with a static MCP extension splint or sagittal band bridge. Splinting continues for approximately 4 to 6 weeks or until extensor tendon subluxation vanishes when actively making a fist. Treatment of this condition represents a rare instance in which the MCP is immobilized in extension, counter to the “safe” position of the hand where the MCP joints are maximally flexed to prevent collateral ligament scarring in a lengthened position. For chronic cases and those with obvious persistent dislocation of the extensor tendon after failed conservative management, a repair is made surgically through a curvilinear dorsal incision, usually with reinforcement or reconstruction using a junctura tendinum or a portion of the extensor retinaculum. In chronic cases, Wheeldon described a surgical technique using the ulnar junctura, which is flipped over and sutured to the radial side. Postrepair immobilization is brief (2 to 3 weeks), but the MCP joint is now flexed 60 degrees to minimize joint contracture.
Few athletes will be comfortable enough to continue competitive play in the acute phase. This situation, coupled with the possibility of further damage to the extensor digitorum communis investments or underlying dorsal capsule from repetitive trauma, leads to the decision to provide treatment in-season in the majority of cases. We are not aware of ways to manage this pathology safely and effectively while allowing athletes (such as baseball or basketball players) to compete at a high level for the remainder of a season as they await out-of-season surgery. Obviously, mild injuries may require only a short period of missed play, whereas more severe injuries may prevent athletes from competing for several months.
Although the hands of any boxer can be subjected to a multitude of injuries, boxer’s knuckle specifically refers to chronic attritional disruption of the dorsal anatomy at the MCP joint. This disruption may include the extensor tendon investments, sagittal band, and/or dorsal capsule. A large capsular aperture may allow for metacarpal head protrusion and persistent flow of synovial fluid from the joint cavity to the subcutaneous space. Athletes who engage in punching and have early symptoms may possibly continue if proper protection is used and supervision is provided. Operative treatment ranges from sagittal band repair or reconstruction to dorsal capsular repair or excisional debridement. Tight dorsal capsular repairs may be counterproductively associated with loss of MCP flexion. Wrapping and gloving strategies with shock-absorbing padding may decrease further injury, but competition rules may restrict the use of some of the more effective types of equipment for these athletes.
“Jersey finger” is an avulsion of the FDP from its insertion on the distal phalanx. This injury classically occurs when an athlete, such as a football or rugby player, forcefully grabs an opponent’s jersey with flexed fingers as the opponent duly escapes the grasp. Various theories have been proposed to explain why the ring finger, as opposed to the long finger, is most commonly affected. The strength of the FDP insertion of the ring finger is significantly less than that of the adjacent digits. As one grips, the distal segment of the ring finger projects farther and becomes more prominent because of the increased mobility at the ring finger CMC joint.
Leddy and Packer described three types of injury, based on the following factors: (1) the presence or absence of a bony fragment radiographically; (2) the level to which the tendon retracted; and (3) the status of the blood supply of the avulsed tendon. The tendon can avulse with or without a bony fragment. The level of the bony fragment as shown on a lateral radiograph does not reliably predict the level of tendon retraction because the tendon end and bone fragment may separate. In a type I injury, the tendon has retracted into the palm, without the presence of a bony fragment. Early repair is required for this injury because retraction of the tendon into the palm and loss of blood supply lead to contraction. Type II avulsions often are accompanied by a small bone fragment and retract only to the level of the PIP joint, and the vinculum longum may still be intact. This injury can be successfully repaired up to 6 weeks after the injury occurs because the tendon length has been maintained. Type III injuries are accompanied by a large bony fragment and are restrained distally by the A-4 pulley ( Fig. 77-17, A ). These injuries also can be successfully repaired weeks after the injury is sustained. Because it is not possible to know the exact position of the avulsed tendon end by examination alone, proceeding with acute repair of all jersey fingers in athletes is justified. After the original three-part description by Leddy and Packer in 1977, a fourth type was added to the classification scheme. This fourth type involves an intraarticular fracture of the distal phalanx and separation of the tendon from the fracture fragment.
Loss of isolated DIP joint flexion is the sine qua non of this injury and is tested by blocking the PIP joint in an extended position while profundus function is checked. Keep in mind that the middle, ring, and small finger profundus tendons are connected to a shared muscle belly in the forearm, whereas the index profundus typically has its own separate muscle belly. Examination may reveal a prominence where the proximal ruptured tendon end is located. For instance, fullness and tenderness at the A-1 pulley area may indicate a type I injury with retraction to the palm level. Radiographs are mandatory. Ultrasonography and magnetic resonance imaging (MRI) are not necessary to diagnose this condition but may be useful adjuncts in equivocal cases in which the timing of surgery may be dictated by the classification of injury.
Surgical repair is best carried out within a week of the injury. The distal FDP insertion site is exposed with either a Bruner zigzag-type incision or use of the long midaxial approach. If the tendon has migrated proximally into the palm, the pulley system and fibro-osseous canal must be maximally preserved. The tendon can be passed distally with a pediatric feeding tube as a leader or by “milking” the tendon distally with smooth forceps from the palm just proximal to the level of the A-1 pulley. Distal insertional repair was historically performed with a pullout suture or wire, although suture anchor fixation recently has been advocated. If additional fracture fragments are present, they are fixed with mini screws ( Fig. 77-17, B ) before tendon repair. After repair, protective dorsal block splinting is provided and a passive Duran flexor tendon protocol is initiated under the supervision of an occupational therapist for the first 4 to 6 weeks. Graduated active flexion is encouraged. Resistive grasp and return to sports are delayed until 10 to 12 weeks after the repair is made.
Players may not seek immediate treatment for an FDP avulsion injury for a number of reasons. They may believe it is a minor injury that can be treated after the season is over, or they may not want to miss playing for a large part of their season. Informing the player of the long-term consequences of neglecting this injury is imperative, and the need for detailed documentation of conversations with the player cannot be overemphasized. Treating a neglected FDP avulsion is never as satisfying as performing a primary repair, and the clinical results are not nearly as functional. The following treatment options can be considered for a neglected FDP avulsion:
Late reinsertion: Late reinsertion is unlikely to be possible if the tendon has retracted a significant amount and the time from injury is beyond 6 weeks.
Acute single-stage reconstruction with a tendon graft: This option is fraught with potential complications, including loss of additional range of motion (in the PIP joint), scarring, and worsening of FDP function.
Two-stage flexor tendon reconstruction: This approach requires a large amount of effort by the patient, surgeon, and therapist and will probably be considered too aggressive a course to regain a small amount of DIP joint flexion. The first stage includes placement of a silicone rod to reconstitute the flexor tendon sheath, followed by exchange for a tendon graft at least 3 months later. A third flexor tenolysis surgery is probable in this treatment course as well.
Stabilization of the DIP joint by fusion or capsulodesis: Stabilization is often the most acceptable choice for the patient when risks and benefits are carefully considered.
Excision: If a retracted tendon is a tender mass in the palm, simple excision of the scarred proximal tendon end may relieve discomfort with grasping activities.
Nonsurgical treatment: Some players choose to do nothing after weighing the pros and cons of the aforementioned possibilities, and the desire to avoid a possible threat to PIP function is not entirely inappropriate.
The fibro-osseous canal and system of pulleys within the digits were elegantly described by Doyle and Blythe in 1977. Biomechanically, the A-2 and A-4 pulleys are critical for normal flexor tendon function and the prevention of “bowstringing.” The A-2 pulley overlies the proximal aspect of the proximal phalanx, whereas the A-4 pulley is at the level of the middle phalanx. Attenuation or frank rupture of a digital pulley occurs most often in rock climbers and baseball pitchers as a result of acute or chronic exposure to forceful contraction of the FDP tendon against a greater than physiologic load. In “free” rock climbers, the flexed DIP joint incredibly supports body weight repetitively and for prolonged intervals of the activity. The rock climbing hand posture of “crimping” specifically places massive strain on the distal part of the A-2 pulley and may understandably result in pulley rupture. Injury to the thumb pulley system is exceedingly rare.
On clinical examination, the patient reports pain over the flexor sheath. Swelling over the pulley may be present, and loss of terminal DIP flexion may be noted. Discomfort often occurs with active digit flexion. The athlete may perceive weakness, and pitchers will lose fastball velocity. The spectrum of injury ranges from partial injury of a pulley to complete rupture of multiple pulleys with overt bowstringing of the flexor tendons. Rarely, both the A-2 and A-4 pulleys fail simultaneously. MRI can aid in confirming the diagnosis and may show edema within the flexor tendon sheath and tendon bowstringing when the images are obtained with applied digital resistance.
Immobilization, rest, and use of antiinflammatory medication are initiated early. Return of complete range of motion is frequently delayed. When an acute pulley rupture is treated nonoperatively, an occupational therapist may fashion an external pulley ring to relieve stress on the pulley system. Buddy strapping and gentle range of motion may begin as edema decreases. PIP flexion contractures can complicate the postinjury course.
With rupture of the entire pulley system, loss of motion and bowstringing are evident. This situation requires surgical reconstruction of the A-2 and/or A-4 pulleys. The principles of reconstruction are to maintain the flexor tendons near the PIP and DIP centers of rotation. Reconstructed pulleys must be sufficiently strong to allow for early mobilization. A tendon autograft (e.g., the palmaris longus, plantaris, or partial flexor digitorum superficialis) or dorsal wrist retinaculum is used to reconstruct the pulleys. At the A-2 pulley level, the graft is placed beneath the extensor mechanism and then envelops the flexor tendons. At the A-4 level, however, the graft is placed over the extensor apparatus. Postoperatively, passive tendon gliding protocols are used, and ring splints help minimize stress to the newly reconstructed pulleys.
Fractures of the Metacarpals and Phalanges
This section highlights select athletic injuries involving the metacarpals and phalanges. A recent epidemiologic study clearly showed the high prevalence of hand fractures sustained during high school sports. Although most closed phalangeal and metacarpal fractures can be treated nonoperatively in the general population, athletes often demand operative approaches for definitive management. Because their predominant mindset is to be “better, faster, stronger,” athletes usually desire options that promote expedited healing and minimal interference with competitive play. Improved implant technology and surgical technique may allow for more aggressive fracture management in elite or professional athletes, but it is important to inform the athlete of all treatment options, possible complications, and realistic time frames for return to his or her respective sport.
Certain principles of injury treatment and fracture fixation are universal for small bone management in the hand. For example, most phalangeal fractures with less than 50% translational displacement, less than 10 degrees of angular deformity, and no shortening or rotational malalignment are often adequately treated by closed means. The same is largely true for metacarpal fractures, although neck and shaft fractures have less tolerance of angular deformity as they progress from ulnar to radial in the hand. Management is guided by a short-term immobilization period of 2 to 3 weeks, followed by gradual return of active range of motion with buddy taping and protective splinting, and lastly by passive joint stretching and progressive strengthening. In general, the hand responds to immobilization poorly, and prolonged casting can lead to tendinous adhesions and contracture of small joint capsules and collateral ligaments. General indications for hand fracture fixation include irreducible and malrotated fractures, displaced intraarticular fractures, open fractures, and multiple fractures. In athletes, the indications may be expanded to include injuries for which secure internal fixation permits an accelerated rehabilitation program. In this section, certain common fracture patterns are featured, and their unique management is highlighted.
Metacarpal Neck Fracture
Fractures at the fragile neck of the metacarpal occur with great frequency, and despite their benign neglect in many “street fighters,” these injuries deserve special attention in the athlete. The usual mechanism is an axial load to the metacarpal head, which often is engendered by a clenched fist injury. Knowledge of the surrounding anatomy is crucial for optimal treatment of these injuries. Metacarpal heads are cam shaped in the sagittal plane, and their collateral ligaments are taut with the MCP joints in 60 to 70 degrees of flexion, which necessitates splinting the MCP joint in at least 60 degrees of flexion after injury. To do otherwise invites the development of an MCP extension contracture, which is notoriously difficult to overcome. MCP extension is a nonfunctional position for grasp and is poorly tolerated, especially in the ring and small rays, the most common sites of metacarpal neck fractures. The lumbrical and interosseous muscles exert a flexion force at the metacarpal level. These muscle actions, combined with the axial load mechanism of injury, result in an apex dorsal angulation deformity for most metacarpal neck and transverse shaft fractures. Posteroanterior, lateral, and oblique radiographs are routinely obtained.
Nondisplaced or minimally displaced neck fractures are often treated with a removable ulnar gutter splint or functional brace with the MCP joints flexed 60 degrees and the wrist in slight extension. Angular deformity is more often a problem than malrotation in these injuries. In cases of displaced metacarpal neck fractures, a closed reduction should be attempted with the patient under a hematoma block or a wrist block. In the Jahss maneuver, the angular deformity is reduced ( Fig. 77-18, A and Fig. 77-19 ) with direct pressure, and the proximal phalanx is used as a plunger, with the MCP joint flexed, to lock the reduction. A plaster splint or cast is applied (see Fig. 77-18, B ), allowing digital motion, and is removed by no later than 3 weeks. Alternatively, Braakman and coworkers reported that simple buddy taping of fifth metacarpal neck fractures produced good results. Another recent study has shown that functional bracing with immediate range of motion produces superior results compared with complete immobilization. For unstable metacarpal neck fractures with significant apex dorsal angulation (especially >70 degrees), reduction and pinning to an adjacent metacarpal works well. A great deal has been written recently about intramedullary (bouquet) pinning for metacarpal shaft and neck fractures. In a well-designed study, intramedullary pinning and transverse pinning worked equally well for unstable neck fractures. Regardless of the method used, composite digital motion must be emphasized in the early postoperative period. Intraarticular extension of a neck fracture is treated with ORIF, using headless compression screws as needed to restore the articular surface without hardware irritation.