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Chirurgie de la main 34 (2015) 155–181

Recent advance

Treatment of chronic extensor tendons lesions of the fingers
Prise en charge secondaire des lésions de l’appareil extenseur des doigts
P. Bellemère
Clinique Jeanne-d’Arc, Institut de la main Nantes Atlantique, 21, rue de Martyrs, 44100 Nantes, France
Received 26 January 2015; received in revised form 12 April 2015; accepted 8 May 2015
Available online 14 July 2015

Chronic finger extensor apparatus injuries are the result of the initial acute treatment having failed or being flawed. Because of their chronic
nature, these injuries present various amounts of tendon retraction, tendon callus lengthening, peritendinous scar adhesions, static and dynamic
imbalances with the flexor apparatus and intrinsic muscles, and joint contractures. This article will review the anatomy of the extensor mechanism
and then will outline by location, the various clinical pictures that are secondary to chronic tendon injury. The clinical presentation of these injuries
can be highly variable but their symptomatology and treatment are very specific. Of the possible therapeutic strategies for chronic mallet finger with
or without associated swan-neck deformity, chronic boutonniere deformity, chronic sagittal band injuries, old ruptures on the dorsum of the wrist
and traumatic defects in multiple tissues, conservative treatment is often the main element. Secondary surgical repair is not free of complications,
and the results are often lacking. Rehabilitation and orthotic bracing are an integral part of the management of these injuries, no matter which
treatment method is being considered.
# 2015 Elsevier Masson SAS. All rights reserved.
Keywords: Finger extensor tendon; Secondary repair; Mallet finger; Swan-neck deformity; Boutonniere deformity; Traumatic injury; Tendon laceration

Les lésions anciennes de l’appareil extenseur des doigts résultent du défaut ou de la faillite de leur traitement initial au stade aigu. Les
conséquences de la chronicité des lésions entraînent à des degrés divers des rétractions tendineuses, des allongements de cals tendineux, des
adhérences cicatricielles péritendineuses, des déséquilibres statiques et dynamiques avec l’appareil fléchisseur et les muscles intrinsèques, ainsi
que des raideurs articulaires. Cet article fait un rappel de l’anatomie de l’appareil extenseur et des différents tableaux cliniques consécutifs à une
lésion tendineuse ancienne selon le siège de la lésion. Les présentations cliniques peuvent être très variées et leur sémiologie ainsi que leur
traitement sont spécifiques : doigt en maillet chronique avec ou sans déformation associée en col de cygne, déformation en boutonnière chronique,
lésion chronique des bandelettes sagittales, ruptures anciennes au dos du poignet ainsi que les lésions avec perte de substance pluritissulaire
répondent à des stratégies thérapeutiques dans lesquelles le traitement orthopédique trouve souvent une large part. Les réparations chirurgicales
secondaires ne sont pas dénuées de complications et leurs résultats sont le plus souvent incomplets. La rééducation et l’appareillage sont
indissociables de la prise en charge de ces lésions, quelle que soit la méthode thérapeutique envisagée.
# 2015 Elsevier Masson SAS. Tous droits réservés.
Mots clés : Tendon extenseur des doigts ; Réparation secondaire ; Doigt en maillet ; Déformation en col de cygne ; Déformation en boutonnière ; Lésion
traumatique ; Rupture tendineuse

E-mail address:
1297-3203/# 2015 Elsevier Masson SAS. All rights reserved.


P. Bellemère / Chirurgie de la main 34 (2015) 155–181

1. Introduction
Chronic injuries of the finger extensor apparatus are the
result of an open (laceration, defect) or closed (rupture,
instability) initial injury that was either not treated or not
treated properly. This may have happened because the injury
was missed, the initial treatment was inappropriate, the
treatment duration was too short or too long, or because the
initial treatment failed, despite being well-conducted. Once
chronic, the tendon injury is associated with varying amounts of
tendon retraction, tendon callus lengthening, peritendinous scar
adhesions, static and dynamic imbalances with the flexor
apparatus and intrinsic muscles, and joint contractures.
Manifestation of these injuries, which is closely related to
their location and therefore the anatomy and physiology of the
extensor mechanism, leads to highly varied clinical pictures
that have equally varied functional consequences. Based on the
significance of the latter, each clinical picture will have specific
symptomatology and respond to specific treatment.
2. Anatomy of extensor mechanism
2.1. Anatomy at the forearm and hand
2.1.1. Standard configuration
The standard configuration of the finger extensor apparatus
(not including the thumb) consists of a common extensor
tendon for each finger and individual extensor muscles for the
second and fifth finger (Fig. 1). In the forearm, about 4 cm from
the wrist joint, the individual extensor tendons for each finger
split from the common extensor digitorum (ED) muscle body
(also known as the extensor digitorum communis). For the fifth
finger, a single tendon arises from the muscle body of the
extensor digiti minimi (EDM), which is also known as the
extensor digiti quinti. For the second finger, the deep extensor
indicis proprius (EIP) has muscle fibers that reach the wrist joint
in 70% of cases [1].
On the dorsum of the distal radius and the radiocarpal joint,
the extensor tendons – surrounded by a synovial sheath – enter
into a narrow osteofibrous canal that is compartmentalized by
septums and has a roof formed by the extensor retinaculum. The
tendon’s excursion is the greatest at this point (up to 41 mm).
The 25-mm long fourth extensor compartment contains the ED
and EIP. The slightly longer fifth compartment is a fibrous canal
that runs over the top of the distal radioulnar joint. It only holds
the EDM. The synovial sheath has a single proximal recess,
5 mm proximal to the proximal edge of the retinaculum. It
terminates beyond the distal edge of the retinaculum by a recess
around each tendon, with the longest one being on the ulnar
side. The extensor retinaculum holds the extensor tendons
against the skeleton during wrist extensor, preventing tendon
bow stringing.
On the dorsum of the hand, the tendons diverge and are no
longer cylindrical; they become flatter as they get closer to the
metacarpophalangeal (MCP) joints. The extensors for the
middle and ring fingers run over the third and fourth
metacarpals. Those of the index and little fingers run over

Fig. 1. Diagram of the finger extensor apparatus on the dorsum of the wrist and
Reproduced with permission of Maîtrise Orthopédique.

the second and fourth intermetcarpal spaces. The common
extensor tendons are held together by fascia, which can be
reinforced in the distal metacarpal region by oblique or
transverse links called intertendinous connections. The
distribution of these intertendinous connections varies as does
their constitution (tendon, ligament, fascia). The most common,
most defined and thickest join the extensor of the middle finger
to that of the fourth finger in 73% to 80% of cases [2,3].
Conversely, the one joining the common extensor of the index
to that of the middle finger is rarer and thinner. The
intertendinous connection joining the fourth finger’s extensor
to that of the fifth finger is often formed by a division of the
latter’s common extensor tendon. The EIP and EDM, which are
located on the ulnar side of the common extensor of the
respective finger, generally do not have any intertendinous
connections. Intertendinous connections help to stabilize the
extensor tendons on the back of the metacarpal heads when the
MCP joints are flexed or laterally deviated. They can participate
in finger extension in certain types of anatomical variations.
2.1.2. Anatomical variations
The greatest anatomical variations in the finger extensor
apparatus are in the area between the forearm and dorsum of the
hand. These consist of varied intertendinous connections,
absence of the fifth finger’s common extensor tendon, tendon
splitting, or presence of extra muscles or tendons such as the
extensor medii proprius, extensor indicis and medii, extensor

P. Bellemère / Chirurgie de la main 34 (2015) 155–181

digitorum brevis manus (called the ‘‘muscle manieux’’ in
French), extensor indicis radialis, and extensor communis
pollicis and indicis [1,2,4,5].

2.2. Anatomy at the fingers
The anatomy of the extensor mechanism is clearly more
complicated at the digits (Fig. 2). On one hand, the extensor
mechanism is stabilized by Zancolli’s assemblage nucleus,
where volar and dorsal capsule, ligament and tendon structures
converge at the MCP and proximal interphalangeal (PIP) joints.
On the other hand, the common extensor tendon is no longer
individualized because it is interconnected with the intrinsic
muscle–tendon system. Interlacing of the tendon fibers and
Landsmeer’s retinacular ligament (transverse and oblique
bands) along with the superimposition of the extensor hood
results in the formation of an extensor aponeurosis that is
inelastic but varies in shape during finger flexion and extension
[6]. This anatomical complexity is difficult to reproduce
secondarily in the presence of old tendon injuries.

Fig. 2. Diagram of the extensor mechanism in a finger. Dorsal (A) and lateral
ulnar (B) views of 1: terminal tendon, 2: triangular ligament, 3: oblique
retinacular ligament, 4: conjoined lateral band, 5: transverse retinacular ligament, 6: central slip, 7: extensor hood (oblique fibers), 8: interosseous tendon, 9:
extensor hood (transverse fibers), 10: sagittal band, 11: deep transverse metacarpal ligament, 12: lumbrical muscle, 13: common extensor tendon, 14: dorsal
interosseous muscle.
Reproduced with permission of Maîtrise Orthopédique.


2.2.1. Metacarpophalangeal joint
The extensor tendon gives rise on its deep surface to a loose
fibrous band that attaches to the dorsal MCP capsule and the
base of the proximal phalanx (P1), but does not contribute to
proximal phalanx extension. Transverse sagittal bands (SB)
from both sides of the tendon link the extensor mechanism with
the volar plate, the intermetacarpal ligament (except for the
radial side of the index and the ulnar side of the fifth finger) and
the flexor mechanism and intrinsic muscle–tendon system by
means of the metacarpophalangeal fibrous nucleus described by
Zancolli [7]. The SB has two sheets: the superficial one covers
the dorsal plane of the tendon and the deeper, thicker one comes
from the deep side of the tendon [8]. The SB on the radial side is
thinner and longer than the one on the ulnar side, particularly
for the middle finger [9], which is why it ruptures more often.
Since they have no firm attachments, the SBs are mobile
structures. The sagittal band’s fiber orientation and tension vary
during flexion-extension. The fibers are perpendicular to the
extensor tendon when the MCP is in neutral position. The SB is
under the least tension when the MCP is flexed 45 degrees [9].
The SB keeps the extensor tendon permanently centered on the
dorsum of the MCP, independent of the joint’s flexion or
deviation, limits its proximal excursion and contributes to the
proximal phalanx’s extension and hyperextension by acting as a
relay between the volar plate and extensor tendon. Its deep
aspect is in close contact with the collateral ligament, over
which it slides during flexion. Its superficial aspect is covered
distally by transverse fibers from the extensor hood. They
merge dorsally and contribute to active tendon stabilization in
addition to the passive stabilization provided by the SBs.
2.2.2. Middle part of proximal phalanx
The common extensor tendon divides into three slips, a
central slip (CS) and two lateral ones. These three slips merge
with the medial and lateral slips from the interossei tendons on
either side of the phalanx, and the lumbrical tendon on the
radial side. The CS merges with the tendinous fibers of the two
intrinsic medial slips to form a combined central tendon, which
inserts on the base of the middle phalanx (P2) and extends it.
Each lateral extensor tendon slip fuses with the lateral slip of
the intrinsic tendons to form a conjoined lateral band, which
crosses the dorsolateral side of the PIP joint. The extensor
hood’s transverse and oblique fibers join the intrinsic medial
and lateral slips with the common extensor tendon. This
complex tendinous layer covers about 75% of the circumference of the proximal phalanx.
On either side of the PIP joint, the transverse retinacular
ligament (TRL), which arises from the volar plate and
cruciform C1 pulley, attaches to the lateral edge of the
conjoined lateral band. Like the sagittal band, the TRL pulls the
conjoined lateral band towards the dorsum of the lateral side of
the PIP during flexion and limits its dorsal displacement during
2.2.3. Middle phalanx
The two conjoined lateral bands become dorsalized and are
joined over the base of the phalanx by a triangular ligament that


P. Bellemère / Chirurgie de la main 34 (2015) 155–181

has transverse fibers. In the distal portion of the middle phalanx,
the two conjoined lateral bands merge into a single terminal
extensor tendon that merges with the dorsal capsule of the distal
interphalangeal (DIP) joint and inserts on the base of the distal
phalanx (P3), 1.4 mm from the nail matrix [10]. The precarious
tendon and skin vascularity in this distal attachment area can
explain its high frequency of spontaneous rupture and healing
problems [11].
The oblique retinacular ligament (ORL) described by
Landsmeer arises from the lateral edge of the distal metaphysis
of the proximal phalanx and the flexor tendon sheath. It takes an
oblique trajectory and crosses the PIP laterally in front of its
flexion-extension axis, to join the volar side of the conjoined
lateral band and merges with it at the middle phalanx’s neck
area, contributing to the formation of the terminal tendon of the
digital extensor mechanism. However, this ligament can be
extremely thin, even missing [12] and its precise role is
controversial [13]. Because its trajectory places it under tension
during PIP extension, it is presumed to provide an active
tenodesis effect that allows DIP extension but limits its flexion
when the PIP is extended.
2.3. Topographic zones
The widely adopted topographic classification for extensor
mechanism injury developed by Verdan and Kleinert has eight
zones [14] (Fig. 3). The even-number zones (2, 4, 6, 8)
correspond to the regions located over a bone’s diaphysis. The
odd-number zones (1, 3, 5, 7) are located over the DIP, PIP,
MCP and wrist joints, respectively. The total extensor tendon
excursion varies nearly linearly relative to the movement
amplitude at the wrist, MCP and PIP joints. It is largest for the
middle finger (50 mm) and smallest for the fifth finger (35 mm)
In each zone, secondary injuries to the extensor mechanism
have very particular anatomical, pathological, clinical and
therapeutic features.
3. Chronic injuries in zone 1: mallet finger

Fig. 3. Topographic zones for extensor tendons.
Reproduced with permission of Maîtrise Orthopédique.

missed initially and left untreated or not treated properly
(unsuitable splint that is not well tolerated or worn
intermittently, overly short immobilization period). Chronic
mallet finger may also reflect a failure of well-conducted initial
treatment that resulted in a lengthened, ineffective tendon

3.1. Definitions
Mallet finger corresponds to a flexion deformity of the
distal phalanx due to loss of active extension (Fig. 4). This
variable flexion deformity reflects lack of continuity in the
terminal extensor mechanism, either due to subcutaneous
rupture, or partial or complete tendon laceration (tendinous
mallet finger), or due to bone avulsion at its insertion on the
P3 base (bony mallet finger). In most cases, it is the sequela
of closed minor trauma that mostly occurs during forced P3
hyperflexion, but occurs in some cases after a hyperextension injury, particularly for bony mallet finger. The fifth
finger, middle finger and ring finger are affected the most
Mallet finger is labeled chronic 4 weeks after the initial
injury event [17]. A non-painful initial injury may have been

Fig. 4. Mallet finger deformity of the fifth finger.

P. Bellemère / Chirurgie de la main 34 (2015) 155–181


3.2. Clinical presentation and functional impairment
The inconvenience related to mallet finger may only be due
to esthetics. Once the extensor lag reaches 30 to 50 degrees, true
functional impairment may interfere with [18] performing
delicate manual work, playing an instrument, typing on a
keyboard or bumping during innocuous movements.
Pressure-sensitive swelling may be present over the DIP
joint or the middle phalanx that corresponds to the callus at the
proximal tendon end; its retraction determines the extent of the
mallet finger. Scheitzer and Rayan have shown that 1 mm of
tendon lengthening triggers a 25-degree DIP extensor lag and
that 4 mm of lengthening leads to more than 60 degrees lag
Associated swan-neck deformity: a swan-neck deformity
due to PIP hyperextension can occur simultaneously with
chronic mallet finger (Fig. 5), particularly in hypermobile
patients. It is exposed during full active finger extension and
can bring about snapping sensations upon the start of PIP
This deformity is the result of imbalance in the action of the
extensor mechanism on the digits, laxity of the PIP volar plate
and progressive TRL weakening. Because the terminal tendon
of the extensor mechanism is ruptured, the central slip is
subjected to the full brunt of the extension forces. In cases of
volar plate laxity or weakness, this leads to PIP hyperextension,
dorsalization and medialization of the lateral slips with
progressive TRL loosening (Fig. 6). Snapping at the start of
PIP flexion is related to sudden ventral shifting of the lateral
slips relative to the P1 condyles. The flexion action of the deep
flexor tendon on the DIP is reinforced by PIP hyperextension,
progressively making the deformity worse. This also reduces
coordination during overall finger flexion because the DIP
flexes before the PIP.
3.3. Clinical assessment
The clinical examination must: 
measure the degree of extensor lag and potentially associated
PIP hyperextension;

Fig. 6. Diagram of the mechanism of swan-neck deformity secondary to mallet
From [60]. Reproduced with permission of Maîtrise Orthopédique. 

assess the amount of active DIP flexion when the PIP is held
in extension, and the amount of active DIP extension; this
reflects on the laxity in the tendon callus at the terminal
extensor mechanism; 
determine if the deformity can be passively reduced with the
finger joints in various positions; 
assess the skin condition over the DIP; 
assess the amount of joint laxity.
Additional examinations: standard radiographs with A/P and
strict lateral views are essential. These are needed for the
diagnosis of bony mallet finger, and to determine the
significance and amount of bone fragment retraction, along
with the severity of osteoarthritis. Volar subluxation of the
distal phalanx is possible if the fragment is larger than one-third
of the articular surface. Ultrasonography and MRI can help to
assess the retraction of the proximal tendon stump, although the
latter is rarely indicated.
3.4. Treatment
Treatment is called for when the patient experiences true
functional impairment. Many chronic mallet fingers are well
tolerated from a functional point of view and do not justify
additional treatment. Conservative treatment must play a very
large role here because surgical correction of mallet finger is
often incomplete and not free of complications.
3.4.1. Conservative treatment
Immobilization of the DIP in extension by an orthotic brace
must be performed systematically for any case of chronic
mallet finger, no matter its duration [17,20,21]. Even if this
treatment was done previously, persistence of significant
residual extensor lag is quite often related to treatment noncompliance in a patient who was not well informed or not
motivated. The patient must be clearly informed of the
treatment’s goal, its duration and how to manage the period of
joint immobilization.

Fig. 5. Swan-neck deformity associated with mallet finger in the index. Goal and principles. The goal is to reduce the
residual DIP extensor lag to the point where it does not impair


P. Bellemère / Chirurgie de la main 34 (2015) 155–181

function (10 to 15 degrees), or even better, is non-existent. This
is possible due to gradual contraction of the tendon callus
during tendon scar maturation, which takes at least 3 months.
Strict DIP immobilization in extension is necessary during this
period; the patient must continuously wear an orthotic brace
that immobilizes the joint for at least 8 weeks. The more the
start of treatment is delayed, the longer this immobilization
period must be, and it can sometimes be 4 months long [20].
The orthotic brace can then be worn only at night for another 1–
3 months. The immobilization period can be shortened for cases
of bony mallet finger because the periosteal continuity of the
fragment contributes to appearance of a bone callus. Types of orthotic braces. There are several types of
orthotic braces: aluminum strips with foam rubber-backing,
premolded plastic splints or custom-molded thermoplastic
splint. In terms of comfort and stiffness, solid thermoplastic
splints that are customized to the patient and water-resistant are
preferable [21]. The numerous volar or dorsal braces available
in stores are often not well tolerated in the long term, and do not
always provide strict DIP immobilization. Moreover, certain
splints also immobilize the PIP joint, which is unnecessary
because the PIP’s motion does not affect the terminal tendon’s
distal retraction; in addition, they are uncomfortable and can
potentially lead to stiffness.
In our practice, we make a dorsal thermoplastic splint that is
glued solidly to the nail and attached to P2 by a removable
Velcro strap (Fig. 7). This leaves the fingertip free, although it
can be supported during intense manual activities with an
additional Velcro strap that protects the glued portion on the
nail. The DIP must be immobilized in a completely straight
position, or even up to 10 degrees hyperextension. Beyond this,
the DIP’s dorsal skin vascularization is compromised because
the dorsal collateral arterial branches are stretched. When a
significant, uncomfortable swan-neck deformity is also present,
we limit PIP extension either with a PIP-stop type dorsal splint
extension or with a Beasley ring (Fig. 8).

Fig. 7. Dorsal thermoplastic brace glued to the nail, leaving the finger pad free.
An additional Velcro strap can be added to protect the portion glued on the nail.

Fig. 8. Beasley-type ring to restricts PIP hyperextension. Appearance with the
joint flexed (a) and extended (b). Results. In a series of 10 cases, Patel et al. found no
residual extensor lag in five cases, a 10-degree lag in four cases
and a 10- to 20-degree lag in one case [20]. The deformity
reoccurred in two patients within a week of the treatment’s end,
but they ultimately had good results with an additional 8-week
immobilization period. Garberman et al. found no differences
in the outcomes of acute and chronic mallet fingers treated with
continuous bracing for 6–10 weeks, and then an additional 4
weeks at night [17]; the mean residual extensor lag was less
than 10 degrees in both groups.
Certain complications have been reported with orthotic
brace treatment: skin intolerance, maceration, pressure sores,
transient nail dystrophy, cold-induced pain [22]. These can be
prevented by regular clinical check-ups during the treatment
3.4.2. Surgical treatment
Five types of procedures can be performed for mallet finger:
tendon callus shortening, tendon grafting, rebalancing of the
finger extensor mechanism, spiral oblique retinacular ligament
(SORL) reconstruction and DIP fusion. These methods have
been described in published retrospective studies that typically
include only a small number of cases and are difficult to
compare to each other. No method has truly been shown to be

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superior relative to another, or relative to conservative treatment.
As a consequence, the indication for surgical treatment is limited
to failure of well-conducted conservative treatment. Tendon callus shortening. Excision of the tendon
callus followed by direct suture is the oldest technique still
being used for treating chronic mallet finger. Simply cutting the
tendon callus and then suturing it leads to mixed results (60%
good and very good) [23]. A tendon callus shortening–suturing
procedure appears to be more appropriate.
Using a bayonet-type dorsal incision, 2–3 mm of the tendon
callus is excised and the tendon sutured with a running 4-0
monofilament. It is protected by pinning the joint in slight
hyperextension for 6 weeks. Levante et al. reported on series of
66 cases with at least 30 degrees extensor lag treated with this
technique after a mean delay of 14 weeks [24]. This was the first
treatment attempted in more than half of the cases. With a mean
follow-up of 26 months, the mean residual extensor lag was 4.5
degrees, and was never greater than 25 degrees. The mean DIP
flexion was 50 degrees. There were two failures due to
extension contracture, one of which was later treated with DIP
fusion. The best results were in the younger patients; the worse
results were in those with bony mallet finger, likely because of
greater tendon shortening after resection of the bone fragment.
Schweitzer and Rayan’s experimental work has shown that it is
very difficult to reinsert the terminal extensor tendon if it is
more than 1 mm retracted [19]. Similar results were obtained
by Ulkür et al. who reinserted the terminal tendon on the P3
base with a bone anchor [25] and with pull-out and pull-in
suture techniques [26,27].
Tenodermodesis or the Brooks-Graner technique is a
variation that avoids the potential devascularization related
to skin detachment and exposure of tendon fragments that the
previous technique has been criticized for. A 2–3 mm block of
skin and tendon over the DIP is excised and the resulting defect
sutured, followed by immobilization with axial pinning of the
fully extended DIP (Fig. 9). In our practice, the incision is
closed using 3-0 or 4-0 non-resorbable suture in a vertical
mattress pattern, with the knot located on the proximal side.
The suture is protected with an axial trans-DIP 1.0 mm K-wire
through the pulp for at least 8 weeks; a removable protective
splint is worn to prevent the K-wire from breaking. Suture
removal is delayed as much as possible, depending on skin
tolerance. The published results with this technique [28–30]
appear equivalent to the ones with the shortening–suturing
technique described by Levante [24], with a residual extensor
lag of 10 degrees or less, and preserved DIP flexion.
The technique recently described by Georgescu leads to
similar results [31]. It makes use of a de-epithelialized pedicled
skin flap to reinforce the extensor tendon, which is distally
reattached using the pull-out technique. Tendon grafting. Tendon grafting techniques after
callus excision have been described more recently. The
indication seems particularly relevant after loss of tendon
substance following an open extensor mechanism injury [32].
The graft can be taken from the palmaris longus, inserted into a

Fig. 9. Diagram of the tenodermodesis technique.
Reproduced with permission of Maîtrise Orthopédique.

bone tunnel on P3 and then sutured at the proximal end as
described by Gu and Zhu [32]. A protective splint is worn for 4
weeks. Wang et al. harvested a bone-tendon graft from the
extensor carpi radialis brevis (ECRB) – including its distal bone
attachment – and secured it to the P3 base [33]. The DIP joint
was pinned in 10–15 degrees hyperextension for 4 weeks.
These two techniques seem to give comparable results to those
of the above-described techniques. In a series of 40 chronic
cases, Gu and Zhu reported restoring 97.6% of the range of
motion of the contralateral DIP joint and having 98.5% good or
excellent results [32]. In the 28 patient series described by
Wang et al., the mean residual postoperative DIP extensor lag
was 4 degrees; 24 patients had an excellent outcome and the
other four had a good outcome [33]. Extensor mechanism rebalancing. Extensor mechanism rebalancing consists of central slip tenotomy (Fowler’s
technique) and related procedures. The principle behind this
technique is to reduce the extension forces placed on the PIP by
releasing the CS insertion. The result is that the lateral slips
transmit extension forces to the terminal tendon and to its
lengthening callus, thereby allowing P3 extension (Fig. 10).
The triangular ligament must be preserved to avoid creating a
boutonniere deformity. The technique described by Fowler can
be performed with local anesthesia using a dorsolateral
approach. By cutting the TRL, the extensor mechanism can
be lifted and reflected. From the deep side of the extensor
mechanism, the CS insertion is then gradually detached
proximally to distally. Active DIP extension can be assessed
intraoperatively if the procedure is performed with a sensory
nerve block [34].
A direct dorsal incision can also be made, and the CS
released over the PIP joint [35]. Through a transverse approach,
Rozmaryn recommended excision of 50% of the central slip’s


P. Bellemère / Chirurgie de la main 34 (2015) 155–181

Fig. 10. Diagram of the principle behind Fowler’s technique used to treat
chronic mallet finger.
Reproduced with permission of Maîtrise Orthopédique.

width (3 of 6 mm), about 5 mm proximal to the joint line to
avoid the lateral bands and triangular ligament [36]. According
to Rozmaryn, this genuine CS tenectomy is justified based on
the conclusions of Hiwatari’s biomechanical study showing
that the residual DIP extensor lag is less when more of the CS
was excised on the dorsal side of P1 [37].
Postoperative PIP splint immobilization in extension for 2
weeks is recommended to avoid or prevent PIP extension deficit
[35,36]. The DIP joint must be immediately mobilized.
Fowler’s technique corrects mallet finger with a mean
residual postoperative extensor lag of 10 degrees or less [35–
40] (Fig. 11). It is not unheard of to observe gradual
improvement in the DIP extensor lag in the months following
the procedure (up to 1 year), along with correction of any
resulting PIP extension deficit [34,35]. The occurrence of
secondary boutonniere deformity is rare, and has been reported
in 4.5% of published cases [35–40]. This can be prevented by
preserving the triangular ligament and lateral bands during the
tenotomy, and transient postoperative PIP immobilization in
extension. Fowler’s technique can be combined with a
procedure on the terminal tendon over the DIP joint, as
recommended by Rozmaryn when the mallet finger’s extensor
lag is significant [36]. Biomechanical studies, performed by
Chao and then Hiwatari, have shown that Fowler’s technique is
not totally effective when the DIP extensor lag is greater than 36
degrees [37,41]. In such cases, Rozmaryn also shortens the
tendon callus by plicature (without excision) with two microbone anchors placed at the P3 base, in combination with DIP
pinning in extension for 4 weeks [36]. Baratz et al. have stated
that Fowler’s procedure should not be performed when the DIP
extensor lag is greater than 45 degrees or when there is no
continuity between the terminal extensor tendon and the distal
phalanx [34]. These contraindications have led them to use the
SORL technique instead (described later on).
When a swan-neck deformity exists with the mallet finger,
Fowler’s technique allows for partial or even full correction of
this deformity, depending on the amount of PIP hyperextension.
In Rozmaryn’s 39-case series, the mean pre-operative PIP
hyperextension of 18 degrees (0 to 70 degrees) was reduced to
4.8 degrees (0 to 30 degrees) using Fowler’s technique [36].

Fig. 11. Treatment of chronic mallet finger with swan-neck deformity using
Fowler’s technique. Preoperative appearance (a). Postoperative result (b).

Nevertheless, this technique is not recommended when PIP
hyperextension exceeds 25 degrees [36,38,42]. This is an
indication for the SORL technique. Spiral oblique retinacular ligament reconstruction
(SORL) technique. This highly ingenious technique is based
on Landsmeer’s anatomical work on the ORL. First described
by Thompson and Littler, it is derived from Littler’s original
technique of isolated ORL reconstruction using a slip of the
lateral band. However, the original technique is difficult to carry
out if the terminal tendon is discontinuous, such as in chronic
mallet finger [42,43]. SORL acts as a dynamic tenodesis. On
one hand, it corrects the deformity of the chronic mallet finger
with swan-neck deformity, and on the other hand, it restores the
synergy of PIP and DIP flexion during finger curling (Fig. 12).
In general, a half-strip of free palmaris longus tendon is used as
the graft, but we also use synthetic materials such as GORETEX1 CV-0 suture. The graft takes a spiral course around the
dorsal side of P3, following the ORL’s trajectory, then crosses
the PIP ventrally between the flexor sheath and the collateral
pedicles to reach the opposite lateral side of the base of P1.
Transosseous fixation of the graft proximally and distally is
performed through a dorsopalmar tunnel at the P3 base and
another transverse tunnel at the P1 base; the sutures are
typically supported on a pull-out button, but bone anchors [42]
and proximal soft tissue fixation can also be used [44].

P. Bellemère / Chirurgie de la main 34 (2015) 155–181

Fig. 12. Diagram of the SORL technique with the ends of the tendon transplant
secured with bone anchors.
Reproduced with permission of Maîtrise Orthopédique.


The primary challenge resides in setting the correct tension
on the grafted tendon. Insufficient tension will not correct the
deformity. Conversely, too much tension will cause DIP
hyperextension and PIP flexion with a boutonniere deformity.
Although Thompson did not pin the reconstruction, Kleinman
and Petersen recommend pinning the DIP in neutral position for
4.5 weeks and the PIP in 15 degrees flexion for 3 weeks [44].
Kanaya et al. recommend placing the PIP in neutral position
and flexing the DIP 15 degrees, while making sure that both the
PIP and DIP can be simultaneously flexed fully passively, and
then pinning the DIP only for 5 weeks [45].
Using the GORE-TEX1 CV-0 suture allows us to create a
double SORL reconstruction. The suture is passed through a
horizontal transosseous tunnel in the P1 base; each strand
followed the SORL trajectory on either side of the finger; one of
the strands returns to the P3 base in the terminal extensor
tendon, or if it is missing, in a horizontal transosseous tunnel;
the two strands are then tied laterally at the neck of the middle
phalanx (Fig. 13). No pinning is performed; the finger is flexed
early on with a Beasley ring for 2–3 weeks. The tension can be
set easily with this technique, and there is no risk of causing
clinodactyly. By using a synthetic suture, a tendon graft does
not need to be harvested; this material is less bulky than the
graft, just as solid and just as well tolerated.

Fig. 13. Intraoperative view of the treatment of a swan-neck deformity secondary to chronic mallet finger using the double SORL technique with a GORE-TEX1 CV0 suture. Palmar view (a). Physiological flexion (b) and extension (c) after adjusting the SORL tension.

P. Bellemère / Chirurgie de la main 34 (2015) 155–181


In the small case series that have been published up to now, the
SORL technique corrects the swan-neck deformity, reduces the
DIP extensor lag to between 0 and 10 degrees, without interfering
with full PIP and DIP flexion. However, DIP hyperextension of
10 to 25 degrees has been observed in 3 of the 12 cases in the
Kleinman and Petersen study, along with one case of joint
contracture; these complications led to two re-operations [44].
This technique does not reconstruct the terminal tendon of the
extensor mechanism but can be used successfully when it is
absent (due to avulsion or trauma-induced defect) or after failed
secondary repair of this tendon [34,45]. Fusion. DIP fusion is indicated when the other
surgical solutions are contraindicated (precarious skin condition, persistent joint stiffness, osteoarthritis pain) or have failed.
The fusion angle is set between 0 and 25 degrees of flexion
depending on the finger involved and the patient’s functional
demands. We recommend ensuring continuity of the terminal
extensor tendon by tenodermodesis suture, so as to reduce the
risk of secondary swan-neck deformity. When the latter is
present, a Fowler-type tenotomy procedure on the central slip
can be performed in combination with the fusion.

tolerated functionally. Two elements must be taken into
consideration: the amount of DIP extensor lag and the presence
of swan-neck deformity. Independent of the chosen therapeutic
method, an 8–12 week treatment period is required.
No method has been shown to be superior to another. None
can ensure complete correction of the deformity, and residual
DIP extensor lag of approximately 10 degrees is very common
The advantages and disadvantages of each treatment method
must be well understood, particularly for any surgical
treatments because of their potential complications: infection,
K-wire migration or breakage, wound healing problem, painful
scar-induced swelling on dorsum of P3 and the DIP joint, nail
deformity due to matrix lesion, DIP or PIP joint contracture,
persistent residual deformity or recurrent deformity.
4. Chronic injuries in zone 2
Chronic zone 2 injuries are the consequence of an initially
open tendon injury that results in DIP contracture due to
peritendinous adhesions or DIP extensor lag (mallet finger) due
to secondary rupture or tendon defect.

3.5. Treatment algorithm for chronic mallet finger

4.1. Contracture caused by adhesions

Fig. 14 summarizes the treatment indication options that can
be put forward in cases of chronic mallet finger that are not well

These are adhesions around one or both lateral bands as a
consequence of an initial partial or total tendon laceration that

Conservative treatment

Swan neck +
No swan neck

PIP hyperextension ≤ 25°

PIP hyperextension > 25°

Tendon defect
DIP extensor lag ≤ 35°

Graft or
DIP fusion

Secondary repair or

Fowler’s technique

Fig. 14. Treatment algorithm for chronic mallet finger.


P. Bellemère / Chirurgie de la main 34 (2015) 155–181

was immobilized for too long after being repaired, or where the
mechanism of injury led to associated bone or skin damage, or
in cases of tendon shortening due to direct suturing of a defect.
Upon examination, the active and passive flexion and/or
extension of the DIP joint is limited or even non-existent.
Treatment must initially consist of manually breaking up the
scar tissue in combination with rehabilitation and physiotherapy, and intermittent wear of a DIP flexion or extension brace if
needed. If the patient experiences persistent functional
impairment, it is important to wait for the initial healing
sequence to be completed (about 6 months) and for any
fractures to be healed before considering a surgical treatment.
If the skin condition allows, tenolysis can be performed by
releasing the peritendinous bone and skin adhesions. Debridement of the tendon ends by partial or total resection of a scared,
non-continuous lateral band may be required, as long as the
other lateral band is continuous and free of adhesions. The
DIP’s ability to flex and extend will not be hindered by doing
this. Anti-adhesion products in the form of gels and resorbable
membranes have been described, but their benefits have not yet
been demonstrated. A skin transplant or local flap procedure
may be necessary if the skin condition is precarious.
Extensive postoperative rehabilitation for PIP and DIP
flexion and extension must be initiated immediately. Posttenolysis complications include infection, recurrent adhesions,
tendon rupture and skin wound healing problems.
4.2. Extension deficit due to tendon rupture or defect
Passive reduction of the mallet finger must be confirmed. As
in Zone 1, conservative treatment with an extension brace must
be started immediately. If this fails, an intercalated tendon graft
can be proposed if the skin conditions allows [33]. The
alternative solution is a SORL reconstruction, especially in the
presence of an associated swan-neck deformity [34].

Fig. 15. Boutonniere deformity.

pulled by the TRL; this further increases the PIP flexion and
DIP hyperextension. This deformity gets its name from the fact
that the PIP slides between the two lateral slips, like a button in
a button hole. Over time, the deformity worsens and becomes
non-reducible with progressive contracture of the PIP and DIP
joints (volar plate and lateral ligaments); this contributes to
ORL retraction that in turn limits passive PIP extension and
active and passive DIP flexion.
Chronic boutonniere deformity is defined by Baratz et al.
[34] as a non-reducible contracture of the PIP and DIP joints.
Posner and Green [47] believe that the duration of the deformity
(beyond 8 weeks) makes it chronic in nature.
Not every old injury to the extensor mechanism in zone 3
will lead to the typical boutonniere deformity. DIP hyperextension can be absent, particularly when the initial injury goes
beyond the CS and extends laterally to the lateral slips,
preventing them from extending the DIP joint. The same thing
occurs when scar adhesions bind the lateral slips to the dorsal
side of the PIP joint.

5. Chronic injuries in zone 3: boutonniere deformity
These injuries involve the central slip of the extensor
mechanism. They are the consequence of either dorsal PIP
laceration or closed trauma (PIP volar dislocation, forced
flexion of the PIP in extension, direct dorsal blow to flexed PIP
joint) leading to CS rupture or avulsion of its distal insertion,
sometimes with a miniscule bone fragment. The chronic course
of these injuries results in boutonniere deformity.
5.1. Definition and pathophysiology
This finger deformity is typical of an old disruption (at least
2 or 3 weeks) [34] in the central slip (Fig. 15). It combines PIP
flexion and DIP hyperextension. Full active PIP extension is
impossible. The CS disruption induces a PIP flexion deformity
and progressive retraction of the extensor mechanism with
transfer of tension to the lateral slips, which in turn
progressively stretches the triangular ligament and induces
DIP extension (Fig. 16). Gradually, the lateral slips migrate in
front of the PIP flexion-extension axis because they are being


Fig. 16. Diagram of the mechanism of the boutonniere deformity.
Reproduced with permission of Maîtrise Orthopédique.


P. Bellemère / Chirurgie de la main 34 (2015) 155–181

5.2. Clinical presentation and functional impairment
The impairment can be appearance-related, but it is mainly
functional: it is due to an active PIP extension deficit that can
cause finger hooking accidents, and to incompletely active DIP
flexion, which limits and weakens the grip during finger
curling. The DIP flexion limitation often is the biggest
contributor to functional impairment (Fig. 17).
The clinical examination is used to: 
measure the active PIP and DIP range of motion during finger
flexion-extension. Early in the development of boutonniere
deformity, Elson’s test is positive: PIP extension against
resistance is weak or limited and leads to DIP extension [48]; 
determine if the PIP extension deficit can be passively
evaluate the possibility of DIP active and passive flexion
when the PIP is passively held in extension. This maneuver
(Haines-Zancolli test or Boyes test) evaluates ORL tension.
When it is retracted, the test is positive because active and
passive DIP flexion is limited or even impossible, but it is
possible with the PIP flexed (Fig. 18); 

measure grip strength, which can be reduced because of the
deficit in DIP active flexion.
5.3. Additional examinations
Standard radiographs with A/P and lateral views of the
extended finger can help reveal avulsion of the CS bony
insertion and evaluate the condition of the joint. Signs of
osteoarthritis may be present in chronic non-reducible
boutonniere deformity. MRI and ultrasound imaging can show
the CS retraction and position of the lateral slips.
5.4. Treatment
It must be stated upfront that it will be difficult to achieve
completely restored function with treatment. The PIP extension
deficit must not be transformed into an extension contracture
that is even less functional. Sensible objectives are to recover
full DIP active flexion and limit the PIP extension deficit to less
than 30 degrees. Although many treatment techniques exist,
they all share the same poor final outcomes, requirement to
wear a brace for an extended period of time and need for
diligent rehabilitation, possibility of deterioration of the
outcome in the long-term along with the occurrence of
complications, such as persistence of the deformity and
functional impairment, joint contracture, infection, painful
and sensitive swelling over the dorsum of the PIP joint.
5.4.1. Items to take into consideration
Several criteria must be analyzed before making a treatment
degree of functional impairment and the patient’s needs,
particularly an inability to flex the DIP joint. Some patients
only want better DIP flexion because the PIP flexion
deformity does not inconvenience them. Active PIP extension
deficit of less than 30 degrees is often well tolerated; 
degree of PIP and DIP joint deformity and possibility that
these deformities can be actively and passively reduced;

Fig. 17. Limited active DIP flexion due to chronic boutonniere deformity.
Appearance in extension (a) and flexion (b).

Fig. 18. Diagram of the Haines-Zancolli or Boyes test showing ORL retraction.
Reproduced with permission of Maîtrise Orthopédique.

P. Bellemère / Chirurgie de la main 34 (2015) 155–181 

skin condition, which can be a contraindication for any local
procedure or justify associated skin reconstruction procedures; 
signs of osteoarthritis in the PIP and/or DIP joint.
5.4.2. Classification
We propose a classification in Table 1 that is derived from
the one set out by Burton [49] and later modified by Strauch.
This classification takes into account the reducibility of the DIP
and PIP deformity, degree of PIP extension deficit (more or less
than 30 degrees), and the presence of osteoarthritis in the last

5.4.3. Conservative treatment
A very large portions of these cases must be treated
conservatively, namely all those in stages I to III.
The goals are to dorsalize the lateral slips by holding the PIP
in extension, to allow the DIP to flex freely, and to correct the
joint contracture, particularly in the PIP. This requires use of a
static and/or dynamic PIP extension orthotic brace, worn day
and night (Fig. 19). By not placing the DIP in the split, it can be
passively and actively flexed. In addition and in parallel,
passive and active DIP flexion and PIP extension mobilization
is carried out during rehabilitation and self-directed rehabilitation. The treatment will last 6 to 12 weeks, until the scar tissue
has matured. It may need to be longer if an old closed injury is
being treated.
If functional impairment persists despite the conservative
treatment due to more than 30 degrees PIP extension deficit or


Table 1
Classification of boutonniere deformity cases.
Stage I: DIP and PIP reducible
Stage II: DIP stiffness and PIP reducible
Stage III: DIP and PIP stiffness
Stage IV: PIP osteoarthritis

PIP deficit
< 308
> 308
< 308
> 308
< 308
> 308

inadequate DIP active flexion, surgical treatment can then be
5.4.4. Surgical treatment
The results of surgical treatment are often incomplete.
Several procedures can be carried out, either alone or in
combination, during the same surgery session. The goals are to:    

lengthen the terminal extensor tendon;
release the lateral slips and reduce their volar dislocation;
reattach or reconstruct the central slip;
make the PIP joint more flexible. Isolated tenotomy of the terminal extensor tendon. This tenotomy technique, which was described by
Fowler then Dolphin [50], reduces the extension forces on

Fig. 19. Conservative treatment of a chronic boutonniere deformity. PIP extension splint that allows DIP flexion (a). Dynamic extension brace used to make a stiff
boutonniere deformity more flexible (b).


P. Bellemère / Chirurgie de la main 34 (2015) 155–181

the terminal tendon at P3 and, by sliding the extensor
mechanism proximally, increases those placed on the PIP
joint. A dorsal skin incision is made on the dorsum of P2. The
extensor tendon can either be cut horizontally, at an angle [34],
in a bayonet configuration or in a chevron shape beyond the
triangular ligament starting at the junction of the middle third
and proximal third of the middle phalanx and proximal to the
distal ORL insertion. We prefer carrying out a mesh-like
lengthening of the terminal extensor tendon by making several
transverse, tiered and irregular small tenotomies that preserve
the extensor’s continuity; this allows rehabilitation to start
immediately (Fig. 20). The procedure is performed under local
anesthesia with a sensory nerve block; this allows the number
and size of the tenotomies to be adjusted according to the
improvement in flexion obtained intraoperatively.
Isolated Fowler/Dolphin tenotomy is indicated for patients
who are only concerned with the DIP flexion deficit or when the
PIP deficit is 30 degrees or less [51,52]. An increase of about 40
degrees in DIP flexion can be achieved [53] and a reduction in
the PIP extension deficit has been observed in nearly half the
cases [53,54]. Absence of residual mallet finger as a
consequence of the tenotomy is related to the pre-existing
contracture of the capsule and DIP collateral ligaments [34]. Release and dorsalization of lateral slips. After
making a curved dorsal incision of the PIP, the TRLs are

divided and then the lateral slips released up to the P1 base.
When performed under distal sensory anesthesia, and in cases
with minor flexion deformity, this procedure can be sufficient to
restore some of the PIP extension during active intraoperative
extension [51]. But in many cases, the triangular ligament must
also be reconstructed to maintain dorsalization of the lateral
slips by suturing them together and making sure not to extend
past the PIP proximally—this ensure its flexion capacity is not
reduced. The ability to passively flex the DIP while keeping the
PIP extended must be verified. Any limitation may require an
associated tenotomy procedure such as the Fowler/Dolphin
one. Release and dorsalization of the lateral slips generally
precedes secondary repair of the central slip in the same surgery
session. [16,34,47,52,55]. Secondary repair of central slip
Several methods are possible: direct repair, local plasty, graft
or tendon transfer. Direct repair. This consists of removing 2–
3 mm of the lengthened callus and suturing the central slip
[52,55–57] or reattaching it at the P2 base using bone anchors or
wire cerclage if avulsed [58]. As many others, we recommend
this procedure whenever possible in cases with significant PIP
extension deficits [34,47,52,55]. Oblique pinning of the joint
with a 1.0 or 1.2 mm K-wire is often necessary, with the K-wire
being placed volar to the lateral slips. It is left in place for at

Fig. 20. Mesh-lengthening of terminal extensor tendon for treating a boutonniere deformity. Same patient as Fig. 17. Intraoperative view of the staged tenotomy
without disruption to the extensor tendon (a). Clinical outcome in extension (b) and flexion (c).

P. Bellemère / Chirurgie de la main 34 (2015) 155–181

least 3 weeks and up to 5 weeks [55]. During this time, active
and passive DIP flexion must be performed regularly by the
patient multiple times each day.
The combination of CS repair and lateral slip release leads to
good and even very good results in 60% of cases with flexible
boutonniere deformity [55–57] (Fig. 21). The average residual
extension deficit is 10 degrees with this technique [51]. In cases
of stiff boutonniere deformity, the outcomes are much worse:
Le Bellec et al. reported 50% poor results and no good or very
good results in their study [55]. Reconstruction of the central slip by local plasty,
grafting or tendon transfer. Reconstruction is indicated if the
CS cannot be directly repaired because of a tendon defect or
precarious healing condition. Many techniques have been
described (Fig. 22). Their principles will be reviewed without
going into the details of the technical modifications made by
various authors. They involve either local plasty, grafting or
tendon transfer.
Local plasty of central slip: various types exist: 
triangular flap of local tissue including a portion of the lateral
slips [59]; 
CS flap divided over the P1 base, folded over itself then
secured to the CS insertion (Snow); although this technique is
often used in traumatology with a fresh injury, it is not very
effective for secondary reconstruction [60];


inverted transposition of lateral slips (Matev) [61]: one of the
slips is divided over the distal section of the triangular
ligament and the other one at the P2 base; the shortest slip is
threaded through the proximal part of the CS and sutured,
while the longest slip is sutured to the distal part of the
contralateral slip; 
distal division of one or both lateral slips (Littler) and
translocation onto the CS insertion [62]. Longitudinal
division of lateral slips into two continuous half-slips that
are brought to the midline; they are sutured together and
secures to the CS insertion (Littler-Burkalter-Aiache)
two central slips, which are previously separated from the
lumbricals and ORL, are turned-over dorsally, divided
distally and then sutured to each other and secured to the
P2 base [62] (Littler-Eaton); 
TRL division just above with the volar plate, which is then
folded-over dorsally and sutured together [65].
All of these plasty procedures also require temporary PIP
pinning, but the DIP can be flexed right away. Indications for
these various techniques depend on the defect size and
whether it only affects the central slip or one or both of the
lateral slips.
Tendon grafting of central slip: this consists of the following

Fig. 21. Treatment of a flexible chronic boutonniere deformity by secondary CS repair, release of lateral slips and PIP pinning. Preoperative appearance (a).
Intraoperative view (b) Clinical outcome (c,d).


P. Bellemère / Chirurgie de la main 34 (2015) 155–181

Fig. 22. Diagram of central slip reconstruction techniques. Snow technique (a) Matev technique (b) Littler-Burkalter-Aiache technique (c). Littler-Eaton technique
Reproduced with permission of Maîtrise Orthopédique. 

short free palmaris longus graft secured to the P2 base and
sutured proximally to the lateral slips [66–68]; 
pedicled flexor superficalis digitorum (FSD) graft [69] that is
completely released proximally; one strip is tunneled
subcutaneously to reconstruct the extensor mechanism and
the other strip is sutured to the flexor sheath to prevent PIP
hyperextension. Amad recently proposed a variation where a
proximally divided FSD slip is passed dorsally through a
bone tunnel in the P2 base to solidly reconstruct the CS and
allow early PIP mobilization [70].
The plasty and tendon grafting techniques used to
reconstruct the CS have led to outcomes that are difficult
to interpret because of the variety of pathologies and
techniques used, which are often described in only a few
cases, along with the outcome measures. In any case, they are
not any better than the ones associated with direct CS repair.
Tendon transfer extended with free long graft (by-pass
technique): the technique proposed by Oberlin et al. uses a
transfer of the extensor indicis proprius muscle that is extended
by a free palmaris longus graft in a by-pass configuration [71].
The graft is passed subcutaneously on the back of the finger and
secured to the CS at the P2 base (Fig. 23). We recommend

stabilizing the graft on the dorsum of the MCP joint to stop it
from dislocationg between the metacarpals and losing its
tension. Contrary to most of the previous techniques, which
require temporary pinning, this active transfer technique allows
for immediate rehabilitation of PIP and DIP flexion and
extension, protected by splinting of the wrist in extension and
MCP in a neutral position for 3 weeks. The outcomes of this
technique seem promising based on the five cases described by
Oberlin et al.: two excellent, two good and one fair result. PIP arthrolysis. Full PIP joint flexibility is needed
before any procedure is performed on the lateral slips and the
central slip. If this cannot be achieved with orthotic bracing and
physiotherapy, arthrolysis will be necessary. This can be the
first procedure performed during surgical treatment of a
boutonniere deformity if the PIP flexion deficit is not significant
(less than 40 degrees). Conversely, if the flexion deficit is more
than 40 degrees, it is best to perform the arthrolysis only;
secondary repair of the extensor mechanism can be considered
once joint flexibility has been restored and maintained
passively after several months of rehabilitation and orthotic
bracing [34,51,55].

P. Bellemère / Chirurgie de la main 34 (2015) 155–181


combined with a Fowler/Dolphin tenotomy, so as to obtain full
active DIP flexion; this provide definite functional improvement, particularly in cases of PIP fusion. Secondary CS repair
can be performed in the same surgical session if arthroplasty is
performed. Treatment algorithm. Many surgeons follow the
treatment sequence proposed by Curtis according to the
deformity correction obtained during the surgery; the
procedures are performed step-by-step under a pure digital
nerve block [1,35,47,49,51,52]. The treatment algorithm
proposed in Fig. 24 takes into account the preoperative
classification (Table 1) and the variables that have a significant
effect on the final outcome: PIP reducibility, magnitude of PIP
deficit, DIP flexibility, arthritic joint.
6. Chronic injuries in zone 4
Since the extensor mechanism broadly covers P1, it is rare to
see chronic injuries in this zone with complete loss of tendon
continuity. Treatment consists of secondary repair after
resection of the tendon callus.
Peritendinous adhesions are much more common however,
and can occur even after closed trauma (P1 fracture),
particularly if the initial trauma included a crush component.
These adhesions lead to finger stiffness, which must be
accurately analyzed clinically. Kilgore’s test shows the

Fig. 23. Diagram of Oberlin’s by-pass transfer technique.
Reproduced with permission of Maîtrise Orthopédique. Fusion and arthroplasty. PIP arthroplasty can be
indicated in chronic boutonniere deformity that coexists with a
painful, stiffened arthritic joint. The alternative is PIP fusion in
a functional position. These procedures on the joint can be

Boutonniere deformity

Conservative treatment

PIP reducible



PIP not reducible



DIP lexible

DIP not lexible
PIP deicit < 30°





PIP deicit > 30°


PIP deicit < 30°



PIP deicit > 30°


No procedure or
CS release or
LB repair

PIP arthritis



LB release
CS repair

LB release
CS repair


Fig. 24. Treatment algorithm for boutonniere deformity according to stage (I to IV). CS: central slip, LB: lateral band.

Fusion or


P. Bellemère / Chirurgie de la main 34 (2015) 155–181

presence of extensor adhesions both in zone 4 and proximal to it
(zones 5 or 6) [72]. In normal cases, active or passive MCP
flexion does not prevent PIP or DIP flexion. If there are extensor
adhesions at P1 or proximally over the MCP or metacarpal,
Kilgore’s test will be positive: the PIP and DIP cannot be flexed
when the MCP is flexed because the extensor is restricted by
adhesions. Conversely, when the MCP is held in extension or
hyperextension, the PIP and DIP can be flexed actively and
passively (Fig. 25). This test is different than the FinochiettoBunnell test that shows tightness due to intrinsic muscle
retraction. The latter test consists of examining passive PIP
flexion with the MCP passively extended and flexed. In cases of
intrinsic muscle tightness, PIP flexion will be greater when the
MCP is flexed than extended. In some old injuries, the two
sources of finger stiffness coexist and it may be hard to
differentiate between them.
If the stiffness persists despite rehabilitation and orthotic
bracing, the treatment consists of tenolysis of the extensor
mechanism by releasing any periosteal and cutaneous adhesions, while making sure the sagittal bands and extensor hood
remain intact.
The Kilgore test and the Finochietto-Bunnell test must be
reproduced intraoperatively once this procedure has been

carried out. If Kilgore’s test is still positive, extensor tendon
retraction is caused by scaring. Kilgore et al. proposed
lengthening the extensor tendon with a partial tenotomy [72]
(Fig. 26); alternatively, Littler proposed resecting the central
tendon at the base of P1 [60]. If the Finochietto-Bunnell test is
positive, the instrinsic muscles are retracted at P1. Treatment
consists of resecting the oblique fibers of the extensor hood; in
more severe cases, the intrinsics are also divided.
It is important to note that, despite immediate and prolonged
postoperative rehabilitation, surgical revision of chronic zone 4
injuries very rarely leads to good results.
7. Chronic injuries in zone 5
These are the consequence of open or closed trauma to the
extensor mechanism over the MCP joints. Several types of
injuries can be observed: complete or partial laceration of the
extensor tendon, sagittal band rupture, longitudinal separation
of the proprius and common extensor tendon at the fifth finger.
Certain types of repeated closed trauma can lead to chronic
dorsal tendon-capsule injuries (boxer’s knuckle).
7.1. Wounds on the dorsum of the MCP joints
Open trauma can lead to complete or more often, partial
laceration of the extensor tendon, often associated with damage
to the underlying joint. Secondary septic lesions are common if
the initial injury was neglected, especially following a bite
wound on the fist. Scar adhesions often limit the function of the
extensor mechanism and the MCP’s ability to flex. An old

Fig. 25. Diagram of the Kilgore test. The test is positive when the PIP can be
flexed with the MCP extended, but it cannot be flexed with the MCP flexed.
Reproduced with permission of Maîtrise Orthopédique.

Fig. 26. Diagram of Kilgore’s technique.
Based on [72]. Reproduced with permission of Maîtrise Orthopédique.

P. Bellemère / Chirurgie de la main 34 (2015) 155–181

sagittal band laceration can lead to subluxation of the extensor
mechanism on the dorsum of the MCP joint.
Secondary treatment of these injuries must be considered if
the functional impairment brought on by finger stiffness is
resistant to rehabilitation and orthotic bracing. Surgical
treatment consists of an incision to remove the pre-existing
scar tissue; the incision is then widened proximally and distally
until it is curvilinear. Samples for microbiology are collected
systematically. The procedure starts by tenolysis while
preserving the sagittal bands. If needed, one sagittal band
can be divided longitudinally close to the extensor tendon to
access the deep side of the tendon and back side of the joint.
This makes it possible to finish the tenolysis and then to
perform dorsal arthrolysis of the MCP if the joint is stiff. If
Kilgore’s test is still positive, the extensor tendon is too short; it
can be lengthened subsequently with a partial tenotomy [72].
If the extensor tendon is ruptured, secondary repair requires
direct suturing of the ends after removing the callus while
making sure not to shorten the tendon too much. The lacerated
sagittal band must be repaired and the stability of the extensor
mechanism on the dorsum of the MCP joint must be verified by
passively flexing the joint.
7.2. Sagittal band rupture
7.2.1. Pathophysiology and clinical consequences
Other than in cases of inflammatory arthropathy, sagittal
band rupture occurs most often following resisted finger
extension or a direct dorsal blow to a flexed MCP joint,
sometimes while simply leafing through book or crumpling a
sheet of paper. It can occur spontaneously, particularly in older
persons, in the context of degenerative articular or periarticular
conditions, sometimes in multiple fingers.
In the majority of cases, the rupture is located on the radial
side, primarily in the middle finger [73] and secondarily in the
ring finger. The greater occurrence in the middle finger can be
explained by the anatomy of its sagittal bands, which extend
more distally in this finger than in the other fingers [74], the
distinct protuberance of the third metacarpal head, the extensor
tendon’s rounder cross-section, which makes it more unstable
than in the neighboring fingers [75], and by the presence of
better developed intratendinous connections on the ulnar size
[76,77]. The clinical picture associates pain and palpable
swelling over the sagittal band, along with extensor tendon
instability on the dorsum of the MCP joint that can be
responsible for a snapping sensation, or even locking during
active MCP extension.
The amount of instability in the extensor tendon depends on
the extent of the sagittal band rupture. Experimentally, one
band must be lacerated proximally by more than 50% to cause
tendon instability. Proximal partial ruptures destabilize the
tendon more than distal ruptures [9,76]. Tendon instability is
revealed during the clinical examination by resisted finger
extension, which causes deviation of the tendon’s contour to the
opposite of side the rupture.
Complete sagittal band rupture leads to subluxation or
dislocation of the extensor mechanism into the intermetacarpal


valley (typically on the ulnar side) during MCP flexion
(Fig. 27). During active MCP extension, the dislocated tendon
suddenly reduces, causing a snapping sensation that is obvious
visually and upon palpation. When the tendon is clearly
dislocated in the intermetacarpal valley, active MCP extension
can be impossible because the tendon is in front of the flexionextension axis. The MCP must be extended passively so that
active extensor contraction can reduce the dislocated tendon
and hold the MCP extension. In the fifth finger, pronounced
ulnar deviation of the proximal phalanx accompanies dislocation on the ulnar side of the MCP of the proprius and common
extensor tendons [78]. In certain chronic forms, the dislocation
can become non-reducible if the ulnar sagittal band retracts,
leading to flexion deformity and ulnar deviation of the MCP
helped by progressive intrinsic muscle retraction (Fig. 27).
Rayan and Murray have described three types of sagittal
band injuries [79]. In type 1, there is a contusion without tear or
tendon instability; in type 2, a tear with tendon subluxation and
snapping; in type 3, the tendon completely dislocates in the
intermetacarpal valley.
Based on Ishisuki’s intraoperative anatomical observations
[8], spontaneous tendon dislocations are due to an injury to the
superficial bundle of the sagittal band close to the extensor
tendon, whereas traumatic dislocation is the consequence of
rupture of both bundles of the sagittal band further away from
the tendon.
When snapping is present, the classical differential
diagnosis is trigger finger due to flexor tenosynovitis; rarer
mechanisms involving a collateral MCP ligament, intratendinous connections or lateral slip snapping at the level of the PIP
in cases of reducible swan-neck deformity have also been
described. Careful clinical examination is essential for

Fig. 27. Rupture of the radial sagittal band of the extensor tendons on the
dorsum of the MCP joint leads to their ulnar subluxation into the intermetacarpal valley.


P. Bellemère / Chirurgie de la main 34 (2015) 155–181

establishing a diagnosis. MRI or ultrasound imaging, particularly dynamic imaging, can be relevant in cases where the
diagnosis is unclear.
Patients will often delay seeking medical attention because
these injuries are functionally well tolerated and because of
misdiagnosis. Most authors consider the injury to be chronic
when it is more than 3 weeks old.
7.2.2. Treatment
Chronic injuries (more than 3 weeks old) of the sagittal band
no longer benefit from conservative treatment and must be
operated on to stabilize the extensor mechanism on the dorsum of
the MCP joint. After making a dorsolateral or dorsal curvilinear
incision over the MCP joint, any scar adhesions on the radial SB
are released. Since dorsalization of the extensor mechanism can
be limited because of ulnar sagittal band retraction, it can be
partially divided (as volar and proximal as possible) or completely
divided if needed. Secondary repair of the radial SB can be
carried out by direct suturing or by using one of the many
variations of the extensor centralization techniques (Fig. 28). Direct sagittal band repair [74] (Keettelkamp). Direct repair is feasible when the tissue quality is sufficient. If the
band is continuous but stretched, plicature with overlapping
sutures can be carried out. If there are multiple old injuries,
repair of the radial SB of the most ulnar finger(s) can be
performed by direct suture to a divided ulnar SB from the
adjacent radial finger. Transposition of distally based extensor tendon
slip. A distally based extensor tendon slip (one-quarter to
one-third of tendon diameter) is harvested proximally over
about 4 cm from the radial side or the ulnar side (Caroll) [80]; if
the latter is used, it can be extended with intratendinous
connections [77]. The slip holds the centralized tendon after
twisting it around the radial collateral ligament [80,81] or

intermetacarpal ligament [77,82,83], or looping it around the
palmar interosseous muscle (Michon) [78]. It is then sutured to
itself and to the extensor tendon or capsule (Michon). Another
technique consists of harvesting a proximally based tendon slip
over P1 and then looping it around the lumbrical tendon
insertion (McCoy) [84]. If an extra tendon such as the proprius
extensor tendon to the middle finger exists, it can be used to
stabilize the reconstruction [85]. Repair with intratendinous connection. An intertendinous connection on the ulnar side is released and shifted to the
radial side (Wheeldon) [75] and then sutured to the radial and
volar stump of the torn SB. Lumbrical tendon transfer [86]. The lumbrical
tendon is passed through the extensor tendon and sutured to
itself. The ulnar SB does not need to be divided during this
active transfer technique, which prevents radial instability. Palmaris longus tendon graft. A palmaris longus
tendon graft is either twisted around the extensor tendon then
secured on both sides of the metacarpal head with 2 bone
anchors [87], or passed through a bone tunnel in the metacarpal
head and then behind the extensor tendon (Kang) [88].
No matter which technique is used, the surgeon must verify
intraoperatively that: 
the extensor tendon is perfectly centered during passive MCP
flexion and extension; 
sufficient tension is placed on the repair: this must be
evaluated with the MCP joint flexed about 50 degrees, while
making sure the MCP can be flexed completely passively; 
the stabilizing transfer on the extensor tendon is located in the
most isometric location possible, ideally at the same height as
the metacarpal neck-head junction [87,88]. More distal

Fig. 28. Diagrams of secondary repair techniques after sagittal band rupture. Keetelkamp’s technique (a). Caroll’s technique (b). McCoy’s technique (c). Wheeldon’s
technique (d).
Reproduced with permission of Maîtrise Orthopédique.

P. Bellemère / Chirurgie de la main 34 (2015) 155–181

fixation will hinder extension, while more proximal fixation
with hinder MCP flexion; 
the repair is strong enough to allow early mobilization.
Postoperative care depends on the technique used and the
strength of the repair. The MCP joint can be immobilized in
about 20 degrees flexion for 3–4 weeks with PIP flexion
allowed. The MCP joint can then be moved with the adjacent
fingers while being protected by a brace that prevents it from
flexing completely for another 3–4 weeks (Fig. 29).
7.3. Longitudinal separation of the extensor tendon at the
fifth finger
This rare injury results from a direct axial blow in a typically
young patient leading to subluxation of the two extensor
tendons (proprius and common) to either side of the joint,
causing a pseudo-boutonniere deformity at the MCP joint [78].
The dorsal capsule may also be torn [89–91]. The clinical
picture shows an active P1 extension deficit without marked
ulnar deviation, which differs from the clinical picture of
simultaneous dislocation of the two extensor tendon to the ulnar
side due to radial SB rupture [78].
When this separation is treated secondarily, surgical
treatment consists of removing any fibrotic areas in the
tendons, abutting the two extensor tendon and suturing them
side-to-side [78,90]. Le Viet et al. combined this procedure with
ulnar SB division; if the radial SB is retracted, it is scarified to
weaken and lengthen it [78].
Postoperative immobilization with a splint at 30 to 40
degrees MCP flexion is used for 2–4 weeks, then continued with
a protective brace that prevents full MCP flexion (Fig. 29). The
results reported in small case series are good, with no
recurrence of the pathology.
7.4. Boxer’s knuckle
This catchy name is used for injuries to the dorsal capsule of
the MCP joint of the long fingers (primarily the middle finger,
but also the index). They are typically chronic and induced by
repetitive impacts during punching movements performed for


certain combat sports, particularly boxing. The primary injury
is a dorsal capsule tear that can be associated with complete or
partial SB rupture, or even longitudinal separation of the
extensor tendons in the fifth finger [90,91]. These injuries cause
pain and dorsal swelling during and immediately after punching
movements are performed. Extensor mechanism instability
may also be present if a sagittal band is completely ruptured.
Once chronic, the joint capsule becomes thickened with nonelastic fibrotic scar tissue. Directly suture repair of the tear can
be carried out in newer injuries [92], but may no longer be
possible in chronic cases because of the risk of interfering with
full MCP flexion. In such cases, Nagaoka et al. [93] recommend
excision of an oval-shaped piece of scar tissue around the
ruptured capsule and the SB, if it is also ruptured. The size of
the resulting tissue defect is measured with the MCP fully
flexed, and then repaired with an extensor retinaculum graft.
There are no reports of SB plasty for the treatment of boxer’s
Postoperative immobilization of the MCP in 60 degrees
flexion is used for 3 weeks. The patient can restart punching
activities 3–6 months after the surgical procedure. The results
reported in various series are good, with no recurrence of the

8. Chronic injuries in zone 6, 7, 8
8.1. Zone 6
On the dorsum of the metacarpals, various chronic extensor
mechanism injuries have been described: loss of continuity due
to simple but neglected lacerations, peritendinous adhesions
after metacarpal fixation or tendon repair, or sequelae of
multiple tissue injuries (skin, tendon, bone) that can require
both bone and skin reconstruction.
In cases where tendon continuity is lost, the MCP joint has a
permanent flexion deformity that cannot be actively reduced.
However, this flexion deformity can be limited if the injury is
located proximal to an intertendinous connection, which takes
over during extension. Proximal secondary tendon retraction is
not significant if the injury is located distal to an intertendinous

Fig. 29. Brace used to protect a zone 5 extensor mechanism repair by limiting full MCP flexion.


P. Bellemère / Chirurgie de la main 34 (2015) 155–181

connection, which remains attached and holds the proximal
tendon end.
Secondary repair by tendon suturing is possible after
excision of the tendon callus. When not possible (excessive
retraction, loss of tendon substance, poor tendon quality),
suture of the distal tendon end by abutting it against the adjacent
finger’s tendon can be considered if it does not interfere with
full MCP flexion. However, there is a risk of causing an
extrinsic extension contracture. A small defect can also be
treated by a turned-over tendon transposition [60].
The extensor can also be rebuilt by transferring a dedicated
finger extensor tendon; the EIP can be used to reconstruct the
middle finger’s extensor tendon; the EDM can be used to
reconstruct the ring finger’s extensor, depending on anatomical
variations in the extensor mechanism in the fifth finger.
Transposition of a tendon slip from the fourth finger has been
proposed as a manner to reconstruct the fifth finger’s extensor
An alternative to tendon transfer is an intercalated tendon
graft using the palmaris longus tendon, or if not available, a toe
extensor tendon. The proximal muscle body must still have the
ability to contract, and cannot be overly retracted, which occurs
when the injury is very old. This more anatomical technique is
indicated if justified by the patient’s functional needs (dexterity,
independent finger extension). Proximal and distal suturing of
the tendon graft must be carried out far away from the extensor
retinaculum, so as to not impinge with it. The sutures must be
solid enough to allow for immediate rehabilitation. We
recommend using a Pulvertaft weave on the distal end. The
proximal end is sutured in zone 7. Appropriate tension is placed
on the repair so that finger extension can be obtained with the
wrist in neutral position [60]. At least 4 weeks of postoperative
immobilization and up to 6 weeks is needed with a static or
dynamic extension brace. This holds the wrist in 30 degrees
extension and MCP in neutral or 15 degrees flexion, with the
PIP and DIP joints free.
If the subcutaneous tissue will not allow effective tendon
gliding, this grafting procedure can be performed in two stages;
a silicone rod is used initially and is replaced a minimum of 2–3
months later with the tendon graft. In some cases, skin
reconstruction with a flap that provides thick subcutaneous
tissue may be necessary; this is performed before or during
secondary repair of the extensor mechanism [95].
Kilgore’s test will be positive if scar adhesions are present.
Rehabilitation and static orthotic bracing, to prevent extension
contracture and help to soften the skin, must be carried out until
the inflammatory scar processes have subsided, generally 6
months after the initial injury event. In case of failure or
incomplete restoration, tenolysis is carried out to release
adhesions and excise peritendinous fibrous scar tissue.
Depending on the presentation, this can be combined with
hardware removal (plate, screw or K-wire) after the metacarpal
bone has healed. This must be followed by immediate
postoperative rehabilitation and orthotic bracing as needed.
Peritendinous absorbable adhesion barriers (gels, membranes)
can be used with the tenolysis procedure, but up to now there is
no proof of their effectiveness in clinical practice.

8.2. Zone 7
If the tendon injury is no longer acute, there is a significant
risk of peritendinous scar adhesions and/or impingement of a
large tendon callus with the extensor retinaculum because this
zone is narrow, compartmentalized and covered with a synovial
Clinical examination will reveal any tendon gliding defects:
when a fist is made, the wrist cannot be flexed or extended.
Moreover, finger extension contracture is evident during wrist
flexion and the fingers cannot be completely extended when the
wrist is extended.
Tenolysis is carried out to release adhesions and impingements. The extensor retinaculum must be opened and certain
septums must be cut to provide more room for gliding. Its
reconstruction at the end of the procedure must be solid enough
to allow immediate and sometimes prolonged rehabilitation,
potentially supplemented by protective night bracing or a static
and/or dynamic brace.
Zone 7 is also a common location for tendon ruptures that
are diagnosed and evaluated secondarily. Other than inflammatory arthropathy, these can have two causes: 
iatrogenic, due to rubbing against a K-wire, sharp edge of a
screw or plate, or on the proximal end of the ulna after the
Sauvé-Kapandji or Darrach procedure, or after cortisone
injection or wrist arthroscopy; 
degenerative, after rupture due to mechanical and inflammatory
causes over an arthritic and unstable distal radioulnar joint. In
these cases, tendon ruptures start with the fingers on the ulnar
side and gradually extend to the radial fingers. They are
sometimes preceded by significant tenosynovial inflammation.
Tendon rupture is diagnosed clinically: active MCP
extension is impossible and passive extension by the tenodesis
effect of wrist flexion is no longer present. Given the long
excursion of the extensor tendon in this zone and the delayed
treatment, the tendon ends can be significantly retracted and
shriveled, making direct suture repair impossible. Several
options are available in these cases: intercalated graft, abutment
to an adjacent finger, intercalary graft, tendon transfer. These
procedures can be combined together depending on how many
extensor tendons are ruptured, how old these ruptures are and
how much the proximal tendon is retracted. The treatment plan
is fairly similar to the one for ruptures secondary to rheumatoid
arthritis. It consists of: 
opening the extensor retinaculum on its ulnar side, marking
the boundary for a rectangular flap with radial hinge; 
extensor tenosynovectomy; 
an appropriate procedure on the distal radioulnar joint,
depending on the etiology of the tendon rupture; 
secondary tendon repair: the classical plan when the extensor
tendons of the fourth and fifth fingers are ruptured is to
transfer the EIP to the common extensor of the fifth finger and
place the middle finger’s common extensor against that of the
index finger on the dorsum of the hand (Fig. 30). If the EIP is

P. Bellemère / Chirurgie de la main 34 (2015) 155–181

Fig. 30. Diagrams of repair techniques for ruptured extensor tendons in zone 7.
EIP transfer and tendon abutment for ruptured extensor tendons in the fourth
and fifth fingers (a). Transfer of the two superficial flexor tendons in a case
where all the finger extensor tendons are ruptured (b).
Reproduced with permission of Maîtrise Orthopédique.


not available, an intercalated tendon graft is a possibility;
however there is a risk of postoperative adhesions. When
extensor tendons are ruptured in three fingers, transfer of the
superficial flexor tendon of the middle or ring finger can be
proposed. The tendon is passed through the interosseous
membrane or around the wrist. It is secured with a Pulvertaft
weave at the distal ends of the torn tendons in the fourth and
fifth fingers; the middle finger can be revived with an EIP
transfer. When four finger extensor tendons are ruptured, the
superficial flexor tendons of both the middle and ring fingers
are used to revive two common extensor tendons each. The
tension placed on the repaired tendon is the same as the one
described in zone 6; 
closing the extensor retinaculum solidly while making sure
there is no impingement that could impede tendon gliding. An
extensor retinaculum plasty procedure is sometimes needed to
isolate the tendon repair from the distal radioulnar joint; 
immobilization and postoperative monitoring is the same as
for zone 6 tendon ruptures (Fig. 31).

Fig. 31. Repair of zone 7 extensor tendon ruptures in the third, fourth and fifth fingers by EIP and superficial flexor tendon transfers. Intraoperative view (a);
postoperative immobilization that allows early flexion (b) and extension (c) movements. Clinical outcome in extension (d) and flexion (e).


P. Bellemère / Chirurgie de la main 34 (2015) 155–181

Fig. 32. Two-stage repair of multiple tissue defects in zones 3, 4 and 5 with initial bone injury. Intraoperative view of the first stage with implantation of silicone rod.
Note the associated sagittal band reconstruction (a). Second stage with palmaris longus grafting performed three months later (b). Postoperative result in flexion (c)
and extension (d).

8.3. Zone 8

9.2. Zones 3, 4, 5

Secondary repairs in the muscle–tendon junction region are
difficult to carry out because of muscle retraction and frequent
muscle and tendon defects. Distal suturing in zone 7 of one or
two ruptured tendons against an adjacent healthy tendon can be
performed. When multiple tendons are ruptured, one or more
superficial flexor tendons can be transferred, along with the
flexor carpi ulnaris tendon, which is long enough to reach zone 8.

Local and regional skin flaps can be used. As previously
stated, secondary tendon repair can be performed at the same
time if the bone and joint structures do not need to be repaired.
Otherwise, or if scar tissue is present that could lead to the
development of early peritendinous adhesions, we recommend
a two-stage repair using a silicone rod (Fig. 32).
9.3. Zones 6, 7, 8

9. Chronic tendon injuries with defects in multiple
It is essential that reliable skin coverage be re-established in
these particular cases. Secondary tendon repair depends on the
zone affected and if bone and joint structures also need to be
repaired. The high risk of sepsis must be kept in mind and
appropriate pre-operative and postoperative preventative
measures taken.

9.1. Zones 1 and 2
DIP fusion in associated with wound coverage using a local
flap or a regional flap (reversed de-epithelialized cross finger
flap) is the most common solution used.

Zones 6, 7 and 8 can be the site of multiple tissue injuries
(rollover hand) leading to extensive skin, tendon, bone and joint
(metacarpal and/or carpal) defects along with injuries to the
interosseous muscles (defects, retraction). The ideal strategy is
to perform a single-stage reconstruction all of the injured
tissues [94,95]. This can be broken up depending on the extent
of the defects, amount of wound contamination and the
patient’s condition (polytrauma). The presence of bone and
joint injuries at the wrist or MCP joints requires that extensor
reconstruction be deferred until the bone injuries and skin
wounds have healed, the risk of sepsis is contained and
maximum wrist and MCP range of motion has been recovered
It is essential for the skin coverage to provide an effective
subcutaneous gliding layer. This can be achieved through a
regional pedicled flap (radial, posterior interosseous, ulnar),

P. Bellemère / Chirurgie de la main 34 (2015) 155–181

distant flap (inguinal) or free flap (external brachial, temporalis
fascia). Secondary tendon reconstruction will require grafting.
If sufficiently good skin coverage has been achieved with the
flap, a silicone rod does not need to be used [96,97]. If the flap is
already in place, we recommend placing the tendon graft
between the fascia and subcutaneous fat to achieve better
gliding further away from the deep scar tissue. Single-stage
tendon grafting would seem to be contraindicated when it
would contact a bone repair because of the significant risk of
secondary adhesions. When large tendon defects exist (greater
than 5 cm) [96], FSD tendon transfer will provided enough
tendon material for the transplant. Depending on the type of
flap, composite vascularized flaps can bring sufficient skin
tissue, gliding tissue and tendon tissue to the site [95–97]. A
composite flap pedicled on the ulnar artery includes the
palmaris longus tendon and a slip from the flexor carpi ulnaris
(Guimberteau). A flap pedicled to the radial artery includes the
palmaris longus tendon, a strip of brachioradialis and a strip
from the flexor carpi radialis (Reid and Moss). A free composite
flap of dorsalis pedis provides four sufficiently long tendons
(Adani). The wound healing sequelae after harvesting these
flaps can be mitigated by using fascia without skin tissue,
particularly for the radial (Adani) and ulnar flaps, or by placing
artificial dermis on the donor site [97].
The results of these secondary multiple tissue repairs seem
positive [96–98] when the passive range of motion of the MCP
and wrist joint are preserved. Residual MCP extension deficit
seems to be the rule [96,98]. Poor outcomes are likely with
extensive bone or joint defects; damage to the interossei
muscles will add significant scar-related stiffening that will
limit finger flexion in particular [96]. Secondary tendon
reconstruction is not justified in these cases, especially since
mechanization of the skin coverage provided by the flap due to
scar adhesions often limits the residual MCP extension deficit.
Disclosure of interest
The author declares that he has no conflicts of interest
concerning this article.
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