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Dupuytren Disease: Anatomy, Pathology, Presentation, and Treatment

Ghazi M. Rayan
J. Bone Joint Surg. Am. 89:189-198, 2007.

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189

Selected
Instructional
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Dupuytren Disease: Anatomy,

Pathology, Presentation, and Treatment
By Ghazi M. Rayan, MD
An Instructional Course Lecture, American Academy of Orthopaedic Surgeons

The disorder called Dupuytren disease
has been recognized for approximately
400 years. Its presentation, although
seemingly rather constant, is actually
extremely variable, depending on which
structures are involved. A thorough
knowledge of palmar fascial anatomy
is essential to the understanding of Du-
puytren disease. There have been re-
cent advances in the pathophysiology
of Dupuytren disease, and these have
added to our knowledge of this disorder
but have not yet changed its treatment.
There are two distinct clinical entities,
classic Dupuytren disease and atypical,
so-called non-Dupuytren palmar fas-
cial disease1,2. These two types differ in
presentation, etiology, treatment, and
prognosis. Authors of future epidemio-
logical and outcome studies should not
confuse these two clinical entities. Sur-
gical treatment is the conventional and
most widely used method of managing
Dupuytren disease.
The earliest published reference
to the disorder that was later to be
called Dupuytren disease was by Felix
Platter, who in 1614 described a case,
attributing the deformity to a flexor
tendon contracture3. In 1777 Henry
Cline recognized that the disorder in-
volved the palmar fascia, in 1822 Sir
Astley Cooper advocated closed fasciot-
omy as a treatment for the condition,
and in 1831 Guillaume Dupuytren gave
a detailed anatomic and pathologic de-
scription of the disease and demon-
strated a surgical case in Paris that
earned him the disease eponym4. By
1900 there were at least 256 publica-
tions related to Dupuytren disease and
at least eight books on the subject2,5-11.
Age, gender, geography, and
ethnicity influence the disease preva-
lence, which has been reported to be as
low as 2% and as high as 42%12-14. Men
are more likely to have it than women
(a ratio of nine to one), and the overall
incidence increases with age, with the
frequency in women catching up to
that in men later in life15. The disease
is common in Scandinavia, Great Brit-
ain, Ireland, Australia, and North
America. It is uncommon in southern
Europe and South America and rare in
Africa and China16,17.
Dupuytren disease is associated
with diabetes18-20. Burge et al. reported a
higher risk of Dupuytren disease in al-
coholics, smokers, people with hyperc-
holesterol, and patients infected with
human immunodeficiency virus21-23.
There is controversy regarding a rela-
tionship between Dupuytren disease
and seizure disorders24,25. The etiology of
Dupuytren disease remains controver-
sial as well, but inflammation, trauma,
neoplasia, and genetics have been im-
plicated as factors26-31. The evidence is
strongest for at least a genetic predispo-
sition. There is a clearly increased inci-
dence in relatives of patients with
Dupuytren disease, and there has been
at least one report of identical twins
with the disease13,32. There seems to be
an autosomal dominant transmission
with variable penetrance.
Anatomy
The radial, ulnar, and central apo-
neuroses, palmodigital fascia, and
digital fascia are all part of the palmar
fascial complex (Fig. 1)33. These struc-
tures are involved to varying degrees in
Dupuytren disease. Each structure
can be subdivided. The radial aponeu-
rosis has four components: the thenar
fascia (an extension of the central apo-
neurosis), the thumb pretendinous
band (small or absent), the distal com-
missural ligament, and the proximal
commissural ligament34. The ulnar apo-
neurosis consists of the hypothenar

Disclosure: The author did not r eceive grants or outside funding in suppor t of his research for or preparation of this manuscript. He did n ot receive
payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed,
or agreed to pa y or direct, any benefits to an y research fund, foundation, educational institution, or other charitable or nonp rofit organization with
which the author is affiliated or associated.

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muscle fascia (an extension of the cen-
tral aponeurosis), the pretendinous
band to the small finger (always present
and very substantial), and the abductor
digiti minimi confluence, which is
enveloped by the fibers of the sagittal
band35,36. The central aponeurosis is the
core of Dupuytren disease activity. It is
a triangular fascial layer with its apex
proximal. Its fibers are oriented longi-
tudinally, transversely, and vertically.
The longitudinal fibers fan out as pre-
tendinous bands in the three central
digits, and each bifurcates distally.
Each bifurcation has three layers37. A
superficial layer inserts into the dermis,
a middle layer continues to the digit as
the spiral band, and a deep layer passes
almost vertically and dorsally. The
transverse fibers make up the natatory
ligament located in the distal part of the
palm and the transverse ligament of the
palmar aponeurosis. The transverse lig-
ament of the palmar aponeurosis is
proximal and parallel to the natatory
ligament and deep to the pretendinous
bands. Its distal, radial extent is the
proximal commissural ligament. The
transverse ligament of the palmar apo-
neurosis gives origin to the septa of
Legueu and Juvara, which protect the
neurovascular structures and provide
an additional proximal pulley to the
flexor tendons. The vertical fibers of the
central aponeurosis are the minute ver-
tical bands of Grapow and the septa of
Legueu and Juvara. The vertical bands
are numerous, small, strong, and scat-
tered along the palmar fascial complex
and are most abundant in the central
aponeurosis38. The vertical septa of
Legueu and Juvara are deep to the pal-
mar fascia and form fibro-osseous
compartments33,39,40. There are eight
septa, one radial and one ulnar for each
finger41. They form seven compart-
ments of two types: four flexor septal
canals that contain the flexor tendons
and three web space canals that contain
the common digital nerves and arteries
and the lumbrical muscles (Fig. 2).
These septa are inserted in a soft-tissue
confluence that consists of five struc-
tures: the A1 pulley, the palmar plate,
the sagittal band, the interpalmar plate
ligament, and the septa of Legueu and
Juvara (Fig. 3). The fascial structures in
the palmodigital region are complex.
The middle layer of the bifurcated pre-
tendinous band spirals on its axis nearly
90°, and the peripheral fibers run verti-
cally adjacent to the metacarpopha-
langeal joint capsule40. They continue
distally deep to the neurovascular bun-
dle and natatory ligaments and emerge
distal to the natatory ligaments to con-
tinue as the lateral digital sheet. This
spiral band therefore is the connection
between the palmar and digital fascial
structures. The proximal fibers of the
natatory ligaments run in a transverse
plane, but the distal fibers form a “u”
and continue longitudinally along both
sides of the digit, forming the lateral
digital sheet. The lateral digital sheet
therefore has deep and superficial con-
tributions from the spiral band and the
natatory ligament. The neurovascular
bundle in the digit is surrounded by
four fascial structures: the Grayson liga-
ment (palmar), the Cleland ligament
(dorsal), the Gosset lateral digital sheet
laterally, and the Thomine retrovascular
fascia medially and dorsally42.

Pathophysiology
The myofibroblast is the offending cell
in Dupuytren disease. It was described
originally by Gabbiani and Majno43 and
further studied by Tomasek et al.44. The
myofibroblast has morphologic charac-
teristics of both a fibroblast and a
smooth muscle cell, and it can actively
contract45. The myofibroblast of Du-
puytren disease expresses alpha-smooth
muscle actin that plays a role in contrac-
Fig. 1 tion46. The Dupuytren myofibroblast
Palmar fascial complex with its five components: the radial aponeurosis (RA), ulnar aponeurosis synthesizes fibronectin, an extracellular
(UA), central aponeurosis, palmodigital fascia, and digi tal fascia. NL = nat atory ligament, PA = glycoprotein, which connects myofibro-
palmar aponeurosis, and TLPA = transverse ligament of the palmar aponeur osis. (Reprinted, blastic cells together and connects myo-
with permission, from: Rayan GM. Palmar fascial complex anatomy and pathology in Dupuytren’s fibroblastic cells to the extracellular
disease. Hand Clin. 1 999;15:75.) stromal matrix with an integrin47,48.

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Myofibroblast contractility can be

influenced by prostaglandins, which
are found in nodules and active stages
of the disease49-51. Fibroblast growth
factor (FGF), transforming growth
factor-alpha (TGF-α), epidermal
growth factor, interleukin-1 (IL-1),
and platelet-derived growth factor
(PDGF) have been found to be ex-
pressed more in Dupuytren disease52.
In Dupuytren disease, normal
fascial bands become diseased cords53.
Dupuytren nodules and cords are
pathognomonic of Dupuytren disease54.
A nodule usually appears first, but
sometimes a cord develops without a
nodule. Typically, the cords progres-
sively shorten, leading to joint and soft-
tissue contracture. The cords involve
the palmar, palmodigital, or digital re-
gions. Shortened cords cause joint de-
formity, and long-standing flexion
deformity leads to contracture of the
Fig. 2
capsuloligamentous tissue and flexion
Interpalmar plate liga ment (IPPL) and septa of Legueu a nd Juvara. PA = palm ar contractures of the metacarpopha-
aponeurosis. (Reprinted, with permission, from: Rayan GM. Palmar fascial complex
langeal and proximal interphalangeal
anatomy and patholog y in Dupuytren’s disease. Hand Clin. 1999;1 5:79.)
joints.
Grapow vertical bands become
microcords leading to skin-thickening,
which is one of the earliest manifesta-

Fig. 3
Soft-tissue confluence and septa of L egueu and Juvara. IPPL = int erpalmar plate ligament and PA = palmar
aponeurosis. (Reprinted, with per mission, from: Ra yan GM. Palmar fascial complex anat omy and pathology in
Dupuytren’s disease. H and Clin. 1999;15:80 .)

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tions of Dupuytren disease. Skin pits
develop from the first layer of the split
pretendinous band and are usually dis-
tal to the distal palmar crease.
The pretendinous cord develops
from the pretendinous band and is the
cord most frequently seen in Du-
puytren disease. It is responsible for
flexion deformity of the metacarpopha-
langeal joint and often extends distally
to continue with digital cords. Occa-
sionally, the pretendinous cord bifur-
cates distally, with each branch
extending into a different digit and
forming a commissural “Y” cord. The
vertical cord is less common and is con-
nected to the pretendinous cord55. The
vertical cord is short thick diseased tis-
sue departing from the pretendinous
cord and extending deeply in between
the neurovascular bundle and the flexor
tendon fibrous sheath. This cord is the
diseased septa of Legueu and Juvara.
Extensive palmar fascial disease is en-
countered in severe conditions and af-
fects a large area of the palm, leading to
diffuse thickening of many compo-
nents of the palmar fascial complex in-
cluding the transverse ligament of the
palmar aponeurosis.
The spiral cord has four origins;
the pretendinous band, the spiral band,
the lateral digital sheet, and the Grayson
ligament56. This cord is encountered
most often in the small finger, but it
may affect the ring finger. In the palm it
is located superficial to the neurovascu-
lar bundle, just distal to the metacar-
pophalangeal joint; it passes deep to the
neurovascular bundle; and in the digit it
runs lateral to the neurovascular bundle
as it involves the lateral digital sheet.
Distally in the digit it is again superficial
to the neurovascular bundle as it in-
volves the Grayson ligament. Initially,
the cord spirals around the neurovascu-
lar bundle, but as it contracts the cord
straightens and the neurovascular bun-
dle spirals around the cord. The dis-
torted anatomy of the neurovascular
bundle, which displaces medially and
centrally, renders it at risk of injury
during surgery57,58. The natatory cord
develops from the natatory ligament,
converting the u-shaped web-space fi-
bers into a v shape and producing a
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contracture of the second, third, and
fourth web spaces. The cord extends
along the dorsal-lateral aspect of the
adjacent digits and can be best detected
by passively abducting the digits and
at the same time flexing one digit and
extending the other at the metacar-
pophalangeal joints. This maneuver al-
lows the natatory cord to become more
prominent.
The most frequently encountered
digital cords are the central, spiral, and
lateral cords. They are responsible for
flexion deformity of the proximal inter-
phalangeal joints. The central cord is an
extension of the pretendinous cord in
the palm. It courses in the midline and
attaches into the flexor tendon sheath
near the proximal interphalangeal joint
or the periosteum of the middle pha-
lanx on one side of the digit. The cen-
tral cord usually does not displace the
neurovascular bundle. The lateral cord
originates from the lateral digital sheet
and attaches to the skin or to the flexor
tendon sheath near the Grayson liga-
ment. The lateral cord leads to contrac-
ture of the proximal interphalangeal
joint but can cause a flexion contracture
of the distal interphalangeal joint. This
cord can displace the digital neurovas-
cular bundle toward the midline by its
volume. The abductor digiti minimi
cord is also known as the isolated digital
cord. It originates from the abductor
digiti minimi tendon, but it may also
arise from the nearby muscle fascia or
base of the proximal phalanx. It courses
superficial to the neurovascular bundle
and infrequently entraps and displaces
it toward the midline. It frequently in-
serts on the ulnar side of the base of the
middle phalanx, but it may attach on
the radial side or have an additional in-
sertion in the base of the distal phalanx,
causing a contracture of the distal inter-
phalangeal joint. The retrovascular cord
is a poorly defined structure but is
thought to develop from the retrovas-
cular band of Thomine and is located
deep to the neurovascular bundle58. It is
different from the checkrein ligament.
The retrovascular diseased tissue does
not cause contracture of the proximal
interphalangeal joint, but if the tissue is
not removed, the proximal interpha-
langeal joint contracture may not be
completely corrected.
The distal commissural cord is
the diseased distal commissural liga-
ment, which is the radial extension of
the natatory ligament, whereas the
proximal commissural cord originates
from the proximal commissural liga-
ment, which is the radial extension of
the transverse ligament of the palmar
aponeurosis. Both of these cords cause
contracture of the first web space. The
thumb pretendinous cord originates
from the thumb pretendinous band and
causes flexion deformity of the thumb
metacarpophalangeal joint59, which is
uncommon.
Diagnosis and Classific ation
In its early stages, Dupuytren disease
can be difficult to diagnose60-62. Skin
changes are the earliest manifestation.
Changes on the dorsum of the hand
consist of either Garrod nodes, which
are rare, or knuckle pads, which are
more common. Garrod nodes are firm
nodules at the proximal interpha-
langeal joints63,64. Knuckle pads are fi-
brosing lesions over the proximal
interphalangeal joints. They are preva-
lent in patients with bilateral disease
and in those with ectopic disease, such
as in the feet and genitals63. Knuckle
pads include loss of wrinkles, thicken-
ing, tethering, or hyperkeratosis. They
are found in just fewer than half of pa-
tients with Dupuytren disease, and the
index finger is the most common digit
involved65,66.
The changes in the palm begin
with the formation of microcords from
the Grapow fibers, which connect the
dermis to the palmar fascia. This pro-
duces a pseudocallus or thickening of
the skin and underlying subcutaneous
tissue. These vertical bands are proba-
bly the first anatomic structures to be-
come affected by Dupuytren disease.
The deep subcutaneous fat becomes
fibrotic near the distal palmar crease67.
As a result, the skin becomes tethered
and adherent to the underlying fascial
structures and loses its normal mobility.
Skin-thickening is often associated with
surface rippling and dimpling. A skin
pit is rarely confused or associated with
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other conditions and therefore it is a re-
liable sign of early Dupuytren disease.
Skin pits are caused by deep full-thickness
skin retraction into the subcutaneous
tissue. The diseased superficial fibers of
the split pretendinous band form a der-
mal cord that pulls the dermal side of
the skin inward. The apex of the cone-
shaped skin pit is often buried deep
within the subcutaneous space and
cannot be seen by the examiner.
A Dupuytren nodule is a firm
soft-tissue mass that is fixed to both the
skin and the deep fascia. The nodule
seems to originate in the superficial
components of the palmar or digital
fascia. It is usually well defined, local-
ized, and raised above the surface, but
it can be only a diffuse thickening of
the deeper fascia. Nodules occur in the
palm or digits. Palmar nodules are adja-
cent to the distal palmar crease, often in
line with the ring and small fingers and
sometimes proximal to the base of the
thumb and small finger. Digital nodules
are usually near the proximal interpha-
langeal joint or at the base of the digit.
Nodules are often painless, but they can
enlarge and become troublesome, caus-
ing pain when they are associated with
stenosing tenosynovitis as a result of di-
rect pressure on the flexor tendons and
A1 pulley or from a vertical cord. Nod-
ules have an abundance of myofibro-
blasts and a rich vascular supply.
Nodules tend to regress sponta-
neously and are replaced by a cord, but
a cord can develop and mature without
nodule regression. The normal bands
discussed previously are the precursors
of pathologic cords54. Early cords can
adhere to the skin and blend with the
nodule, making it difficult to ascertain
where a nodule ends and a cord begins.
The cord later becomes prominent and
acquires the appearance and consis-
tency of a tendon. Cords are located in
the palm, the palmodigital area, or the
digits. A mature cord has only sparse
myofibroblasts but abundant collagen.
The disease has early, intermedi-
ate, and late phases. Skin changes with
loss of normal architecture and for-
mation of skin pits is the early phase.
Nodules and cords form during the
intermediate phase, and contractures
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mark the late phase. The late phase
tends to go through four stages of con-
tracture, with contracture of the meta-
carpophalangeal joint of the ring finger
in stage I; contractures of the metacar-
pophalangeal and proximal interpha-
langeal joints of the ring finger and the
metacarpophalangeal joint of the small
finger in stage II; contractures of the
metacarpophalangeal and proximal in-
terphalangeal joints of the ring finger,
the metacarpophalangeal and proximal
interphalangeal joints of the small fin-
ger, and the metacarpophalangeal joint
of the long finger in stage III; and stage-
III contractures as well as distal inter-
phalangeal joint hyperextension of the
ring or small finger in stage IV. This
progression is not immutable. In many
cases, palmar fascial disease or contrac-
ture remains confined to the palm and
does not progress enough to cause digi-
tal flexion deformity. Palmar involve-
ment usually precedes extension of the
disease into the digits; however, the dis-
ease may also begin and remain in the
digits. The ring finger is the most com-
monly involved digit, followed in order
of frequency by the small, long, and in-
dex fingers and lastly by the thumb. The
anatomy of the neurovascular bundle
can be distorted as the spiral cord con-
tracts. A palpable interdigital soft-tissue
mass is an indication that the neurovas-
cular bundle is involved, but it is not a
reliable indicator57,68.
Dupuytren disease may affect
locations other than the hand, and
patients with Dupuytren disease
should be examined for ectopic sites
of involvement. Ectopic disease can be
either regional in the upper extremity
or distant in other parts of the body.
Garrod nodes or knuckle pads occur
on the dorsum of the hand and are al-
most always limited to the fingers.
Three reports have noted disease ex-
tension into the wrist area69-71.
Dupuytren contractures have
been reported in more proximal loca-
tions in the upper extremity72,73. Distant
ectopic disease occurs occasionally, and
patients with knuckle pads are more
likely to have distant involvement66. The
most common distant ectopic disease is
fibromatosis restricted to the plantar
fascia. This is usually asymptomatic and
rarely causes flexion contracture of the
toes74,75. Wheeler and Meals76 reported
on a patient with Dupuytren disease
who had bilateral palmar contracture,
bilateral plantar nodules, and nodular
fasciitis of the popliteal space.
There is a clinical condition that is
similar to Dupuytren disease but should
not be confused with it. It is termed non-
Dupuytren disease1,2. Classic Dupuytren
disease occurs mostly in white people,
whereas non-Dupuytren disease occurs
mostly in a diverse ethnic group. Non-
Dupuytren disease is unilateral, usually
involving a single digit, and it is not in-
frequently associated with trauma, in-
cluding surgery. Patients with this
disease rarely need surgical treatment,
and the condition can spontaneously
improve. Confusing these two condi-
tions can produce contrasting epidemio-
logical data.
In addition to non-Dupuytren dis-
ease, there are other soft-tissue changes
that can mimic early Dupuytren disease,
and certain pathologic processes can be
mistaken for established Dupuytren dis-
ease. Epithelioid sarcoma has masquer-
aded as Dupuytren disease77,78. Also, skin
changes and nodules in Dupuytren dis-
ease should be distinguished from occu-
pational thickening, hyperkeratosis, and
callus formation that are caused by
chronic friction and pressure on a work-
ing person’s hand61. McGrouther de-
scribed changes in the edematous hand
that cause bulging of the subcutaneous
adipose tissue between fibrous bands
with exaggeration of normal anchorage
of the fascia to the skin, giving the ap-
pearance of early Dupuytren disease62.
Large Dupuytren nodules should be
differentiated from palmar soft-tissue
subcutaneous lesions such as localized
pigmented villonodular synovitis (soft-
tissue giant-cell tumor), palmar gangli-
ons, and inclusion cysts. Stenosing
tenosynovitis without triggering can be
associated with thickening and adher-
ence of the skin to the underlying flexor
tendon sheath. Prominence of flexor ten-
dons due to attenuation of anular pul-
leys, as is found in rheumatoid arthritis,
can be confused with pretendinous
cords79. Digital joint flexion deformity
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such as that seen following ulnar nerve
lesions and posttraumatic contracture
also should be differentiated from long-
standing Dupuytren disease. The pres-
ence of other manifestations in the typi-
cal disease can reinforce its diagnosis.
Accurate diagnosis and differentiation
between the types of palmar fascial con-
tracture are necessary to gain insight into
the disease prognosis and to achieve a
satisfactory treatment outcome.
Treatment
Observation is indicated for a patient
who has static Dupuytren disease with
minimal contracture and without com-
promise of function. Recent basic-science
research has shown the potential of cer-
tain local agents in the treatment of
Dupuytren disease. These include the
calcium channel blockers nifedipine
and verapamil45 for early stages of the
disease and collagenase80 for advanced
stages. Enzymatic fasciotomy with trypsin
and hyaluronidase followed by forced
extension of the digit has been reported81.
Steroid injection into nodules has been
used to suppress the disease82. Intrale-
sional injections of gamma-interferon83
decrease the symptoms and the size of
the lesions in both Dupuytren disease
and hypertrophic scars, probably by de-
creasing expression of alpha-smooth
muscle actin and production of col-
lagen. There is no consensus regarding
local injection for the treatment of Du-
puytren disease.
Surgery is the most widely used
treatment for advanced Dupuytren dis-
ease. Flexion contracture of the meta-
carpophalangeal joint of >30° and
flexion contracture of the proximal in-
terphalangeal joint of 15° interfere with
function and, in the presence of a well-
developed cord, are indications for sur-
gical treatment. Treatment of metacar-
pophalangeal joint contractures is more
successful than that of proximal inter-
phalangeal joint contractures.
Percutaneous fasciotomy was
first used by Astley Cooper and has
been advocated for palmar cords in
older patients84,85. In severe cases, this
technique may be useful as a prelimi-
nary procedure86. There is a risk to the
flexor tendons and the nerves, and re-
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flex sympathetic dystrophy has been re-
ported after percutaneous releases87.
The technique of percutaneous release
utilizes a stab wound adjacent to the
cord and a number-11 blade to cut the
cord while the digit is extended.
Fasciectomy is associated with
a lower recurrence rate than is fasciot-
omy (15% compared with 43%). Par-
tial, regional, or limited fasciectomy
remains the most conventional and
widely used technique among hand
surgeons today88,89. Partial fasciectomy
is the excision of the diseased tissue
only and was first described by Goyrand
in 1834. Freehafer and Strong recom-
mended that treatment with use of
multiple small longitudinal incisions88.
In segmental aponeurectomy,
multiple small incisions are created in
the palm and digits, and segments of
diseased tissue are excised without re-
moval of all tissue. Russ first described
this minimally invasive technique, and
the results are comparable with those of
other methods of treatment, with a re-
currence rate of 21%89,90. The procedure
is done through a series of c-shaped in-
cisions, and 1-cm segments of diseased
tissue are excised.
McIndoe and Beare performed a
total fasciectomy through a transverse
palmar incision and digital z-plasties
without excising the skin, which they
reported on in 195891. Zachariae com-
pared this procedure with a limited
fasciectomy and found nearly equal
functional results, but other authors
reported a higher incidence of compli-
cations with total fasciectomy92.
Dermofasciectomy involves si-
multaneous excision of skin and dis-
eased tissue10,93. The recurrence rate
after this procedure is lower than that
after other surgical techniques. When it
was combined with skin-grafting, there
were no recurrences beneath the graft
even when the method was used to treat
recurrent disease93-95. A midterm review
revealed recurrent nodule formation
limited to graft insets in 10% of pa-
tients, without recurrence of cords.
There were few other complications,
but an increase in disease extension was
found between three and thirteen years
after dermofasciectomy94,96. This tech-
nique is best suited for recurrent and
severe primary disease, when the skin is
adherent to the underlying Dupuytren
disease tissue, but it is not indicated for
all recurrent and severe cases. Roush
and Stern reported the total range of
motion after operative treatment of re-
current Dupuytren disease to be better
after fasciectomy and flap coverage than
after skin-grafting or arthrodesis97. An
attempt should always be made to dis-
sect the skin from Dupuytren disease
tissue, but skin that cannot be saved
should be excised and skin graft should
be used if necessary.
Severe flexion deformity of the
proximal interphalangeal joint can re-
sult in a residual contracture after exci-
sion of the offending digital cord. This
contracture may be due to attenuation
of the central slip of the extensor ten-
don, which is placed at risk by a pro-
longed contracture of the proximal
interphalangeal joint, especially when
the deformity exceeds 60°. If the proxi-
mal interphalangeal joint remains con-
tracted after a digital fasciectomy,
extension splinting for several weeks
can help to restore the tone of the cen-
tral slip95,96,98-100. Surgical release of a
proximal interphalangeal joint contrac-
ture after fasciectomy is indicated if the
residual deformity is >40°.
Preoperative and postoperative
skeletal traction with an external fixa-
tion device has been utilized to im-
prove correction of severe contractures
of the proximal interphalangeal joint. In
severe cases, a continuous-elongation
technique prior to fasciectomy has
been shown to decrease the deformity,
facilitate surgery, minimize the need for
amputation, and alter the collagen ori-
entation and even the metabolism of
the fascia101,102. Although this technique
is an additional option for treating diffi-
cult cases, it is associated with a high
rate of complications such as infection,
pin-loosening, recurrence, and even
amputation.
Salvage procedures may be neces-
sary for severe digital deformities (for
example, a flexion contracture of the
proximal interphalangeal joint in ex-
cess of 70°) and especially for recurrent
cases with an exuberant amount of
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scarring. Dorsal wedge osteotomy of
the proximal phalanx is a method to
prevent amputation103. Another option
is arthrodesis of the proximal interpha-
langeal joint combined with resection
of a portion of the proximal phalanx to
shorten the digit, allowing extension
without tension on the neurovascular
structures. Arthroplasty of the proxi-
mal interphalangeal joint with a silicone
implant can correct some of the defor-
mity and retain motion but is associ-
ated with the risk of further flexion
deformity of the joint. Amputation at
the proximal interphalangeal joint or
through the proximal phalanx may be
necessary when nerve and vascular
damage results in loss of sensory func-
tion and cold intolerance.
Primary closure should be used
whenever possible. McGrouther illus-
trated about sixty diagrams in the liter-
ature of surgical incisions used for the
treatment of Dupuytren disease62. How-
ever, the most commonly used are the
Bruner zigzag incision and the midline
longitudinal incision that is closed with
multiple z-plasties.
When primary closure is not
possible, the wounds can be left open.
Dupuytren was the first to leave
wounds open after making a transverse
palmar incision. McCash used the same
method with minor modifications104.
The palmar incision is left open to heal
by secondary intention. Reports of satis-
factory results of this method, with less
pain, better motion, and low compli-
cation rates, continue to appear in the
literature105-108.
A full-thickness skin graft from
the wrist, the ulnar side of the hand, or
the antecubital area is most useful for
recurrent or severe cases when primary
closure is not possible. A distally based
dorsal hand flap, rotation flaps from
the side of the fourth and fifth digits,
and a cross-finger flap from an adja-
cent digit can be used. A butterfly flap
is useful for coverage after excision of a
natatory cord from a digital web space
in order to minimize web-space con-
tracture formation. Simple and four-
flap z-plasties can be used for the first
web space.
Complications of surgery for
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Dupuytren disease are either technique-
related, such as neurovascular injury,
hematoma, and infection, or related to
patient physiology, such as stiffness and
reflex symptomatic dystrophy. Boyer
and Gelberman classified complications
temporally as intraoperative, early post-
operative, and late postoperative109.
The risk of digital nerve injury is asso-
ciated with severe contractures of the
metacarpophalangeal and proximal in-
terphalangeal joints, with altered nerve
anatomy by a spiral cord, and, espe-
cially in recurrent cases, with exuber-
ant amounts of scar tissue. Preventive
measures include isolation of the neu-
rovascular bundle by careful dissection,
with use of loop magnification and
on the basis of knowledge of the patho-
logic anatomy. The dissection is carried
out in a proximal-to-distal direction,
sometimes in combination with a distal-
to-proximal approach, prior to re-
moval of the diseased cord. If the nerve
is transected, a primary repair should
be done.
A vascular injury can be an arte-
rial laceration, arterial spasm, intimal
hemorrhage, or vessel rupture result-
ing from vigorous correction of a se-
vere digital joint contracture. Arterial
laceration that results in vascular com-
promise requires immediate repair
or placement of an interposition vein
graft. Arterial spasm and intimal
hemorrhage are treated first by re-
positioning the digit in flexion, then
irrigating with warm saline solution,
applying topical lidocaine, and even
administering intravenous heparin.
If all else fails, vascular reconstruction
should be done.
Separating diseased tissue from
adherent skin is difficult, especially in
recurrent cases. To reduce the risk of
buttonholing the skin, the use of a
number-15C scalpel and the back of the
knife as a dissector allows separation of
diseased tissue from normal skin. In ad-
dition, using an operating room light to
transilluminate from the epidermal side
of the skin allows visualization of the
thickness of the flap and can alert the
surgeon when the dissection is becom-
ing too superficial.
Hematoma is prevented by tour-
niquet deflation and then achieve-
ment of adequate hemostasis prior to
wound closure. Deflating the tourni-
quet and assessing the skin vascularity
prior to closure to ensure adequate cir-
culation is the best way to prevent skin
necrosis. Closure under tension should
be avoided, and skin-grafting or use
of the open palm method should be
considered if a primary closure is too
tight. If skin necrosis develops, exci-
sion of necrotic tissue and skin-grafting
or flap coverage are performed.
Reflex sympathetic dystrophy,
also referred to as a “flare” reaction
and “complex regional pain syndrome,”
may occur after surgery. The patient has
swelling, hyperemia, dysesthesias, and
pain out of proportion to that expected.
Direct trauma to the nerves and exces-
sive dissection are thought to be pre-
disposing factors. The simultaneous
performance of a carpal tunnel release
with the surgery for Dupuytren disease
is a predisposing factor, especially in
women. An atraumatic surgical tech-
nique and gentle handling of nerves
and other tissues during surgery should
minimize the development of this com-
plication. If a specific cause cannot be
identified, the treatment is therapy for
pain control. In recalcitrant cases, a se-
ries of stellate sympathetic ganglion
blocks can be helpful.
Inclusion cysts can occur near
the scar as a result of entrapment of
dermal tissue in the subcutaneous
space and can be prevented by careful
attention to skin approximation dur-
ing wound closure. Hypertrophic
scar formation is lessened by careful
attention to the placement of the skin
incisions.
The recurrence rate ranges be-
tween 2% and 60%, with an average
of 33%104-108,110. This may represent true
recurrence (disease at the operative
site) or disease extension (disease out-
side of the area of the prior surgery).
Recurrence is more common in pa-
tients with proximal interphalangeal
joint involvement, a diseased small fin-
ger, and more than one digit affected
as well as in those who present a longer
time after surgery or after a secondary
fasciectomy.
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THE JOURNAL OF BONE & JOINT SURGER Y · JBJS.ORG
VO L U M E 89-A · N U M B E R 1 · J A N U A R Y 2007
Ghazi M. Rayan, MD
Upper Extremity, Hand and Microsurgery
Center, Baptist Physicians Building D, 3366
N.W. Expressway, Suite 700, Oklahoma City,
OK 73112
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P R E S E N T A T I O N , A N D TR E A T M E N T
Printed with permission of the American
Academy of Orthopaedic Surgeons. This arti-
cle, as well as other lectures presented at the
Academy’s Annual Meeting, will be available
in February 2007 in Instructional Course Lec-
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