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T HE J OURNAL OF B ONE & J OINT S URGER Y JBJS . ORG D UPUYTREN D ISEASE : A NATOMY , P ATHOLOGY , V OLUME 89-A N UMBER 1 J ANUAR Y 2007 P RESENTATION , AND T REATMENT Dupuytren Disease: Anatomy, Pathology, Presentation, and

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THE JOURNAL OF BONE & JOINT SURGER Y · JBJS.ORG VOLUME 89-A · NUMBER 1 · JANUAR Y 2007 DUPUYTREN DISEASE: ANATOMY, PATHOLOGY, PRESENTATION, AND TREATMENT

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 recent advances in the pathophysiology

f 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 fascial disease

1,2. 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 contracture

3. In 1777 Henry

Cline recognized that the disorder involved the palmar fascia, in 1822 Sir Astley Cooper advocated closed fasciot-

my 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 eponym

4. By

1900 there were at least 256 publica- tions related to Dupuytren disease and at least eight books on the subject

2,5-11.

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 life

15. 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 diabetes

18-20. Burge et al. reported a

higher risk of Dupuytren disease in al- coholics, smokers, people with hyperc- holesterol, and patients infected with human immunodeficiency virus

21-23.

There is controversy regarding a rela- tionship between Dupuytren disease and seizure disorders

24,25. 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 aponeurosis has four components: the thenar fascia (an extension of the central aponeurosis), the thumb pretendinous band (small or absent), the distal commissural ligament, and the proximal commissural ligament

34. The ulnar apo-

neurosis consists of the hypothenar

Disclosure: The author did not receive grants or outside funding in support of his research for or preparation of this manuscript. He did not receive payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed,

r agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with

which the author is affiliated or associated.

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THE JOURNAL OF BONE & JOINT SURGER Y · JBJS.ORG VOLUME 89-A · NUMBER 1 · JANUAR Y 2007 DUPUYTREN DISEASE: ANATOMY, PATHOLOGY, PRESENTATION, AND TREATMENT

muscle fascia (an extension of the central 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 band

35,36. 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 pretendinous bands in the three central digits, and each bifurcates distally. Each bifurcation has three layers

37. 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 ligament 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 aponeurosis 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 vertical 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 aponeurosis

38. The vertical septa of

Legueu and Juvara are deep to the palmar fascia and form fibro-osseous compartments

33,39,40. 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 structures: 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 pretendinous band spirals on its axis nearly 90°, and the peripheral fibers run vertically adjacent to the metacarpophalangeal joint capsule

40. They continue

distally deep to the neurovascular bundle and natatory ligaments and emerge distal to the natatory ligaments to continue 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 ligament (palmar), the Cleland ligament (dorsal), the Gosset lateral digital sheet laterally, and the Thomine retrovascular fascia medially and dorsally

42.

Pathophysiology The myofibroblast is the offending cell in Dupuytren disease. It was described

riginally by Gabbiani and Majno

43 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-

tion46. The Dupuytren myofibroblast

synthesizes fibronectin, an extracellular glycoprotein, which connects myofibro- blastic cells together and connects myo- fibroblastic cells to the extracellular stromal matrix with an integrin

47,48.

Fig. 1

Palmar fascial complex with its five components: the radial aponeurosis (RA), ulnar aponeurosis (UA), central aponeurosis, palmodigital fascia, and digital fascia. NL = natatory ligament, PA = palmar aponeurosis, and TLPA = transverse ligament of the palmar aponeurosis. (Reprinted, with permission, from: Rayan GM. Palmar fascial complex anatomy and pathology in Dupuytren’s

disease. Hand Clin. 1999;15:75.)

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THE JOURNAL OF BONE & JOINT SURGER Y · JBJS.ORG VOLUME 89-A · NUMBER 1 · JANUAR Y 2007 DUPUYTREN DISEASE: ANATOMY, PATHOLOGY, PRESENTATION, AND TREATMENT

Myofibroblast contractility can be influenced by prostaglandins, which are found in nodules and active stages

f the disease

49-51. 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 disease

52.

In Dupuytren disease, normal fascial bands become diseased cords

53.

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 capsuloligamentous tissue and flexion contractures of the metacarpophalangeal and proximal interphalangeal joints. Grapow vertical bands become microcords leading to skin-thickening, which is one of the earliest manifesta-

Fig. 2

Interpalmar plate ligament (IPPL) and septa of Legueu and Juvara. PA = palmar

aponeurosis. (Reprinted, with permission, from: Rayan GM. Palmar fascial complex

anatomy and pathology in Dupuytren’s disease. Hand Clin. 1999;15:79.)

Fig. 3

Soft-tissue confluence and septa of Legueu and Juvara. IPPL = interpalmar plate ligament and PA = palmar

aponeurosis. (Reprinted, with permission, from: Rayan GM. Palmar fascial complex anatomy and pathology in

Dupuytren’s disease. Hand Clin. 1999;15:80.)

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THE JOURNAL OF BONE & JOINT SURGER Y · JBJS.ORG VOLUME 89-A · NUMBER 1 · JANUAR Y 2007 DUPUYTREN DISEASE: ANATOMY, PATHOLOGY, PRESENTATION, AND TREATMENT

tions of Dupuytren disease. Skin pits develop from the first layer of the split pretendinous band and are usually distal 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 metacarpophalangeal joint and often extends distally to continue with digital cords. Occa- sionally, the pretendinous cord bifurcates 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 cord

55. The

vertical cord is short thick diseased tissue 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 encountered in severe conditions and af- fects a large area of the palm, leading to diffuse thickening of many components 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 ligament

56. 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 neurovascular bundle, just distal to the metacarpophalangeal 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 involves the Grayson ligament. Initially, the cord spirals around the neurovascular bundle, but as it contracts the cord straightens and the neurovascular bundle spirals around the cord. The distorted anatomy of the neurovascular bundle, which displaces medially and centrally, renders it at risk of injury during surgery

57,58. The natatory cord

develops from the natatory ligament, converting the u-shaped web-space fibers into a v shape and producing a 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 metacarpophalangeal joints. This maneuver allows 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 interphalangeal 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

r the periosteum of the middle pha-

lanx on one side of the digit. The central cord usually does not displace the neurovascular bundle. The lateral cord

riginates 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

f the distal interphalangeal joint. This

cord can displace the digital neurovascular 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 inserts 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 interphalangeal joint. The retrovascular cord is a poorly defined structure but is thought to develop from the retrovascular band of Thomine and is located deep to the neurovascular bundle

58. 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 interphalangeal joint contracture may not be completely corrected. The distal commissural cord is the diseased distal commissural ligament, which is the radial extension of the natatory ligament, whereas the proximal commissural cord originates from the proximal commissural ligament, 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 joint

59, which is

uncommon. Diagnosis and Classification In its early stages, Dupuytren disease can be difficult to diagnose

60-62. 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 interphalangeal joints

63,64. 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 genitals

63. Knuckle

pads include loss of wrinkles, thickening, tethering, or hyperkeratosis. They are found in just fewer than half of patients with Dupuytren disease, and the index finger is the most common digit involved

65,66.

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 become affected by Dupuytren disease. The deep subcutaneous fat becomes fibrotic near the distal palmar crease

67.

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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THE JOURNAL OF BONE & JOINT SURGER Y · JBJS.ORG VOLUME 89-A · NUMBER 1 · JANUAR Y 2007 DUPUYTREN DISEASE: ANATOMY, PATHOLOGY, PRESENTATION, AND TREATMENT

ther 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 dermal 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 adjacent 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 interphalangeal joint or at the base of the digit. Nodules are often painless, but they can enlarge and become troublesome, causing pain when they are associated with stenosing tenosynovitis as a result of direct pressure on the flexor tendons and A1 pulley or from a vertical cord. Nod- ules have an abundance of myofibroblasts and a rich vascular supply. Nodules tend to regress spontaneously and are replaced by a cord, but a cord can develop and mature without nodule regression. The normal bands discussed previously are the precursors

f pathologic cords
54. 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, intermediate, and late phases. Skin changes with loss of normal architecture and formation of skin pits is the early phase. Nodules and cords form during the intermediate phase, and contractures mark the late phase. The late phase tends to go through four stages of contracture, with contracture of the metacarpophalangeal joint of the ring finger in stage I; contractures of the metacarpophalangeal and proximal interphalangeal joints of the ring finger and the metacarpophalangeal joint of the small finger in stage II; contractures of the metacarpophalangeal and proximal interphalangeal joints of the ring finger, the metacarpophalangeal and proximal interphalangeal joints of the small finger, and the metacarpophalangeal joint

f the long finger in stage III; and stage-

III contractures as well as distal interphalangeal joint hyperextension of the ring or small finger in stage IV. This progression is not immutable. In many cases, palmar fascial disease or contracture remains confined to the palm and does not progress enough to cause digital flexion deformity. Palmar involvement usually precedes extension of the disease into the digits; however, the disease may also begin and remain in the

digits. The ring finger is the most com-

monly involved digit, followed in order

f 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 neurovascular bundle is involved, but it is not a reliable indicator

57,68.

Dupuytren disease may affect locations other than the hand, and patients with Dupuytren disease should be examined for ectopic sites

f involvement. Ectopic disease can be

either regional in the upper extremity

r distant in other parts of the body.

Garrod nodes or knuckle pads occur

n the dorsum of the hand and are al-

most always limited to the fingers. Three reports have noted disease extension into the wrist area

69-71.

Dupuytren contractures have been reported in more proximal locations 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 toes

74,75. Wheeler and Meals 76 reported

n 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 disease

1,2. 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 infrequently 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 epidemiological data. In addition to non-Dupuytren disease, 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 disease

77,78. Also, skin

changes and nodules in Dupuytren disease 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 hand

61. McGrouther de-

scribed changes in the edematous hand that cause bulging of the subcutaneous adipose tissue between fibrous bands with exaggeration of normal anchorage

f the fascia to the skin, giving the ap-

pearance of early Dupuytren disease

62.

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-

ns, 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 tendons due to attenuation of anular pul- leys, as is found in rheumatoid arthritis, can be confused with pretendinous cords

79. 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 presence of other manifestations in the typi- cal disease can reinforce its diagnosis. Accurate diagnosis and differentiation between the types of palmar fascial contracture 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 certain local agents in the treatment of Dupuytren disease. These include the calcium channel blockers nifedipine and verapamil

45 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 disease

82. 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 interphalangeal joint of 15° interfere with function and, in the presence of a well- developed cord, are indications for surgical treatment. Treatment of metacarpophalangeal joint contractures is more successful than that of proximal interphalangeal joint contractures. Percutaneous fasciotomy was first used by Astley Cooper and has been advocated for palmar cords in

lder patients

84,85. In severe cases, this

technique may be useful as a prelimi- nary procedure

86. There is a risk to the

flexor tendons and the nerves, and reflex sympathetic dystrophy has been reported 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-

my (15% compared with 43%). Par-

tial, regional, or limited fasciectomy remains the most conventional and widely used technique among hand surgeons today

88,89. Partial fasciectomy

is the excision of the diseased tissue

nly and was first described by Goyrand

in 1834. Freehafer and Strong recom- mended that treatment with use of multiple small longitudinal incisions

88.

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

ther methods of treatment, with a re-

currence rate of 21%

89,90. The procedure

is done through a series of c-shaped incisions, 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 1958

91. Zachariae com-

pared this procedure with a limited fasciectomy and found nearly equal functional results, but other authors reported a higher incidence of complications with total fasciectomy

92.

Dermofasciectomy involves simultaneous excision of skin and diseased tissue

10,93. 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 disease

93-95. A midterm review

revealed recurrent nodule formation limited to graft insets in 10% of patients, without recurrence of cords. There were few other complications, but an increase in disease extension was found between three and thirteen years after dermofasciectomy

94,96. 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 recurrent Dupuytren disease to be better after fasciectomy and flap coverage than after skin-grafting or arthrodesis

97. 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 result in a residual contracture after excision of the offending digital cord. This contracture may be due to attenuation

f the central slip of the extensor ten-

don, which is placed at risk by a prolonged contracture of the proximal interphalangeal joint, especially when the deformity exceeds 60°. If the proximal interphalangeal joint remains con- tracted after a digital fasciectomy, extension splinting for several weeks can help to restore the tone of the central slip

95,96,98-100. Surgical release of a

proximal interphalangeal joint contracture 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

f 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 fascia

101,102. Although this technique

is an additional option for treating difficult cases, it is associated with a high rate of complications such as infection, pin-loosening, recurrence, and even amputation. Salvage procedures may be necessary 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 amputation

103. Another option

is arthrodesis of the proximal interphalangeal joint combined with resection

f 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 deformity and retain motion but is associated 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 function and cold intolerance. Primary closure should be used whenever possible. McGrouther illus- trated about sixty diagrams in the literature of surgical incisions used for the treatment of Dupuytren disease

62. 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 modifications

104.

The palmar incision is left open to heal by secondary intention. Reports of satisfactory results of this method, with less pain, better motion, and low compli- cation rates, continue to appear in the literature

105-108.

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 adjacent 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 contracture formation. Simple and four- flap z-plasties can be used for the first web space. Complications of surgery for 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-

perative, and late postoperative

109.

The risk of digital nerve injury is associated with severe contractures of the metacarpophalangeal and proximal interphalangeal joints, with altered nerve anatomy by a spiral cord, and, especially in recurrent cases, with exuberant amounts of scar tissue. Preventive measures include isolation of the neurovascular bundle by careful dissection, with use of loop magnification and

n the basis of knowledge of the patho-

logic anatomy. The dissection is carried

ut 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 arterial laceration, arterial spasm, intimal hemorrhage, or vessel rupture result- ing from vigorous correction of a severe digital joint contracture. Arterial laceration that results in vascular com- promise requires immediate repair

r 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 addition, using an operating room light to transilluminate from the epidermal side

f 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

f 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

r 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 predisposing 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 series 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 during wound closure. Hypertrophic scar formation is lessened by careful attention to the placement of the skin incisions. The recurrence rate ranges between 2% and 60%, with an average

f 33%

104-108,110. This may represent true

recurrence (disease at the operative site) or disease extension (disease outside of the area of the prior surgery). Recurrence is more common in patients with proximal interphalangeal joint involvement, a diseased small finger, 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 VOLUME 89-A · NUMBER 1 · JANUAR Y 2007 DUPUYTREN DISEASE: ANATOMY, PATHOLOGY, PRESENTATION, AND TREATMENT Ghazi M. Rayan, MD Upper Extremity, Hand and Microsurgery Center, Baptist Physicians Building D, 3366 N.W. Expressway, Suite 700, Oklahoma City, OK 73112 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- tures, Volume 56. The complete volume can be ordered online at www.aaos.org, or by calling 800-626-6726 (8 A.M.-5 P.M., Central time).

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