Chapman’s Orthopaedic Surgery
3rd Edition

James S. Thompson
Clayton A. Peimer
J. S. Thompson: Carolina Hand Surgery Associates; Mission-St. Joseph’s Health System, Asheville, North Carolina, 28801.
C. A. Peimer: University at Buffalo School of Medicine and Biomedical Sciences, State University of New York; Millard Fillmore Health System, Buffalo, New York, 14209.
“The hand,” wrote Sterling Bunnell, “includes exact machinery of much refinement and tissues of great delicacy and specialization” (8). The extensor mechanism is a prime example of the “machinery” Bunnell was describing. Because of its subcutaneous vulnerability, it is one of the most frequently injured structures in the hand.
Many anatomists have appreciated the complexity of the extensor mechanism, among them Albinus, who presented the first detailed structural description in 1734 (46). Reconstructive surgeons who attempt surgical correction of hand dysfunction resulting from extensor tendon injury or imbalance quickly gain respect for the structure.
Intrinsic muscle abnormalities aside (see Chapter 63), the diagnosis of most extensor lesions (acute and chronic) is relatively simple. Likewise, the surgical exercise of tendon suture is not as technically demanding as it is for flexor tendons, because the extensors are primarily extrasynovial. The thin nature of the extensors within the digits, however, as well as the intimate proximity of the extensor mechanism to periosteum and bone (to which it readily adheres) and the influence of the digital extensors on the critical function of the interphalangeal joints (49,58), all contribute to potentially poor functional results following surgical treatment of extensor tendon injuries (19,20,22,23,25,36,45,51,74).
In the fingers, proximal interphalangeal (PIP) and distal interphalangeal (DIP) motion are interdependent, and


lack of or excess of extension in either joint reciprocally affects the other. The swan-neck or boutonnière positions are the classic examples of this interphalangeal reciprocity (see Fig. 49.10). The entire extensor mechanism, the total digital deformity, and the lack of motion or presence of abnormal motion at each joint must be considered in planning reconstruction (13). Eaton has aptly described the extensor mechanism as a “sleeping giant which is not appreciated until it becomes disorderly or out of balance. When out of control it can create great disturbances” (17).
Figure 49.10. The dorsopalmar translation of the conjoined lateral bands is demonstrated in the two classic reciprocal digital deformities: swan-neck (top) and boutonnière (bottom). The insets are transaxial representations of the condyles of the proximal phalanx, showing the normal positions of the conjoined lateral bands in extension and flexion of the PIP joint. The abnormal positions of the conjoined lateral bands in each deformity are represented in black.
Restoring a normally functioning extensor mechanism can be more difficult than reconstructing a flexor system. A surgeon contemplating such a restorative attempt must approach the problem with complete understanding and great care. Failure to comprehend the diverse and complex structure’s functional anatomy and to appreciate the need for proper dressing and appropriate rehabilitation may contribute to poor results in extensor reconstruction, regardless of the anatomic level or the mechanism of injury (22).
This chapter is not meant to be a compendium of procedures but rather a description of principles and concepts useful for devising appropriate management for each case. The primary focus of the chapter is the finger extensor mechanism; the thumb extensor system and the wrist extensor will be discussed briefly. Table 49.1 lists abbreviations and terminology that will be used.
Table 49.1. Abbreviations and Terminology
The digital extensor system consists of three joints extended by a single confluent tendinous mechanism (Fig. 49.1, Fig. 49.2) formed by the interlinkage of two separate and neurologically independent components: tendons of the extrinsic, radial-nerve-innervated muscle and tendons of the intrinsic, ulnar/median-nerve-innervated muscles.
Figure 49.1. The extensor mechanism of the wrist and dorsum of the hand. The six extensor compartments at the wrist contain (1) the abductor pollicis longus (APL) and extensor pollicis brevis (EPB); (2) the extensor carpi radialis longus (ECRL) and brevis (ECRB); (3) the extensor pollicis longus (EPL); (4) the extensor digitorum communis (EDC) II–V and extensor indicis proprius (EIP); (5) the extensor digiti quinti (EDQ); and (6) the extensor carpi ulnaris (ECU). An important anatomic detail is the presence of a synovial sheath around each tendon unit within each fibro-osseous canal. These sheaths are often involved in rheumatoid disease.
Figure 49.2. Digital extensor mechanism. A: Dorsal view. B: Lateral view.
The radially innervated extrinsic extensors contributing to the extensor mechanism, and their fingers of action, are the extensor digiti communis (EDC) (all fingers), the extensor indicis propius (EIP) (index), and the extensor digiti quinti (EDQ) (little finger) (Fig. 49.1). While this arrangement is considered normal, subtle variations in extrinsic extensor tendon anatomy are fairly common (2,15,27,67,77,79,83), especially the presence or absence of a discrete separate EDC tendon to the little finger (60). After passing beneath the extensor retinaculum (69) (through synovial sheaths within each extensor compartment), the extrinsic extensor tendons are interconnected by juncturae tendinum on the dorsum of the hand (66,78,80). Laceration of individual extrinsic extensor tendons proximal to the juncturae may be masked by partial metacarpophalangeal (MP) extension transmitted through the juncturae by the adjacent tendons (15,66,78,80). The juncturae tendinum may act as force vectors in the dynamic stabilization of the MP joints during flexion (1).
At the MP level, the sagittal bands (Fig. 49.2, Fig. 49.3), which act to maintain centralization of the extensor tendons, form the most proximal insertion of the extensor mechanism (37). The sagittal bands surround the metacarpal heads and insert into the MP volar plate and intervolar plate ligaments (Fig. 49.3B). The sagittal bands also prevent dorsal prolapse of the extrinsic extensor tendons during MP hyperextension (Fig. 49.4).
Figure 49.3. A: Radial sagittal band of the middle finger. There is a natural cleavage plane (through which the scissors penetrate) between the transverse fibers of the sagittal band and the oblique fibers from the lateral slip (arrows) to the central slip (CS). B: Transaxial view at the MP level of the sagittal bands and their insertion into the periphery of the volar plate (VP) and intervolar plate ligament. Note the relationship of the interossei and lumbrical to the MP axis of rotation and intervolar plate ligament.
Figure 49.4. Hand of a 39-year-old woman with systemic lupus erythematosus, treated for 20 years with oral steroids. All five extensor tendons subluxate with digital flexion. With extension, marked MP hyperextension/dorsal prolapse of the EDC tendons is present due to incompetence of the MP sagittal bands.

Attenuation or injury to the radial aspect of a sagittal band may allow subluxation of the extensor tendon into the ulnar intermetacarpal sulcus with MP flexion (36). If this subluxation is reducible, the physical finding may simply be painful snapping as the tendon moves to and fro with MP flexion or extension (Fig. 49.5) (30,33,34,58,59). If, however, the extensor tendon becomes permanently fixed palmar to the MP axis of rotation in the ulnar intermetacarpal sulcus (frequently seen in rheumatoid disease; see Chapter 70), it becomes a strong MP flexor and contributes significantly to ulnar deviation of the fingers (56).
Figure 49.5. A: Ulnar subluxation of the EDC of the middle finger (arrow) with finger flexion in an elderly patient with extremely atrophic skin. B: Reduction of the subluxation occurs with finger extension.

Because the MP joint is proximal to the zone of convergence (Fig. 49.6) of the intrinsic and extrinsic contributions to the digital extensor mechanism, these two separate and distinct systems act as antagonists at this level. The intrinsics, being palmar to the MP rotational axis, act as MP flexors; the extrinsics, being dorsal, are MP extensors (Fig. 49.2B). This paradox of action at the MP joint is a primary factor contributing to difficulty in understanding the digital extensor mechanism (17,43).
Figure 49.6. The zone of convergence of the digital extensor mechanism, which begins at about the midportion of the proximal phalanx and ends at the level of the central slip insertion into the dorsal base of the middle phalanx. Proximal to the zone of convergence, the extrinsic and intrinsic components of the extensor mechanism are separate: The central slip is extrinsic, while the lateral slips are intrinsic. Within the zone of convergence there is complete reciprocal crossover of fibers from the central slip and lateral slips. The products of the completed convergence are the central slip insertion and the conjoined lateral bands, both of which have dual muscular activity (intrinsic and extrinsic) for extension of both interphalangeal joints. PIP, proximal interphalangeal joint; TRL, transverse retinacular ligament; ORL, oblique retinacular ligament; E, extrinsic contribution to conjoined lateral bands; I, intrinsic contribution to central slip insertion.
An insertion point of the extrinsic extensor is present in the dorsal MP capsule and dorsal base of the proximal phalanx (Fig. 49.7, Fig. 49.8). Although the insertion point has been described as indifferent (17) and variable (46), it is consistently present and represents the second of the insertion points of the extensor system, the first being the sagittal bands (Fig. 49.3) (75). These two insertion points are not firmly fixed bony insertions in the pure sense, as are those at the dorsal base of the middle and distal phalanges. In fact, these insertions have an excursion approximately equal to the excursion of the central slip at the PIP joint (Table 49.2) and therefore become taut only when the PIP joint is in full extension (18).
Figure 49.7. Lateral aspect of a finger demonstrating the four insertion points of the extensor mechanism. (1) Insertion through the sagittal bands into the volar plate and intervolar plate ligament. (2) Extensor insertion into the dorsal MP joint capsule and base of the proximal phalanx. This is a loose or indifferent insertion. (3) Central slip insertion into dorsal base of middle phalanx. (4) Terminal extensor insertion into dorsal base of distal phalanx.
Figure 49.8. Extensor insertion into the dorsal MP capsule and dorsal base of the proximal phalanx (arrow). This insertion is filmy and loose and has an excursion equal to the extensor amplitude at the PIP joint. This “insertional excursion” allows PIP and DIP flexion while the MP joint is in maximum hyperextension. With PIP extension, however, this insertion becomes taut and assists extension of the proximal phalanx (PP). MC, metacarpal.
Table 49.2. Extensor Tendon Excursiona
This function can be easily demonstrated in a normal finger by maintaining the MP joint in maximum hyperextension and actively flexing and extending the interphalangeal (IP) joints. A fixed insertion of the extrinsic extensor at the MP level would obviate the possibility of this maneuver. If the entire extensor mechanism is lacerated at the proximal phalangeal level (rarely the case in isolated laceration of the tendon, because of its broad convex shape, but frequently seen in dorsal guillotine-type injuries with transection of the bone), the extensor mechanism retracts only a distance equal to or less than the available insertional excursion.
The intrinsic muscle group contributing to the extensor mechanism is composed of the interossei (all ulnar-innervated), the fourth and fifth lumbricals (ulnar-innervated), and the second and third lumbricals (median-innervated). Along the proximal phalangeal segment, the fibers of the intrinsic tendons (lateral slips) merge, winglike, into the central slip (Fig. 49.9A). This configuration explains the necessity of the triangular (wing) excision (Fig. 49.9B) in cases of intrinsic muscle contracture proposed by Littler for complete intrinsic release (41). A smaller excision or simple lateral slip tenotomy will not completely eliminate the influence of abnormal intrinsic muscle tension on the central slip and its attendant limitation of IP flexion.
Figure 49.9. A: Anatomic preparation demonstrating winglike configuration of intrinsic contribution to the digital extensor mechanism. B: The wing excision of Littler that is necessary for complete elimination of intrinsic influence on the digital extensor mechanism. CS, central slip; LS, lateral slip.
At about the midportion of the proximal phalanx, the central slip begins its trifurcation. Distal to this level of trifurcation, there is free exchange of fibers from the central slip to the lateral slips and from the lateral slips to the central slip (Fig. 49.6). Distal to the anatomic zone of convergence, the central slip and conjoined lateral bands are truly a dual extensor mechanism with both intrinsic and extrinsic contributions, either (or both) of which is capable of powering active IP extension.

Fowler recognized this dual nature of the extensor assembly in 1949 (24). Even Bunnell had held a different functional view of the extensor mechanism before Fowler’s observations (D. C. Riordan, personal communication, 1987) (8,46). This duality of extensor motor power at the IP joint (29,54), plus the mechanical concept of a dynamic IP tenodesis [the oblique retinacular ligament (ORL)], forms the basis for many procedures involving redistribution of forces in IP joint extensor dysfunction (42,47,73,76).
At the PIP joint, the transverse retinacular ligaments (TRL) act to gently maintain the conjoined lateral bands within certain limits of dorsopalmar excursion (Fig. 49.2B). This dorsopalmar translation of the conjoined lateral

bands (Fig. 49.10) was presented in 1923 by Hauck (31). Palmar displacement of the conjoined lateral bands occurs normally with PIP flexion, allowing synchronized distal interphalangeal (DIP) flexion (62). Smooth, unrestricted DIP flexion depends on normal PIP flexion, which allows relaxation of the conjoined lateral bands and oblique retinacular ligament.
Lax PIP volar plates (VP) in some people allow DIP flexion while the PIP joint is maintained in extension (usually slight hypertension). This maneuver is possible only in people with PIP-VP laxity and normal supple intrinsic muscles. Repeating this “trick” may result in further VP laxity, stretching of the TRL, allowing further dorsal migration of the conjoined lateral bands and development of painful locking of the PIP joint in hyperextension, a dynamic swan-neck deformity (Fig. 49.10, Fig. 49.11).
Figure 49.11. Dynamic swan-neck deformity in a professional musician with PIP volar plate laxity. The conjoined lateral bands (arrows) bowstring dorsally as the transverse retinacular ligament stretches (see Fig. 49.10). The finger is locked in extension at the PIP joint, causing occupational disability. Successful surgical treatment was flexor superficialis tenodesis of the PIP joint blocking PIP hyperextension; this allowed complete DIP extension.

This phenomenon clearly illustrates the participation of the static VP in the normal and abnormal dynamics of extension. Littler has emphasized the importance of the VP as an adjunct to the dynamic process of normal digital extension (49). VP stretching or contracture also contributes to the fixed reciprocal deformities, including the swan-neck deformity (PIP hyperextension and DIP flexion) and the boutonnière deformity (PIP flexion and DIP hyperextension).
The central slip terminates in a broad, strong bony insertion at the dorsal base of the middle phalanx (Fig. 49.12). The conjoined lateral bands merge over the dorsum of the middle phalangeal segment to form the terminal extensor tendon (Fig. 49.2A), which inserts into the dorsal base of the distal phalanx (Fig. 49.13). The triangular ligament is composed of transverse fibers between the conjoined lateral bands distal to the central slip insertion and proximal to the merging of the bands (Fig. 49.6) (37).
Figure 49.12. Broad insertion of central slip (CS) into the dorsal base of the middle phalanx. The glistening, gliding layer is seen covering the dorsal aspect of the proximal phalanx.
Figure 49.13. Bony insertion of the terminal extensor (TE) into the dorsal base of the distal phalanx. The proximal ends of the conjoined lateral bands (arrows) are visible at the PIP joint level.
The ORL may play a unique and integral role in the extensor system. The existence and biomechanical significance of the ORL in normal digits is controversial (53,55,65). Weitbrecht illustrated this structure in 1742 and named it the retinaculum tendini longi (82). The ORL

(Fig. 49.14) originates palmar to the PIP axis of rotation from the periosteum of the proximal phalanx and flexor sheath and passes dorsally and distally to join the terminal extensor tendon (63). Walsh clearly demonstrated the ORL in a prize-winning monograph in 1897 (81). Landsmeer subjected the ligament to a sophisticated dynamic analysis, and the soundness of the mechanical basis of a “dynamic interphalangeal tenodesis” concept has induced procedures designed to augment DIP extension based on active PIP extension (38,39 and 40,42,73). ORL tightness may also contribute to pathologic conditions such as fixed DIP hyperextension in the boutonnière deformity and DIP extension contracture in digital Dupuytren’s disease (see Chapter 62).
Figure 49.14. The oblique retinacular ligament, elevated by the probe, originates along the proximal phalangeal periosteum and flexor sheath, passes volar to the PIP axis of rotation, and joins the terminal extensor tendon. The principle of “dynamic interphalangeal tenodesis” is based on the biomechanical fact that a structure of fixed length extending from the proximal phalanx to the distal phalanx, palmar to the PIP axis, and dorsal to the DIP axis will relax with PIP flexion and tighten with PIP extension.
Complete understanding of the extensor mechanism is elusive, but functional understanding requires only time and assimilation of many small bits of information. The complete mechanism (Table 49.3)—extrinsic and intrinsic motors, merging tendons, dynamic and static retaining ligaments, and other contributing components—when functioning normally has been described as a “fugue of motion” (J. W. Littler, personal communication, 1987).
Table 49.3. Components of the Digital Extensor System
The abductor pollicis longus (APL) inserting on its dorsal base and into the fascia of the thenar intrinsic muscles provides extension and abduction of the first metacarpal (Fig. 49.1). The multiple slips of this muscle–tendon unit make it very useful in reconstructive procedures at the base of the thumb (70).
The variable extensor pollicis brevis (EPB) inserts into the dorsoradial base of the proximal phalanx and the extensor pollicis longus (EPL) into the dorsal base of the distal phalanx (Fig. 49.1). These two muscle–tendon units exert extensor influence on multiple joints: the EPB on the trapeziometacarpal joint (extension/abduction) and MP joint (extension); and the EPL on the trapeziometacarpal

joint (extension/abduction), MP joint (extension), and IP joint (extension).
The intrinsics of the thumb [abductor pollicis brevis (APB), flexor pollicis brevis (FPB), and adductor pollicis (AP)] contribute to IP extension through the extensor hood at the MP joint and frequently confuse the inexperienced examiner in cases of suspected EPL laceration (48). The intact thenar intrinsics will extend the IP joint to a near-neutral position, but the diagnosis of EPL rupture or laceration is obvious if the entire thumb ray is compared with that of the uninjured thumb.
A “dropped joint” (lack of full extension with posture in flexion) at the site of extensor muscle tendon action is the simple sign of complete extensor functional deficit (43). An MP drop is seen with extrinsic extensor laceration or rupture, a PIP drop with complete central slip laceration or rupture, and a DIP drop (mallet) with terminal extensor tendon laceration or rupture.
In the thumb, laceration of the contents of the first extensor compartment (EPB, APL) will present as flexion/adduction of the first metacarpal and a lag in full extension of the MP joint. The EPL functions as both MP and IP extensor in this situation. Isolated laceration of the EPB is rare, and repair of this tendon is optional, depending on the functional deficit at the MP joint. This lesion is frequently undiagnosed in the emergency situation because of the presence of MP extension through the intact EPL. EPL extension of the MP joint, however, will usually be incomplete when compared with that of the opposite, uninjured side. The magnitude of the MP extensor lag secondary to EPB laceration is variable, and this factor determines whether EPB repair is warranted.
Two basic patterns of EPL laceration are seen, and the presentation depends on whether the laceration site is proximal or distal to the MP joint. Proximal to the MP joint, the entire thumb ray is affected and demonstrates metacarpal adduction, incomplete MP extension, and IP extension lag (some IP extension remains, by virtue of intact thumb intrinsics). The EPL retracts significantly when lacerated proximal to the MP extensor hood, and retrieval from the synovial extensor compartment or the distal forearm may be difficult and may require a proximal counterincision.
Extensor pollicis longus laceration distal to the MP joint is simpler, easily diagnosed by consideration of the injury location and loss of IP hyperextension. The tendon cannot retract more than a few millimeters because of its attachment to the MP extensor hood. It should be repaired and treated as a sharply lacerated terminal extensor tendon of a finger (discussed later).
Several simple maneuvers will establish the location of restriction of gliding (tenodesis) of the extrinsics or contracture/fibrosis of the intrinsic components (Table 49.4). The level of extrinsic tenodesis is frequently made obvious by scars. Intrinsic contracture and contracture of the ORL, however, cannot be appreciated without the use of clinical tests (43).
Table 49.4. Clinical Tests for Tightness or Entrapment of Extensor Mechanism Components
Bunnell in 1922 was the first surgeon to enumerate the reasons for poor results after tendon surgery (7). He was primarily discussing flexor tendons, and the reasons remain valid and apply equally well to extensor tendons (Table 49.5).
Table 49.5. Reasons for Poor Results after Extensor Tendon Surgery
The integrity of the gliding layer between the extensor mechanism and the phalanges is important. This layer is often described as periosteum, and indeed the deep portion of the layer is phalangeal periosteum. The superficial cellular components of the gliding layer, however, are more areolar in nature and cannot be distinguished from paratenon. Absence of the gliding layer makes adherence to bone much more likely. Repair of a cleanly lacerated gliding layer, when possible, improves chances for more normal extensor excursion. Preserving the gliding layer in

the exposure for reconstruction of phalangeal fractures improves the postoperative range of motion (14,58). Careful preservation of the gliding layer improves results after other elective procedures, and this specialized tissue should be considered an integral part of the extensor mechanism (71).
Surgical approaches that involve splitting the extensor tendon and gliding layer are unnecessary and should not be used. They do not facilitate bone reduction but rather create severe extensor mechanism trauma, resulting in adherence and loss of tendon amplitude. Incisions preserving the entire extensor mechanism allow access and reduction of all phalangeal fractures (14,52).
The major dualities in the digital extensor mechanism should be fixed in the surgeon’s mind (Table 49.6). A knowledge of these redundancies in the system facilitates

decision making in both acute repairs and late reconstructions. A common power-saw injury, for instance, results in an untidy laceration of a lateral slip and portion of the central slip over the proximal phalangeal segment with destruction of the underlying gliding layer and abrasion or cortical chipping of the phalanx. Such an injury is best treated by debridement of the shredded tendon followed by early initiation of motion.
Table 49.6. Extensor System Dualities
Unnecessary repair of tendons in these circumstances is done when the surgeon does not realize that there is enough undamaged extensor mechanism to perform IP extension. Adequacy of the mechanism can be checked easily after digital anesthesia by asking the patient to straighten the finger. Recognizing the redundancy of the extensor mechanism, and therefore the expendability of certain elements, should prevent one of the complications of extensor repairs seen by hand surgeons—unnecessary suture of partial lacerations resulting in digits stiffly fixated in extension.
Little has been written about the repair of lacerated wrist extensor tendons, and the subject deserves mention. The wrist extensors maintain balanced alignment of the hand and provide stabilization of the hand during grip. They should be repaired when possible. Isolated laceration of a wrist extensor is rare, because of the intimate anatomic arrangement of the extensor complex in the forearm and wrist. Wrist extensor tendon lacerations are therefore usually associated with laceration of one or more of the digital extensors.
Careful physical examination to rule out associated neurovascular injuries is mandatory (stab wounds in the forearm with small entry wounds may be very misleading), followed by complete surgical exploration and repair. Dorsal laceration in the proximal forearm frequently involves branches of the radial nerve. Explore and repair them if feasible. Muscle bellies of the extensor muscles can be opposed with nonabsorbable or synthetic absorbable sutures (Table 49.7).
Table 49.7. Suture Materials for Extensor Tendon Repaira
Fibrous septae within the substance of muscles, when identifiable, afford the most secure purchase for suture placement. Synthetic, slowly absorbed sutures are now preferred for peripheral sutures of muscle and tendon. The details of extensor repair—positioning after surgery, proper dressings and splints, patient education, and appropriate type and timing of therapy—are more important than the type of suture material used (72).
Because the brachoradialis (BR), extensor carpi radialis longus (ECRL), extensor carpi radialis brevis (ECRB), EDC, and EDQ have their origins from the lateral epicondyle, elbow flexion (in addition to wrist extension) facilitates repair (15). After surgery, use a long-arm dressing with elbow at 90° flexion, the forearm in neutral rotation, the wrist extended 45°, and the MP joints flexed about 15°. Allow the IP joints full, unrestricted motion throughout treatment of the injury. Allow active motion of the MP joints at 3 weeks, and of the elbow at 4 weeks (Table 49.8). At 5 weeks, gently institute wrist motion under the guidance of a hand therapist. Use a removable splint that maintains the neutral or slightly extended position between exercise sessions and at night for an additional 3 to 4 weeks. The development of sufficient tensile strength to allow application of significant stress across the repair requires at least 5 weeks (50). However, some motion at the juncture site is beneficial for the return of maximum postoperative tendon excursion.
Table 49.8. Postoperative Management of Extensor Tendon Repairs in the Forearm and Wrista
The keys to the best results, therefore, are protection that is adequate for the specific repair and some motion that is prompt enough to achieve early tendon gliding. The surgeon determines the immobilization method and mobilization sequence. Observe the juncture directly before wound closure and assess the effects of passive MP and IP flexion. Because about 60% of the digital extensor amplitude occurs at the wrist, immobilization of the wrist in extension affords significant protection for extensor repairs (45). Graduated institution of range of motion for each of the joints possibly affected by extensor injuries, rather than prolonged immobilization of all joints, contributes to improved results (6,21).
In addition to individualized mobilization of joints, frequent

clinical evaluation by the surgeon and close supervision by an informed, experienced hand therapist are necessary to achieve optimum results following extensor repair or reconstruction (6,21,61).
Laceration of a single tendon of the EDC may be masked by juncturae tendini pull-through. Laceration of the EIP and EDQ results in loss of independent MP extension of the index or little finger. Repair all of these tendons (3) using appropriate core and outer sutures (Table 49.7).
The method of immobilization (Table 49.9) is similar to that for lacerations in the forearm and wrist. Involvement of the EDC tendons necessitates inclusion of all fingers in the dressings and splints, but isolated lacerations of the EIP and EDQ may be treated with immobilization of only the involved digit and the wrist.
Table 49.9. Postoperative Management of Extensor Tendon Repairs in the Dorsum of the Hand
Delayed repair of a lacerated extensor tendon and MP joint capsule is prudent. The rationale for wound irrigation, inspection, open wound treatment, splinting, and delayed repair after 5 to 10 days of antibiotic treatment is to minimize the risk of infection from human bites, which is increased by primary closure (16). Primary closure, an inappropriate treatment for a human bite, frequently leads to septic destruction of the MP joint (see Chapter 73). Perform primary closure of lacerations of the extensor tendon and MP joint only if you are confident of the history, and if the wound appears compatible with that history. The methods and duration of immobilization are the same as those described for extensor lacerations on the dorsum of the hand (Table 49.8).
Extensor Subluxation
Closed subluxation of the extensor tendon at the MP joint (Fig. 49.5) can frequently be managed successfully with extension splinting for 4 to 6 weeks (57). Repair acute sharp injuries to the radial sagittal band of the MP joint to prevent ulnar extensor tendon subluxation. Chronic subluxation that does not respond to MP extension splinting requires surgical treatment. Release the ulnar sagittal band and, if possible, reef the radial sagittal band. If adequate substance for repair is not present in the radial sagittal band, several surgical reconstructions have been described using juncturae or strips of the tendon secured to soft tissue on the radial side of the joint to prevent the ulnar subluxation (10).
Complete laceration of the extensor mechanism at the proximal phalanx is very rare without transection of the

digit. Therefore, lacerations over the proximal phalanx are usually partial and affect only the tendon over the convex portion of the phalanx. These tendon injuries do not retract significantly, do not result in loss of extension at the IP joints, and are usually diagnosed only through direct visual inspection of the wound.
Repair of the central slip is indicated, but lateral slip repair, especially if the gliding layer is disrupted, is optional. Treat untidy injuries of a single lateral slip with debridement of the crushed tendon ends. Initiate motion after 10 days of splinting. Remember the dualities of the system and the concept of expendability in crushing and abrading injuries. Fine, synthetic, slowly absorbable sutures are preferable for repair of the central slip.
After repair of partial laceration of the central slip, ask the patient to actively flex and extend the MP and PIP joints. This exercise provides some indication of whether early motion will jeopardize the repair. If no tension on the repair is demonstrated with active flexion/extension of the MP or PIP joints, consider early motion. If there is significant tension on the repair, follow the postoperative regimen for laceration of the extensor tendon at the PIP joint (Table 49.10).
Table 49.10. Postoperative Management of Extensor Tendon Repairs of the PIP Joint (Acute Boutonnière Deformity)
Untreated laceration of the central slip at the PIP joint allows development of the buttonhole (boutonnière) deformity. The inevitable flexion of the middle phalangeal segment due to unopposed FDS pull encourages herniation of the proximal phalangeal condyles through the central slip defect. As the PIP flexion deformity progresses, the conjoined lateral bands slide palmar to the PIP axis, maintaining and increasing PIP flexion and tightening the terminal extensor, which produces DIP hyperextension (Fig. 49.10). The boutonnière deformity, when allowed to progress, is one of the most difficult reconstructive challenges to confront a hand surgeon (9,47,61,76).
The key to prevention, in sharp injuries, is careful exploration of all wounds over the PIP dorsum and extensor tendon repair. If there is a complete PIP extension deficit, the PIP joint should be maintained in full extension with a transarticular Kirschner wire before tendon repair. If the PIP extension deficit is not severe (less than 30° to 40°), tendon repair and external splinting will usually suffice. Careful postoperative management (Table 49.10) is necessary for optimum results.
Closed dorsal injury at the PIP level is the cause of many late-presenting, difficult, fixed boutonnière deformities. Prevention in these cases is simply based on an awareness of the potential problem and a high index of suspicion. Immobilize the PIP joint in extension and observe it with careful follow-up examinations. Unrestricted finger flexion after blunt trauma to the dorsum of the PIP region with central slip contusion/rupture may lead to severe deformity. PIP flexion, therefore, should be instituted gradually

and only after follow up examinations reveal full active PIP extension. If there is significant periarticular swelling and pain with attempted flexion, a prudent assumption is that the injury is a closed boutonnière deformity until proven otherwise; adherence to the regimen presented in Table 49.10 is indicated.
At least seven classifications of classic mallet-finger deformity (dropped distal phalanx) exist.
  • Closed rupture of the terminal extensor tendon
  • Intraarticular avulsion fracture of the terminal extensor insertion (dorsal base of the distal phalanx) without palmar DIP subluxation
  • Intraarticular avulsion fracture of the terminal extensor insertion (dorsal base of the distal phalanx) with palmar DIP subluxation
  • Open laceration of the terminal extensor at the middle phalanx or DIP level
  • Dorsal abrasion/degloving-type composite tissue injury with loss of tendon substance
  • Extraarticular fracture at the base of the distal phalanx in adults with marked palmar angulation
  • Transepiphyseal fracture of the distal phalanx in children with marked palmar angulation
Most mallet fingers fall into the first four groups, and it is these that are the basis for discussion of mallet fingers in this chapter. Fortunately, injuries in the fifth group are relatively rare; they often require flap or graft coverage (see Chapter 8, Chapter 38) before extensor tendon reconstruction can be considered. The last two groups of fractures, because of marked palmar angulation at the fracture site, are usually associated with nail-root avulsions and are treated relatively easily (see Chapter 38, Chapter 40).
All mallet fingers involving loss of terminal extensor contact with the distal phalanx (groups 1 through 5) may present with PIP recurvatum (swan-neck deformity), the magnitude of which depends on the ability of the PIP VP to resist the increased extensor force (central slip plus conjoined lateral bands) on the middle phalanx.
Mallet fingers in groups 1 and 2 can be managed satisfactorily by closed means in Stack splints (11,26,65). In group 2, the area of articular surface on the fracture fragment of the distal phalanx is not critical, as long as the DIP joint is not palmarly subluxated (11). Even though anatomic reduction may be impossible in a splint, results are good if joint alignment is maintained (11).
The presence of palmar subluxation of the distal phalanx

indicates that enough of the DIP collateral ligament insertion is present on the fracture fragment to allow the unopposed FDP insertion to palmarly displace the distal phalanx. This circumstance usually does not occur until 50% or more of the articular surface of the distal phalanx is present on the fracture fragment (11).
If palmar subluxation of the distal phalanx is present, treat the injury surgically with reduction of the DIP joint, transarticular Kirschner wire fixation (Table 49.11), and open reduction of the fracture fragment. Methods for fragment fixation are diverse, and none have a clear advantage. The clear disadvantage of open treatment of any mallet deformity is loss of DIP flexion. A certain amount of flexion loss is the cost of accurate joint and fracture reduction in group 3 mallet deformities and tendon repair in group 4 mallet deformities. A patient who is advised about this problem in advance of surgery is usually satisfied with the surgeon’s efforts, while the unprepared patient is often disappointed.
Table 49.11. Transarticular Kirschner Wire Sizesa
The postoperative management of mallet deformity (Table 49.12) is also used in the treatment of closed mallet injuries. Open mallet deformities (group 4) are also managed as shown in Table 49.12. Place fine, synthetic, absorbable sutures in the tendon after the DIP joint has been fixed in neutral extension with a transarticular Kirschner wire.
Table 49.12. Postoperative Management of Extensor Tendon Repair Over the Middle Phalanx or at the DIP Joint (Acute Mallet Deformity)a
Delayed extensor reconstruction is controversial, and many procedures have been described. The following are a few simple guidelines divided into general anatomic levels for the management of chronic extensor deficits.
Wrist and MP extension are the functional losses accompanying disruption of wrist extensors and extrinsic digital extensors. Without wrist extensors, the grasp function of the hand is disabled. Loss of MP extension eliminates the placement arc of the fingers, while digital encompassment (IP flexion through FDP/FDS, and IP extension through intact intrinsic musculature) is maintained (49). Loss of

either wrist extension or MP extension results in marked disability. Tenodesis and stiffened joints may also contribute to the clinical presentation.
Reconstructive goals are independent wrist or MP extension using a technique that provides satisfactory power and amplitude to meet functional requirements. Normal amplitude is rarely achieved, but adequate power for extensor function is a reasonable goal, since normal digital extensor strength is 10% of that of all the muscles below the elbow, and digital extensor work capacity is less than one third of that of the digital flexors (5). Indeed, according to Brand, the FDS and FDP of the middle finger alone are as strong as the extensors of all the other fingers (5).
The three options available for late reconstruction of extrinsic wrist and digital extensor loss are attempted delayed repair, interpositional tendon graft, and redistribution of power through tendon transfer. In general, tendon transfers are the most successful. Delayed repair and interpositional tendon graft suffer in comparison because the lacerated muscle–tendon unit is usually compromised by retraction, adherence, and weakness. There are multiple options for tendon transfers to restore wrist and MP extension; these methods are most fully described in treatises dealing with reconstruction following radial nerve palsy (see Chapter 55) (64). If composite tissue loss on the dorsum of the hand or forearm necessitates flap coverage, the use of silicone rods beneath the flap will facilitate later tendon transfer (61).
Posttraumatic tenodesis of the extensor tendons over the metacarpals and phalanges is a relatively common clinical problem, presenting after extensor tendon injuries with or without fractures. The gliding layer has been disrupted in these cases and dense adhesions are present between the bone and extensor tendon. Extensor tenolysis in the hand or digit with or without use of synthetic interpositional material (silicone sheets, which eventually require removal) is a worthy surgical attempt to improve functional range of motion. The long-term results, however, are highly variable.
The gains in range of motion may be dramatically good in some patients and dismally poor in others. Adhesions may extend far beyond the level of injury; other factors, both objective (e.g., stiffened MP or IP joints, loss of muscle amplitude, altered tendon nutrition) and subjective (e.g., pain perception and tolerance, patient understanding and motivation), are as important as simply lysing tendon from bone. The gains in flexion will be more significant than the reduction in extensor lag, and the necessity for joint capsulotomy will decrease the overall benefit of extensor tenolysis (12). If the joints are supple, however, and a well-motivated patient understands the rigors of maintaining postoperative tendon excursion, tenolysis is an acceptable surgical option.
The PIP joint, which accounts for 85% of final interphalangeal encompassment, is most affected by extensor tenodesis of the central slip over the proximal phalanx (48,49). Consider the feasibility of separation of the extrinsic and intrinsic contributions to the extensor mechanism at the proximal phalangeal level. The extrinsics would then be isolated as MP extensors. Excise the area of tenodesis to eliminate the extensor tether of the PIP joint. If the lateral slips are normal and the area of tenodesis is proximal to the zone of convergence (Fig. 49.6), the intrinsic muscles then become the sole IP extensors. When possible, this solution to the problem can be very successful (44,45).
Few patients complain of loss of DIP flexion after extensor injury followed by tenodesis over the middle phalanx, even though DIP flexion is uniformly decreased after such injuries. Tenolysis at the middle phalangeal level could be considered in a patient with unique occupational demands (e.g., a professional musician, requiring maximum DIP range of motion).
Reconstruction of the chronic boutonnière deformity is not easily accomplished and often frustrates the most experienced hand surgeons. The fixed or flexible nature of the PIP flexion deformity is extremely important in operative planning. All reconstructions in late boutonnière deformities depend on attainment of maximum passive PIP extension followed by appropriate distribution of the available extensor power (9,13,45,58,61,68,76).
Many innovative reconstructive procedures have been proposed and used in restoration of swan-neck deformity. If the DIP joint assumes the extended position when PIP hyperextension is blocked at neutral or slight flexion, direct treatment simply at limiting PIP extension to a neutral or slightly flexed position.
A more challenging swan-neck deformity follows rupture of the terminal extensor in patients with lax PIP volar plates. The increased extensor pull on the middle phalanx (Fig. 49.10) causes progressive PIP hyperextension. In these cases, surgical management can be divided into two basic categories: procedures designed to shift extensor pull from the middle to the distal phalanx, and procedures using the dynamic interphalangeal tenodesis concept to limit PIP hyperextension and augment DIP extension.
The prime example of an extensor shift procedure is the Fowler central slip tenotomy (4,28,32). Tenotomy of the central slip reduces extensor tone on the PIP joint and

allows proximal shift of the conjoined lateral bands, increasing DIP extensor tone. This procedure is simple and is usually effective in improving DIP extension and reducing PIP hyperextension. DIP extension will not be complete in most cases, however, and PIP extension lag is a potential problem following central slip tenotomy (71). Use this procedure exclusively in swan-neck deformities resulting from rupture and separation of the terminal extensor tendon.
Several procedures have been described that create a strong oblique retinacular ligament homologue; they have been reported to be effective (30,42,43,73). These procedures provide predictable methods for correcting loss of DIP extension and PIP hyperextension.
If the deformity is purely DIP extension loss (mallet finger) with no tendency toward PIP hyperextension, direct treatment toward reconstituting the terminal extensor tendon by excision of interposed scar and secondary repair, tendon graft, or tendodermadesis (34).
Late extensor deficits are less common in the thumb ray than in the fingers because of the thumb’s recessed and palmar abducted position, which provides relative protection from longitudinal dorsal trauma. The thumb of the nondominant glove hand in baseball and softball is an exception to this rule, but athletes tend to sustain fractures and ligament injuries rather than extensor tendon deficits after thumb trauma.
Most late extensor deficits in the thumb occur secondary to the deformities of rheumatoid disease or attritional rupture of the EPL following a distal radial fracture. Reconstruction of the rheumatoid thumb is discussed in Chapter 70. Tendon transfer, especially EIP, provides the most satisfactory solution to late EPL deficit, if the joints are supple (70). All procedures discussed in this chapter regarding late mallet deformities are applicable, but rarely applied, to the thumb.
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