Download CME Extensor Tendon: Anatomy, Injury, and Reconstruction

CME
Extensor Tendon: Anatomy, Injury, and
Reconstruction
W. Bradford Rockwell, M.D., Peter N. Butler, M.D., and Bruce A. Byrne, M.D.
Salt Lake City, Utah
Learning Objectives: After studying this article, the participant should be able to: 1. Describe the anatomy of the extensor
tendons at the wrist, hand, and fingers. 2. Describe acute and chronic pathologic conditions affecting the extensor
mechanism. 3. Understand physiology and techniques for repair of traumatic injuries. 4. Understand reconstructive
options for chronic disorders.
Although seemingly simple in its anatomy and function, the extensor mechanism of the hand is actually a
complex set of interlinked muscles, tendons, and ligaments. A thorough understanding of the extensor anatomy is required to understand the consequences of injury
at various levels. Reconstructive options must restore normal function. Whereas primary repair of anatomic structures is frequently possible in acute injury, it is rarely
possible in chronic situations. Technically exacting procedures may be necessary to restore function. (Plast. Reconstr. Surg. 106: 1592, 2000.)
proprius and extensor digiti minimi are usually
ulnar and deep to the extensor digitorum communis at the metacarpophalangeal joints. The
extensor digitorum communis to the little finger is present less than 50 percent of the time.3
When absent, it is almost always replaced by a
junctura tendinum from the ring finger to the
extensor apparatus of the little finger.4 The
juncturae tendinum join the extensor digitorum communis tendons proximal to the metacarpophalangeal joint. Lacerations proximal to
the juncturae may still allow extension of the
involved digit by pull from an adjacent finger
passing through the juncturae. The four extensor digitorum communis tendons originate
from a common muscle belly and have limited
independent action. The extensor indicis proprius and extensor digiti minimi have independent muscle bellies and are common donor
tendons for transfer.
At the wrist, the extensor tendons are more
round and have sufficient bulk to hold a suture. Over the hand, they are thin and flat with
longitudinal fibers that do not hold suture
well.5 The extrinsic extensor tendons have four
insertions—the metacarpophalangeal joint
palmar plate through the sagittal bands, a tenuous insertion on the proximal phalanx, and
stout insertions on the middle and distal phalanges.6 At the metacarpophalangeal joint
level, the extensor tendons are held in place by
the intrinsic tendons and the sagittal band that
The anatomy and function of the extensor
mechanism of the hand are more intricate and
complex than those of the flexor system. The
extensor apparatus is a linkage system created
by the radial nerve innervated extrinsic system
and the ulnar nerve and median nerve innervated intrinsic system.1 These interconnecting
components can compensate for certain deficits in function.
The muscle bellies of the extrinsic extensors
arise in the forearm and enter the hand
through six compartments formed by the extensor retinaculum, a fibrous band that prevents bowstringing of the tendons (Fig. 1). At
the wrist, tendons are covered by a synovial
sheath, but not over the dorsal hand or fingers.
The extensor pollicis brevis, abductor pollicis
longus, extensor pollicis longus, extensor digitorum communis, extensor indicis proprius,
and extensor digiti minimi have independent
origins and functions.2 The extensor indicis
From the Division of Plastic Surgery, University of Utah Health Sciences Center. Received for publication November 3, 1999; revised June
13, 2000.
1592
Vol. 106, No. 7 /
1593
EXTENSOR TENDON
arises from the palmar plate and the deep
intermetacarpal ligament. The extrinsic extensor tendons extend the metacarpophalangeal
joint primarily and the interphalangeal joints
secondarily.6
The intrinsic tendons are composed of four
dorsal interossei (abductors), three palmar interossei (adductors), and four lumbrical muscles. The interossei originate from the lateral
sides of the metacarpals and run distally on
both sides of the fingers except the ulnar side
of the little finger. The interossei tendons enter the finger dorsal to the intermetacarpal
ligament. The lumbricals arise from the radial
side of the flexor digitorum profundus tendon
and pass palmar to the intermetacarpal ligament. The tendons of these intrinsic muscles
join to form the lateral bands, all passing palmar to the axis of the metacarpophalangeal
joint (Fig. 2). The lateral bands join the extrinsic extensor mechanism proximal to the midportion of the proximal phalanx and continue
to the distal finger dorsal to the axis of the
proximal interphalangeal and distal interphalangeal joints.7 The intrinsic muscles flex the
metacarpophalangeal joint and extend the
proximal and distal interphalangeal joints.
At the midportion of the proximal phalanx,
the central slip of the extensor mechanism
trifurcates.8 Distal to this level, there is an exchange of fibers from the central slip to the
lateral bands and from the lateral bands to the
central slip. The central slip primarily attaches
to the base of the middle phalanx, but both
components are capable of proximal and distal
interphalangeal extension.
At the proximal interphalangeal joint, the
transverse retinacular ligament maintains the
position of the extensor mechanism and creates limits on its dorsal-palmar excursion.9 The
oblique retinacular ligament arises proximally
from the middle third of the proximal phalanx
and the A2 pulley and inserts into the lateral
portion of the extensor tendon along the middle phalanx. When coursing palmar to the
proximal interphalangeal joint, it helps stabilize the lateral bands.8 Its previously described
role of mechanically linking simultaneous
proximal and distal interphalangeal extension10 has been discounted.8,11 The triangular
ligament connects the lateral bands over the
dorsum of the middle phalanx, maintaining
them in close proximity.
Excursion of the extensor tendons over the
finger is less when compared with the flexor
tendons. At the proximal interphalangeal
joint, excursion may vary from 212,13 to 8 mm.14
This small excursion contributes to a system
with a delicate balance among its various components. Preservation of relative tendon length
between the central slip and lateral bands is
important. Once the balance is disturbed, the
deformities are progressive, and restoration of
normal balance may be very difficult.
Overlapping linkage systems also contribute
to this balance.6 The components of the linkage system pass palmar to one joint and dorsal
to the next. The intrinsic tendons create the
linkage at the metacarpophalangeal and proximal interphalangeal joints, and the oblique
retinacular ligaments function at the proximal
and distal interphalangeal joints. Because of
this interrelationship of joints, a deformity at
one joint may cause a reciprocal deformity at
an adjacent joint. The boutonnière and swanneck deformities are examples. When evaluating a deformity at a particular joint, be mindful
of the tendon pathways and their relationship
to the flexion-extension axis of that joint and
adjacent joints.
The extensor mechanism of the thumb is
different from that of the fingers in that each
joint has an independent tendon for extension. The extensor pollicis longus extends the
interphalangeal joint, the extensor pollicis brevis extends the metacarpophalangeal joint, and
the abductor pollicis longus extends the carpometacarpal joint. The abductor pollicis longus
almost always has multiple tendon slips,
whereas the extensor pollicis brevis usually has
one.15 The intrinsic muscles of the thumb primarily provide rotational control, but also contribute to metacarpophalangeal flexion and interphalangeal extension. On the radial side,
the abductor pollicis brevis tendon continues
to insert on the extensor pollicis longus. On
the ulnar side, fibers of the adductor pollicis
also insert on the extensor pollicis longus.
These two muscles can extend the interphalangeal joint to neutral, significantly masking an
extensor pollicis longus laceration.
ACUTE INJURY
Extensor tendon injuries are encountered
much more frequently than flexor tendon injuries because of their less protected anatomic
location. However, because of the misconception that they are comparatively simple to treat,
they are often treated in the emergency room
by uninitiated physicians who underestimate
1594
PLASTIC AND RECONSTRUCTIVE SURGERY,
December 2000
jury and outcome is an important concept. The
type of injury, deformity, and surgical outcome
are varied because structural and functional
systems are different from fingertip to forearm.
This led to the categorization of tendon injuries into anatomical zones. Verdan’s12 zone system is the most widely accepted and allows for
a more logical discussion of treatment plans
and outcomes associated with each area. Verdan defined eight zones—four odd-numbered
zones overlying each of the joints and four
FIG. 1. The extensor tendons enter the hand through six
fibrous tunnels that are made by the extensor retinaculum at
the wrist. A small sheath is present around each individual
tendon at the wrist, but not in the hand or fingers. The
extensor indicis proprius (EIP) and the extensor digiti
minimi (EDM) are typically ulnar and deep to the communis
tendons at the metacarpophalangeal joint. Juncturae tendinum provide interconnections between the extensor digitorum communis (EDC) tendons in the distal portion of the
dorsal palm. ECU, extensor carpi ulnaris; EPL, extensor pollicis longus; EPB, extensor pollicis brevis; APL, abductor pollicis longus; ECRL, extensor carpi radialis longus; ECRB, extensor carpi radialis brevis.
the injury.16 The management of extensor injuries demands the same degree of skill and
knowledge required for the care of flexor tendon injuries. Recent clinical reports advocate
the importance of initial treatment and postoperative rehabilitation of extensor tendon injuries, because good outcomes are not always
as easily obtained as once assumed.17 Because
excursion of the extensor tendon over the finger is less than with the flexors, preservation of
length is far more critical to restore normal
tendon balance.12–14,18
The relationship between the location of in-
FIG. 2. The extrinsic extensor tendons contribute the
central slip to the extensor mechanism in the finger. The
intrinsic system contributes the lateral bands that pass palmar
to the axis of the metacarpophalangeal (MP) joint and dorsal
to the axis at the proximal interphalangeal (PIP) and distal
interphalangeal (DIP) joints. The sagittal band centralizes the
extensor tendon over the metacarpal head at the metacarpophalangeal joint. The intermetacarpal ligament separates
the lumbrical tendon that is palmar from the interossei tendons that are dorsal. The transverse retinacular ligament
stabilizes the extensor tendon at the proximal interphalangeal joint. The oblique retinacular ligament is a component
of the linkage system, passing palmar to the rotational axis of
the proximal interphalangeal joint and dorsal to the joint axis
at the distal interphalangeal joint. The triangular ligament
helps maintain close proximity of the lateral bands over the
middle phalanx. The extensor tendon has four insertions,
with one being on the metacarpophalangeal palmar plate
through the sagittal band. The tendon then inserts on the
base of the proximal, middle, and distal phalanges. Over the
distal portion of the proximal phalanx, the central slip trifurcates as the central slip and lateral bands share fibers. The
central slip inserts on the base of the middle phalanx, whereas
the lateral band component continues to insert on the base
of the distal phalanx.
Vol. 106, No. 7 /
1595
EXTENSOR TENDON
even-numbered zones overlying the intervening tendon segments and increasing in number from distal to proximal.
Zone 1 Injury (Mallet Finger)
Disruption of continuity of the extensor tendon over the distal interphalangeal joint produces the characteristic flexion deformity of
the distal interphalangeal joint. A mallet finger
may be open, but is more often closed. The
mechanism for the closed injury is most commonly a sudden, forceful flexion of the distal
interphalangeal joint in an extended digit.
This results in rupture of the extensor tendon
or avulsion of the tendon often, with a bony
fragment from its insertion in the distal phalanx. When left untreated for a prolonged
time, hyperextension of the proximal interphalangeal joint (swan-neck deformity) may develop because of proximal retraction of the
central band.19
Mallet finger injuries are classified into four
types:
• Type I: Closed, with or without avulsion fracture.
• Type II: Laceration at or proximal to the
distal interphalangeal joint with loss of tendon continuity.
• Type III: Deep abrasion with loss of skin,
subcutaneous cover, and tendon substance.
• Type IV: (A) Transepiphyseal plate fracture
in children; (B) hyperflexion injury with
fracture of the articular surface of 20 to 50
percent; and (C) hyperextension injury with
fracture of the articular surface usually
greater than 50 percent and with early or
late palmar subluxation of the distal phalanx.
The management of mallet finger is still a
topic for debate. In the vast majority of cases,
splinting alone is sufficient. For type I injuries,
the recommended treatment is continuous
splinting of the distal interphalangeal in extension for 6 weeks, followed by 2 weeks of night
splinting. An Alumafoam splint (Millpledge
Healthcare, Nottinghamshire, U.K.) is used to
keep the distal interphalangeal joint at 0 degrees. The patient must understand that splinting must be continuous (e.g., using the thumb
to apply extension force to the distal phalanx
of the injured finger when showering). The
physician should be aware that there are complications with splinting, including dorsal skin
necrosis, especially with acute swelling. Alternatively, and only in rare circumstances,
Kirschner wire fixation of the distal interphalangeal joint in extension, with the wire cut off
beneath the skin to allow the patient to continue working, will achieve the same results.
Kirschner wire should be left in place for 6
weeks, followed by 2 weeks of night splinting.
Type II injures may be repaired with a simple
figure-of-eight suture through the tendon
alone or a roll-type suture (dermatotenodesis)
incorporating the tendon and skin in the same
suture.9 The distal interphalangeal joint is
splinted in extension for 6 weeks, followed by 2
weeks of night splinting. Type III injuries with
loss of tendon substance require immediate
soft-tissue coverage and primary grafting or
late reconstruction using a free tendon graft.
Type IV-A is best managed by closed reduction,
followed by splinting for 3 to 4 weeks. Mallet
finger deformity in a child is usually a transepiphyseal fracture of the phalanx.20 The extensor mechanism is attached to the basal
epiphysis, so closed reduction results in correction of the deformity. In type IV-B, where there
is no palmar subluxation, splinting for 6 weeks
with 2 weeks of night splinting yields good
results. Excellent remodeling of the articular
surface occurs in most mallet fractures. Type
IV-C with palmar subluxation of the distal phalanx is usually best managed operatively with
open reduction and internal fixation using a
Kirschner wire and possibly a pull-out wire or
suture (Fig. 3). This should also be protected
with a splint for 6 weeks, after which the Kirschner wire is removed and motion started. The
fracture fragment size is a less important consideration than the fragment’s location.21 A
proximally displaced fragment not in continuity with the distal phalanx may also require
open reduction and internal fixation.
Zone 2 Injury (Middle Phalanx)
In contrast to zone 1 injuries, zone 2 injuries
are usually secondary to a laceration or crush
injury rather than an avulsion. If less than 50
percent of the tendon width is cut, the treatment involves routine wound care and splinting for 7 to 10 days, followed by active motion.
Injuries involving more than 50 percent of the
tendon should be repaired primarily, followed
by 6 weeks of splinting.
1596
FIG. 3. A closed mallet injury without a fracture or with a
nondisplaced fracture can be treated with closed splintage. A
mallet fracture with joint subluxation requires reduction and
internal fixation. Through a dorsal approach over the distal
interphalangeal joint, the fragments are isolated. A Kirschner
wire is passed antegrade through the bulk of the distal phalanx. Reduction is then completed and the Kirschner wire is
passed retrograde through the fragment (if possible) and
into the middle phalanx. Intraoperative radiographs confirm
appropriate reduction. The Kirschner wire is removed in 6
weeks.
PLASTIC AND RECONSTRUCTIVE SURGERY,
December 2000
passive extension of the joint23; and (3) failed
nonoperative treatment. The usual method of
repair is to pass a suture through the central
tendon and secure it to the middle phalanx
with or without the bony fragment. Kirschner
wire fixation of the proximal interphalangeal
joint is maintained for 10 to 14 days, followed
by an extension splint until there is radiographic evidence of bony union. If primary
repair of the central slip is not possible, portions of the lateral bands can be sutured together in the dorsal midline of the finger to
reconstruct the central slip (Fig. 4). A flap may
be raised from the proximal portion of the
central slip to restore active extension (Fig. 5).
For open injuries, surgical repair might be
avoided by splinting, because the tendon ends
do not retract in this area. However, in a true
boutonnière deformity, both central slip and
lateral band injuries should be expected. In
the elderly, the period of absolute immobilization can be reduced to 2 weeks to help them
regain full flexion. Results are still fairly good.24
Zone 3 Injury (Boutonnière Deformity)
The boutonnière deformity is caused by disruption of the central slip at the proximal interphalangeal joint. This results in the classic
deformity with loss of extension at the proximal interphalangeal joint and hyperextension
at the distal interphalangeal joint. The injury
can be closed or open, and the central slip may
avulse with or without a bony fragment.
The early injury may be associated with localized swelling, but no deformity. The boutonnière deformity then develops gradually, especially in closed trauma. It usually appears 10 to
14 days after the initial injury.16 Diagnosis is
best made after splinting the finger straight for
a few days and reexamining it after swelling
subsides. Absent or weak active extension of
the proximal interphalangeal joint is a positive
finding.22 Initial treatment for closed injury
should be splinting of the proximal interphalangeal joint in extension. The distal interphalangeal, metacarpophalangeal, and wrist joints
are left free. Length of time for splinting
ranges from 4 to 6 weeks, with reapplication of
the splint if the deformity recurs.
Surgical indications for closed boutonnière
deformity are: (1) displaced avulsion fracture
at the base of the middle phalanx13; (2) axial
and lateral instability of the proximal interphalangeal joint associated with loss of active or
FIG. 4. Acute disruption of the extensor tendon over the
proximal interphalangeal joint may not be amenable to primary repair of the central slip. The lateral bands can be
divided longitudinally over a distance of 2 cm, centered over
the proximal interphalangeal joint. The middle segments are
sutured in the midline to reconstruct the function of the
central slip. This technique will help prevent formation of a
boutonnière deformity.
Vol. 106, No. 7 /
1597
EXTENSOR TENDON
FIG. 5. If primary repair of a central slip laceration is not
possible, a distally based central slip flap may be created from
the proximal portion of the extensor tendon. The flap remains attached to its local portion of tendon. The more
proximal portion of the flap is then folded distally and sutured to the distal portion of the central slip. The resulting
defect in the proximal portion of the central slip is primarily
repaired.
Zone 4 Injury (Proximal Phalanx)
Zone 4 injuries usually involve the broad
extensor mechanism, are usually partial, and
usually spare the lateral bands. Diagnosis can
only be made by direct inspection.12 However,
when there is no loss of extension in the interphalangeal joints, repair is rarely required.
Splinting the proximal interphalangeal joint in
extension for 3 to 4 weeks without repair is
equivalent to repair of the tendon with 5-0
nonabsorbable suture.17 For partial injuries,
early motion should be considered. For complete lacerations, primary repair should be performed, followed by 6 weeks of splinting in
extension.11
Zone 5 Injury (Metacarpophalangeal Joint)
Injuries over the metacarpophalangeal joint
are almost always open and should be treated
as a human bite until proven otherwise. The
injury more often occurs with the joint in flexion, so the tendon injury will actually be proximal to the dermal injury. Primary tendon repair is indicated after thorough irrigation. All
involved structures should be repaired separately, including partial injuries. The sagittal
bands should be repaired to prevent lateral
migration of the extensor digitorum communis tendon and subsequent metacarpophalangeal extension loss.16,17 Immobilization of the
wrist in 30 to 45 degrees of extension and the
metacarpophalangeal joint in 20 to 30 degrees
of flexion is performed with the proximal interphalangeal joint free. Early dynamic splinting has also improved outcome.
When associated with a human bite, the incidence of complications is directly related to
the time from injury to treatment. The wound
is extended for thorough inspection and debrided, irrigated, and left open.9 Arthrotomy
of the metacarpophalangeal joint should be
considered in cases of bite injury or suspected
pyarthrosis. Wound cultures should be taken
before irrigation and the patient started on
broad-spectrum antibiotics. The hand is
splinted with the wrist in 45 degrees of extension and the metacarpophalangeal joint in 15
to 20 degrees of flexion. The wound usually
heals within 5 to 10 days, and secondary repair
is rarely needed.9,16
Zone 6 Injuries (Dorsal Hand)
Single or partial tendon lacerations in zone 6
may not result in loss of extension at the metacarpophalangeal joint because extensor forces
are still transmitted from adjacent extensor
tendons through the juncturae tendinum. Diagnosis, therefore, is best made by direct inspection. Because the tendons are thicker and
more oval, repair should be performed with
stronger, core-type sutures. Conventional
splinting places the wrist and fingers in extension for 4 to 6 weeks. If the extensor digitorum
communis is involved, all fingers should be
splinted. If just a proprius tendon is involved,
only the affected finger need be splinted with
the wrist.18 Again, use of early dynamic splinting has been shown to improve results.
Zone 7 Injuries (Wrist)
Controversy exists whether excision of part
of the retinaculum over the injury site is necessary to prevent postoperative adhesions.25,26
If early dynamic splinting is used, adhesions
are less likely. In any case, partial release of the
retinaculum is required in most cases to gain
exposure to the lacerated tendons, which retract significantly in this area.16 However, at
least some portion of the retinaculum should
be preserved to prevent extensor bowstringing.
1598
A four-strand nonabsorbable core suture is
used.
Zone 8 Injuries (Dorsal Forearm)
Multiple tendons may be injured in this area,
making it difficult to identify individual tendons. In this situation, restoration of independent wrist and thumb extension should be
given priority.27 Difficulty also may be encountered with injuries at the musculotendinous
junction because the fibrous septa retract into
the substance of the muscles. When repairing
the muscle bellies, multiple figure-eight sutures are used with a slowly absorbing material.
Static immobilization of the wrist in 45 degrees
of extension and metacarpophalangeal joints
in 15 to 20 degrees of flexion is maintained for
4 to 5 weeks.11 Also, because the extensors
originate from the lateral epicondyle, splinting
the elbow in flexion may also be beneficial.
Dynamic motion of the metacarpophalangeal
joints may be started at 2 weeks and has improved results.
Thumb Injuries
Although anatomically the thumb interphalangeal and finger distal interphalangeal joints
are similar, the terminal extensor tendon is
much thicker on the thumb. Therefore, mallet
thumbs are rare,28 especially as closed injuries.
There is little data comparing operative and
nonoperative treatments. For open injuries,
most would recommend primary repair, followed by splinting for 6 weeks. For closed injuries, splinting for 6 weeks without surgical
repair is appropriate, although some would
still opt for surgical repair.29
Because of the broad extensor expansion at
the metacarpophalangeal joint of the thumb,
traumatic division of all components of thumb
extension is rare. Isolated laceration of the
extensor pollicis brevis at this level is also rare
and its repair is optional but recommended,
because extension of the metacarpophalangeal
joint is possible with an intact extensor pollicis
longus. There is an extension lag in both metacarpophalangeal and interphalangeal joints
with extensor pollicis longus injury, and it
should be repaired. All tendons and the capsule should be repaired separately using coretype sutures. Splinting should be for 3 to 4
weeks, with the wrist in 40 degrees of extension
and slight radial deviation and the thumb
metacarpophalangeal joint in full extension.
In zones 6 and 7, the abductor pollicis lon-
PLASTIC AND RECONSTRUCTIVE SURGERY,
December 2000
gus retracts significantly when divided and usually requires that the first compartment be released for successful repair.12 Splinting is for 4
to 5 weeks, with the wrist in radial deviation
and the thumb in maximal abduction. Treatment of the thumb extensors at the forearm
level is identical to that of the fingers.
Dynamic Splinting for Extensor Injuries
Since its introduction by Kleinert et al.,30
early controlled motion has been used after
flexor repair to overcome the adhesions associated with repair in “no man’s land.” Early
controlled motion with a dynamic extensor
splint has been found to decrease adhesions
and subsequent contractures.26,31 It has been
most effective when used for injuries in zones 5
to 8.9 Its usefulness in the more distal zones is
less apparent, although several studies are
promising. The technique should only be used
in the cooperative patient, and is most advantageous when a skilled hand therapist is available to fabricate the splint and monitor the
patient. The splint allows incomplete active
flexion and passive extension. After 4 weeks,
full active extension is initiated.
CHRONIC INJURY
To understand better extensor tendon reconstruction, several key points should be reemphasized. The extensor mechanism has
much less tolerance for changes in tendon
length than the flexor mechanism.2,6 Finger
extension is synergistic with wrist flexion, and
controlled wrist function is essential to normal
finger extensor mechanics. Therefore, wrist
flexors are excellent tendon transfer donors
for finger extension. The delicate balance of
the extensor complex is partially based on a
series of overlapping linkage systems, lying palmar to the axis of rotation at a proximal joint
and dorsal at the next distal joint.4,6 The precise tension in this system changes with joint
flexion and contraction. Thus, late extensor
disorders are reciprocal at adjacent joints (e.g.,
proximal interphalangeal flexion is associated
with distal interphalangeal extension in the
boutonnière deformity). Evaluation of established extensor disorders must include all
three joints as they are interrelated, and treatment is usually directed at the most proximal
involved joint.32
Preoperatively, ensuring patient education is
paramount, because bad outcomes are likely
for patients who cannot understand or partic-
Vol. 106, No. 7 /
EXTENSOR TENDON
ipate in postoperative therapy and those who
have unrealistic goals. Joint contractures are
contraindications to reconstruction of extensors. The hand surgeon must remember that
many established imbalances will respond to
nonoperative treatment.
Inability to extend the finger metacarpophalangeal joint or radially abduct the thumb despite intact radial nerve function indicates a
problem proximal to the metacarpophalangeal
joint.33 Unless held to length by the juncturae,
the motor unit undergoes myostatic contraction, precluding secondary tendon repair.
The extensor pollicis longus tendon is a
commonly ruptured tendon, usually associated
with distal radius fractures and rheumatoid arthritis, but the other finger extensors also have
a significant propensity to rupture.34 Tendon
transfers are the most reliable technique for
reconstruction of chronic extensor tendon deficits at this location. The extensor indicis proprius or palmaris longus is frequently used for
extensor pollicis longus functional transfer,
whereas the extensor indicis proprius, flexor
carpi ulnaris, or side-to-side extensor digitorum communis transfers are used for extensor
digitorum communis ruptures. For wrist extensors, the pronator teres is the common
choice.35
Technical points in this procedure include
passing the transfer subcutaneously rather
than beneath the retinaculum because wrist
flexion is synergistic with finger extension,36
and around the wrist rather than through the
interosseous membrane to lessen scarring. Setting tension properly with the wrist maximally
extended and the fingers flexed is essential.
The procedure concludes with the wrist
splinted in moderate extension and the metacarpophalangeal joints splinted at 70 degrees
flexion. This should be continued for 3 to 4
weeks, followed by active range of motion for 1
to 2 weeks and later passive ranging,31 although
dynamic splinting may be used in motivated,
reliable patients. Complications after repair of
lesions proximal to the metacarpophalangeal
joint include adhesions of the tendons (most
common), rupture or attenuation, donor deficits, and joint stiffness.
The sagittal bands wrap around the metacarpophalangeal joint, stabilizing the extrinsic extensors centrally with attachment to the palmar
plate.1,6 With rupture or attenuation of these
bands, usually on the radial side, the extensor
slips off the metacarpal head fulcrum and loses
1599
its mechanical advantage for extension. This
situation occurs most commonly with not only
rheumatoid arthritis, but also with traumatic,
congenital, epileptic, and degenerative states.37
This can be an acute or chronic finding. Physical findings include “catching,” extensor lag,
ulnar deviation of the digit, and pain and swelling. The patient cannot extend from flexion;
but, if passively extended, the tendon reduces,
and the patient can hold this position.
When diagnosed during the first 2 weeks,
this subluxation can be effectively treated with
metacarpophalangeal extension splinting and
encouraged proximal interphalangeal motion.38 After 2 weeks, this condition generally
should be surgically corrected by delayed primary repair that is technically difficult, dorsal
tenodesis, or a sling procedure.6,35,37,39 The latter two procedures take a sling of extensor
digitorum communis to recentralize the tendon. The metacarpophalangeal joints must remain in extension for several weeks while the
other joints are ranged.
If the extrinsic extensor becomes adherent
or foreshortened, flexion at the metacarpophalangeal causes an extension force at the proximal interphalangeal by dorsal tenodesis restraint. These patients with extrinsic extensor
tendon tightness are not able to fully flex the
involved fingers.1,6 Clinically, the patient can
flex the proximal interphalangeal only with the
metacarpophalangeal extended. Most patients
respond well to exercises that emphasize extensor excursion and splinting, especially if this is
begun early.
Operative treatment of this condition includes tenolysis or extrinsic extensor release.
However, these procedures should not be considered until a 6-month trial of hand therapy
has been completed. Tenolysis is best for fingers with scarring but adequate tendon length.
Although the sagittal bands must be preserved,
the extensor retinaculum is expendable in this
procedure. Littler’s technique of extrinsic extensor tendon release is indicated for short
tendons or long lengths of scarring.1,6 This procedure separates the extrinsic and intrinsic extensors. The central portion of the extensor
assembly is excised over the proximal phalanx,
preserving the sagittal bands and the central
slip distally at its insertion on the base of the
middle phalanx. It is recommended that both
of these procedures be performed while allowing the patient to move the fingers actively on
1600
the table. Range of motion is begun almost
immediately.
In contrast, intrinsic tendon tightness (Fig.
6) is diagnosed by the inability to flex the
proximal interphalangeal joint when the metacarpophalangeal joint is brought into full extension, putting maximum tension on the intrinsics.40 This condition usually responds well
to exercise and splinting.41 For patients in
whom nonoperative treatment fails, surgical
treatment includes eliminating the dual control of proximal interphalangeal joint extension by excision of the oblique fibers and lateral band of the extensor hood over the
middle of the proximal phalanx.6 Be aware that
this does not address the palmar plate laxity in
the swan-neck deformity.
Swan-neck deformity describes a finger with
proximal interphalangeal joint hyperextension
and distal interphalangeal flexion. Although it
is a dynamic imbalance initially, it may progress
to a fixed deformity. This posture can result
from various causes, including palmar plate
laxity at the proximal interphalangeal joint,
spastic conditions such as cerebral palsy and
stroke, rheumatoid arthritis, malunion of middle phalanx fractures, and mallet deformity
with coexistent palmar plate laxity.42 Pathomechanically, the incompetent palmar plate allows hyperextension at the proximal interphalangeal joint, causing the lateral bands to
migrate dorsally. This creates laxity in the distal
tendon because of the fixed attachment of the
central tendon at the proximal interphalan-
FIG. 6. Intrinsic tightness is caused by shortening of the
intrinsic musculotendinous apparatus. Testing for intrinsic
tightness is performed by passively extending the metacarpophalangeal joint. This will create tension on the more distal
extensor apparatus, making passive proximal interphalangeal
flexion difficult. If the condition will not resolve with therapy,
surgical resection of the lateral bands over the proximal phalanx will relieve intrinsic tightness.
PLASTIC AND RECONSTRUCTIVE SURGERY,
December 2000
geal joint. The unopposed flexor digitorum
profundus deforms the distal phalanx into flexion.6
Conservative splinting and exercises are not
helpful in the treatment of swan-neck deformity, fixed or dynamic.43 Surgical correction
must recognize the underlying cause: only the
mallet deformity need be corrected if this is the
cause. Correction of the malunited middle
phalanx is the appropriate treatment of this
cause. When compliance with postoperative
splinting and exercises is difficult, as with spastic patients, arthrodesis of the proximal interphalangeal joint is appropriate. In rheumatoid
patients, one must correct the metacarpophalangeal joint deformity first.44 When intrinsic
tightness is present, intrinsic release must also
be performed.
For those cases where rebalancing of the
extensor mechanism with correction of the
proximal interphalangeal palmar plate incompetence is necessary, two general techniques
are commonly used: oblique retinacular ligament reconstruction or superficialis tenodesis.
Oblique retinacular ligament reconstruction
involves creating a tenodesis that passively
tightens and extends the distal interphalangeal
joint as the proximal interphalangeal joint actively extends, while remaining palmar to the
proximal interphalangeal joint axis and dorsal
to the distal interphalangeal joint axis. The
original method described by Littler45 uses the
lateral band either ipsilaterally or spiraling palmarly attached at the base of the proximal
phalanx for oblique retinacular ligament reconstruction. A modification of this, spiral
oblique retinacular ligament technique, uses a
free tendon graft to spiral palmarly to reconstruct the oblique retinacular ligament (Fig. 7)
with Kirschner wire fixation of the proximal
interphalangeal joint in 20 degrees of flexion.46
The superficialis tenodesis technique uses one
slip of the flexor digitorum superficialis attached distally and affixed proximally to the
proximal phalanx.47 This method does not rebalance the extensor mechanism at the distal
joint.
Postoperatively, the Kirschner wire is removed at 4 weeks and replaced by a dorsal
blocking splint. A realistic goal is 5 to 10 degrees flexion at the proximal interphalangeal
joint rather than complete extension. Complications include recurrence of the deformity
caused by attenuation, excessive proximal interphalangeal joint flexion deformity from too
Vol. 106, No. 7 /
EXTENSOR TENDON
FIG. 7. Swan-neck deformities are characterized by proximal interphalangeal hyperextension and distal interphalangeal flexion. Oblique retinacular ligament reconstruction
can be conducted with existing local tissue or with a tendon
graft. The grafted tendon is placed dorsal to the distal interphalangeal joint and palmar to the axis of rotation of the
proximal interphalangeal joint. Tension in the tendon graft
is adjusted to correct the original deformity.
tight of a tenodesis, and flexor adhesions, especially after superficialis tenodesis.
Boutonnière deformity refers to a finger posture with the proximal interphalangeal joint
flexed and the distal interphalangeal joint hyperextended (Fig. 8). Like swan-neck deformity, it begins as a dynamic process that can
lead to a fixed deformity.48 It is primarily
caused by disruption of the cental slip and
transverse retinacular fibers at the proximal
FIG. 8. (Above) The boutonnière deformity is usually the
result of the central slip rupturing at the proximal interphalangeal joint. Extensor tone at that joint is decreased but the
force of the extensor mechanism is passed through the lateral
bands to the distal interphalangeal joint where hyperextension occurs. (Below) In the chronic condition, the lateral
bands move palmar to the axis of the proximal interphalangeal joint. They may adhere in this position, creating a fixedflexion deformity.
1601
interphalangeal joint, allowing the lateral
bands to migrate palmar to the axis of the
proximal interphalangeal joints, and become
flexors of this joint. The oblique retinacular
ligament shortens along with the lateral bands.
If the condition is left untreated, the distal
interphalangeal hyperextends.48 Three stages
have been described, including dynamic imbalance, established tendon contracture with supple joints, and fixed-joint changes.35
Similar to many other extensor imbalances,
boutonnière deformity is best treated with
splinting and exercises, especially before the
deformity occurs. This cannot be stressed
enough because surgical repair is fraught with
complications, and results with conservative
therapy may be as good or better than with
surgery. The exercises include active-assisted
proximal interphalangeal joint extension that
will cause worsening of the distal interphalangeal extension. Secondly, active-forced flexion
of the distal interphalangeal joint with the
proximal interphalangeal in extension will
cause stretching of the oblique retinacular ligament. Splinting supports the proximal interphalangeal joint and the two proximal phalanges only.
Perhaps a systematic approach to the management of chronic boutonnière deformity is
best. Curtis et al.49 described a four-stage approach progressing from tenolysis to transverse
retinacular ligament sectioning to lengthening
of lateral bands over the middle phalanx to
repair of the central slip. One technique to
repair late boutonnière deformity uses the central slip primary repair with reattachment of
the lateral bands dorsal to the proximal interphalangeal joint axis, with or without division
of the terminal extensor insertion on the distal
phalanx to restore distal interphalangeal function. However, probably the most reliable procedure is that advocated by Littler and Eaton50
This involves lengthening of the lateral band
by incomplete transection of the extensor
mechanism over the middle of the middle phalanx, but leaving the oblique retinacular ligament intact. Littler originally described this
technique with suturing of the lateral bands
dorsally. For any reconstruction, a supple proximal interphalangeal joint with satisfactory passive motion is a prerequisite.
Occasionally, the central tendon deficit is so
large that it requires a tendon graft passed
through a bone tunnel at the dorsal base of the
middle phalanx and criss-crossed to be sutured
1602
PLASTIC AND RECONSTRUCTIVE SURGERY,
to the lateral bands.51 Lateral band tendon
transfers have also been described by Littler52
and Matev.53 The hyperextension deformity at
the distal interphalangeal joint may cause
greater difficulty for the patient than the lack
of proximal interphalangeal joint extension. A
tenotomy of the terminal extensor mechanism
alone may be sufficient.54
The complexity of the extensor mechanism
is created by a delicately balanced musculotendinous system controlled by two linkage systems. Anatomical and functional knowledge is
a prerequisite to provide care for extensor deficits, both acute and chronic.
W. Bradford Rockwell, M.D.
Division of Plastic Surgery
University of Utah Health Sciences Center
50 North Medical Drive, 3B205
Salt Lake City, Utah 84132
[email protected]
REFERENCES
1. Eaton, R. G. The extensor mechanism of the fingers.
Bull. Hosp. Joint Dis. 30: 39, 1969.
2. Kaplan, E. B. Anatomy, injuries and treatment of the
extensor apparatus of the hand and fingers. Clin. Orthop. 13: 24, 1959.
3. Riordan, D. C., and Stokes, H. M. Synovitis of the extensors of the fingers associated with extensor digitorum brevis manus muscle: A case report. Clin. Orthop.
95: 278, 1973.
4. Von Schroeder, H. P., Botte, M. J., and Gellman, H.
Anatomy of the juncturae tendinum of the hand.
J. Hand Surg. (Am.) 15: 595, 1990.
5. Minamikawa, Y. Extensor Repair and Rehabilitation. In
C. Peimer (Ed.), Surgery of the Hand and Upper Extremity.
New York: McGraw-Hill, 1996.
6. Littler, J. W. The finger extensor mechanism. Surg. Clin.
North Am. 47: 415, 1967.
7. Schultz, R. J., Furlong, J., and Storace, A. Detailed anatomy of the extensor mechanism at the proximal aspect
of the finger. J. Hand Surg. (Am.) 6: 493, 1981.
8. Harris, C., and Rutledge, G. L., Jr. The functional anatomy of the extensor mechanism of the finger. J. Bone
Joint Surg. (Am.) 54: 713, 1972.
9. Doyle, J. R. Extensor Tendons: Acute Injuries. In D. P.
Green (Ed.), Operative Hand Surgery, 3rd Ed. New York:
Churchill Livingstone, 1993.
10. Landsmeer, J. M. F. The coordination of finger joint
motions. J. Bone Joint Surg. (Am.) 45: 1654, 1963.
11. El-Gammal, T. A., Steyers, C. M., Blair, W. F., and Maynard, J. A. Anatomy of the oblique retinacular ligament of the index finger. J. Hand Surg. (Am.) 18: 717,
1993.
12. Verdan, C. E. Primary and Secondary Repair of Flexor
and Extensor Tendon Injuries. In J. E. Flynn (Ed.),
Hand Surgery, 2nd Ed. Baltimore: Williams & Wilkins,
1975.
13. Boyes, J. H. Tendons. In J. H. Boyes (Ed.), Bunnell’s
Surgery of the Hand, 5th Ed. Philadelphia: Lippincott,
1970.
December 2000
14. Minamikawa, Y., Peimer, C. A., Yamaguchi, T., et al.
Wrist position and extensor tendon amplitude following repair. J. Hand Surg. (Am.) 17: 268, 1992.
15. Minamikawa, Y., Peimer, C. A., Cox, W. L., and Sherwin,
F. S. De Quervain’s syndrome: Surgical and anatomical studies of the fibroosseous canal. Orthopedics 14:
545, 1991.
16. Hart, R. G., Uehara, D. T., and Kutz, J. E. Extensor
tendon injuries of the hand. Emerg. Med. Clin. North
Am. 11: 637, 1993.
17. Blair, W. F., and Steyers, C. M. Extensor tendon injuries. Orthop. Clin. North Am. 23: 141, 1992.
18. Thompson, J. S., and Peimer, C. A. Extensor Tendon
Injuries: Acute Repair and Late Reconstruction. In
M. W. Chapman (Ed.), Operative Orthopaedics. Philadelphia: Lippincott, 1998.
19. Evance, D., and Weightman, B. The pipeflex splint for
treatment of mallet finger. J. Hand Surg. (Br.) 13: 156,
1988.
20. Edmonson, A. S., and Crenshaw, A. H. Campbell’s Operative Orthopedics, 6th Ed. St. Louis: Mosby, 1980.
21. Wehbe, M. A., and Schneider, L. H. Mallet fractures.
J. Bone Joint Surg. (Am.) 66: 658, 1984.
22. Elson, R. A. Rupture of the central slip of the extensor
hood of the finger: A test for diagnosis. J. Bone Joint
Surg. (Br.) 68: 229, 1986.
23. Tubiana, R. Surgical repair of the extensor apparatus of
the finger. Surg. Clin. North Am. 48: 1015, 1968.
24. McFarlane, R. M., and Hampole, M. K. Treatment of
extensor tendon injuries of the hand. Can. J. Surg. 16:
366, 1973.
25. Newport, M. L., Blair, W. F., and Steyers, C. M. Longterm results of extensor tendon repair. J. Hand Surg.
(Am.) 15: 961, 1990.
26. Browne, E. Z., Jr., and Ribik, C. A. Early dynamic splinting for extensor tendon injuries. J. Hand Surg. (Am.)
14: 72, 1989.
27. Willson, R. L. Management of Acute Extensor Tendon
Injuries. In J. M. Hunter, L. H. Schneider, and E. J.
Mackin (Eds.), Tendon Surgery in the Hand. St. Louis:
Mosby, 1987.
28. Patel, M. R., Lipson, L.-B., and Desai, S. S. Conservative
treatment of mallet thumb. J. Hand Surg. (Am.) 11: 45,
1986.
29. Din, K. M., and Meggitt, B. F. Mallet thumb. J. Bone Joint
Surg. (Br.) 65: 606, 1983.
30. Kleinert, H. E., Kutz, J. E., Atasoy, E., and Stommo, A.
Primary repair of flexor tendons. Orthop. Clin. North
Am. 4: 865, 1973.
31. Lee, V. H. Rehabilitation of Extensor Tendon Injuries.
In J. M Hunter, L. H. Schneider, E. D. Mackin, and
A. D. Callahan (Eds.), Rehabilitation of the Hand, 2nd
Ed. St. Louis: Mosby, 1984.
32. Urbaniak, J. R., and Hayes, M. G. Chronic boutonnière
deformity: An anatomic reconstruction. J. Hand Surg.
(Am.) 6: 379, 1981.
33. Aulicino, P. L. Acute injuries of the extensor tendons
proximal to the metacarpophalangeal joint. Hand
Clin. 11: 403, 1995.
34. Mannerfelt, L., Oetker, R., Ostlund, B., and Elbert, B.
Rupture of the extensor pollicis longus tendon after
Colles fracture and by rheumatoid arthritis. J. Hand
Surg. (Br.) 15: 49, 1990.
35. Burton, R. I., and Melchior, J. Extensor Tendons: Late
Reconstruction. In D. M. Green, R. N. Hotchkiss, and
Vol. 106, No. 7 /
36.
37.
38.
39.
40.
41.
42.
43.
44.
45.
1603
EXTENSOR TENDON
W. C. Petersen (Eds.), Operative Hand Surgery, 4th Ed.
New York: Churchill Livingstone, 1999.
Palmer, A. K., Skahen, J. R., Werner, F. W., and Glisson,
R. R. The extensor retinaculum of the wrist: An anatomical and biomechanical study. J. Hand Surg. (Br.)
10: 11, 1985.
Inoue, G., and Tamura, Y. Dislocation of the extensor
tendons over the metacarpophalangeal joints. J. Hand
Surg. (Am.) 21: 464, 1996.
Kilgore, E. S., Jr., Graham, W. P., Newmeyer, W. L., and
Brown, L. G. Correction of ulnar subluxation of the
extensor communis. Hand 7: 272, 1975.
Carroll, C., Moore, J. R., and Weiland, A. J. Posttraumatic ulnar subluxation of the extensor tendons: A
reconstructive technique. J. Hand Surg. (Am.) 12: 227,
1987.
Smith, R. J. Non-ischemic contractures of the intrinsic
muscles of the hand. J. Bone Joint Surg. (Am.) 53: 1313,
1971.
Parkes, A. The lumbrical plus finger. Hand 2: 164, 1970.
van der Meulen, J. C. Causes of prolapse and collapse
of the proximal interphalangeal joint. Hand 4: 147,
1972.
van der Meulen, J. C. The treatment of prolapse and
collapse of the proximal interphalangeal joint. Hand
4: 154, 1972.
Nalebuff, E. A., and Millender, L. H. Surgical treatment
of the swan-neck deformity in rheumatoid arthritis.
Orthop. Clin. North Am. 6: 733, 1975.
Littler, J. W. The Digital Extensor-Flexor System. In
46.
47.
48.
49.
50.
51.
52.
53.
54.
J. M. Converse (Ed.), Reconstructive Plastic Surgery, Vol.
6. Philadelphia: Saunders, 1977.
Thompson, J. S., Littler, J. W., and Upton, J. The spiral
oblique retinacular ligament (SORL). J. Hand Surg.
(Am.) 3: 482, 1978.
Littler, J. W. The Hand and Wrist. In M. B. Howorth
(Ed.), A Textbook of Orthopedics. Philadelphia: Saunders, 1952.
Salisbury, R. E., and Bevin, A. G. Boutonnière Deformity. In Atlas of Reconstructive Surgery. Philadelphia:
Saunders, 1981.
Curtis, R. M., Reid, R. L., and Provost, J. M. A staged
technique for the repair of the traumatic boutonnière
deformity. J. Hand Surg. (Am.) 8: 167, 1983.
Littler, J. W., and Eaton, R. G. Redistribution of forces
in correction of boutonnière deformity. J. Bone Joint
Surg. (Am.) 49: 1267, 1967.
Nichols, H. M. Repair of extensor tendon insertions in
the fingers. J. Bone Joint Surg. (Am.) 33: 836, 1951.
Littler, J. W. Principles of Reconstructive Surgery of the
Hand. In J. M. Converse (Ed.), Reconstructive Plastic
Surgery. Philadelphia: Saunders, 1964.
Matev, I. Transportation of the lateral slips of the aponeurosis in treatment of long-standing “boutonnière
deformity” of the fingers. Br. J. Plast. Surg. 17: 281,
1964.
Meadows, S. E., Schneider, L. H., and Sherwyn, J. H.
Treatment of the chronic boutonnière deformity by
extensor tenotomy. Hand Clin. 11: 441, 1995.
Self-Assessment Examination follows on
page 1604.
Self-Assessment Examination
Extensor Tendon: Anatomy, Injury, and Reconstruction.
by W. Bradford Rockwell, M.D., Peter N. Butler, M.D., and Bruce A. Byrne, M.D.
1. WHAT PERCENTAGE OF PEOPLE HAVE AN EXTENSOR DIGITORUM COMMUNIS TENDON TO THE LITTLE
FINGER?
A) 100 percent
B) 98 percent
C) 90 percent
D) 80 percent
E) Less than 50 percent
2. INDICATIONS FOR OPERATIVE MANAGEMENT FOR CLOSED BOUTONNIÈRE DEFORMITY INCLUDE ALL
OF THE FOLLOWING EXCEPT:
A.) Failure of conservative, nonoperative management.
B) Palmar migration of the lateral bands 7 to 10 days after injury.
C) Displaced avulsion fracture of the base of the middle phalanx.
D) Axial and lateral instability of the proximal interphalangeal joint associated with loss of active or passive proximal interphalangeal
joint extension.
3. ZONE 6 (DORSAL HAND) INJURIES ARE BEST DIAGNOSED BY:
A) Loss of active extension of distal interphalangeal joint.
B) Loss of active extension of proximal interphalangeal joint.
C) Loss of active extension of metacarpophalangeal joint.
D) Direct inspection.
E) Intrinsic tightness plus posture of finger.
4. THE RECOMMENDED TREATMENT FOR CLOSED MALLET FINGER IS:
A) Surgical repair of tendon.
B) Percutaneous Kirschner wire fixation of distal interphalangeal joint in extension.
C) Splinting of only distal interphalangeal joint in extension.
D) Splinting of proximal interphalangeal and distal interphalangeal joint in extension.
E) Controlled early motion of distal interphalangeal joint.
5. WHICH OF THE FOLLOWING STATEMENTS IS TRUE?
A) Intrinsic tightness refers to resistance of proximal interphalangeal joint flexion while the metacarpophalangeal joint is flexed.
B) Joint contractures are contraindications to extensor reconstruction.
C) Swan-neck deformity refers to a finger posture of proximal interphalangeal joint flexion and distal interphalangeal joint
hyperextension.
D) When the extrinsic extensor subluxates off the metacarpal head, it usually falls to the radial side.
E) Extrinsic tightness causes a posture of metacarpophalangeal flexion, proximal interphalangeal extension and distal interphalangeal
extension.
6. ALL OF THE FOLLOWING CONDITIONS USUALLY RESPOND WELL TO SPLINTING AND EXERCISE
PROGRAMS EXCEPT:
A) Extrinsic extensor tightness.
B) Intrinsic extensor tightness.
C) Swan-neck deformity.
D) Boutonnière deformity.
E) Mallet finger.
To complete the examination for CME credit, turn to page 1673 for instructions and the response form.