EXTENSOR TENDON INJURIES: ACUTE REPAIR AND LATE RECONSTRUCTION

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.

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).

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).

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).

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).

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.

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).

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).

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).

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).

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).

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).

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.

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.

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).

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.

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.

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.

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.