The Journal of Bone & Joint Surgery

The Journal of Bone & Joint Surgery, Volume 89, Issue 1

Selected Instructional Course Lecture | January 01, 2007

Dupuytren Disease: Anatomy, Pathology, Presentation, and Treatment

Ghazi M. Rayan, MD¹

¹ Upper Extremity, Hand and Microsurgery Center, Baptist Physicians Building D, 3366 N.W. Expressway, Suite 700, Oklahoma City, OK 73112

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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, or 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.

Printed with permission of the American Academy of Orthopaedic Surgeons. This article, as well as other lectures presented at the Academy's Annual Meeting, will be available in February 2007 in Instructional Course Lectures, Volume 56. The complete volume can be ordered online at , or by calling 800-626-6726 (8 a.m.-5 p.m., Central time).

An Instructional Course Lecture, American Academy of Orthopaedic Surgeons

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J Bone Joint Surg Am, 2007 Jan 01;89(1):189-198

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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 Dupuytren disease. There have been recent 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 fascial 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. Surgical treatment is the conventional and most widely used method of managing Dupuytren disease.

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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 Dupuytren disease. There have been recent 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 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. Surgical 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 involved the palmar fascia, in 1822 Sir Astley Cooper advocated closed fasciotomy as a treatment for the condition, and in 1831 Guillaume Dupuytren gave a detailed anatomic and pathologic description of the disease and demonstrated a surgical case in Paris that earned him the disease eponym⁴. By 1900 there were at least 256 publications related to Dupuytren disease and at least eight books on the subject^2,5-11.

Age, gender, geography, and ethnicity influence the disease prevalence, 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 Britain, Ireland, Australia, and North America. It is uncommon in southern Europe and South America and rare in Africa and China^16,17.

Dupuytren disease is associated with diabetes^18-20. Burge et al. reported a higher risk of Dupuytren disease in alcoholics, smokers, people with hypercholesterol, and patients infected with human immunodeficiency virus^21-23. There is controversy regarding a relationship between Dupuytren disease and seizure disorders^24,25. The etiology of Dupuytren disease remains controversial as well, but inflammation, trauma, neoplasia, and genetics have been implicated as factors^26-31. The evidence is strongest for at least a genetic predisposition. There is a clearly increased incidence in relatives of patients with Dupuytren disease, and there has been at least one report of identical twins with the disease^13,32. There seems to be an autosomal dominant transmission with variable penetrance.

Anatomy

Anatomy | Pathophysiology | Diagnosis and Classification | Treatment | References

The radial, ulnar, and central apo-neuroses, palmodigital fascia, and digital fascia are all part of the palmar fascial complex (Fig. 1)³³. These structures 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 apo-neurosis), the thumb pretendinous band (small or absent), the distal commissural ligament, and the proximal commissural ligament³⁴. The ulnar apo-neurosis consists of the hypothenar 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 longitudinally, transversely, and vertically. The longitudinal fibers fan out as pretendinous 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 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 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 vertical bands of Grapow and the septa of Legueu and Juvara. The vertical bands are numerous, small, strong, and scattered along the palmar fascial complex and are most abundant in the central aponeurosis³⁸. 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 compartments 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 capsule⁴⁰. 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 contributions 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 dorsally⁴².

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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.)

Pathophysiology

Anatomy | Pathophysiology | Diagnosis and Classification | Treatment | References

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 characteristics of both a fibroblast and a smooth muscle cell, and it can actively contract⁴⁵. The myofibroblast of Dupuytren disease expresses alpha-smooth muscle actin that plays a role in contraction⁴⁶. The Dupuytren myofibroblast synthesizes fibronectin, an extracellular glycoprotein, which connects myofibroblastic cells together and connects myofibroblastic cells to the extracellular stromal matrix with an integrin^47,48. Myofibroblast contractility can be influenced by prostaglandins, which are found in nodules and active stages of the disease^49-51. Fibroblast growth factor (FGF), transforming growth factor-alpha (TGF-a), epidermal growth factor, interleukin-1 (IL-1), and platelet-derived growth factor (PDGF) have been found to be expressed more in Dupuytren disease⁵².

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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.)

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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.)

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 progressively shorten, leading to joint and soft-tissue contracture. The cords involve the palmar, palmodigital, or digital regions. Shortened cords cause joint deformity, 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 manifestations 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 Dupuytren disease. It is responsible for flexion deformity of the metacarpophalangeal joint and often extends distally to continue with digital cords. Occasionally, 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 connected to the pretendinous cord⁵⁵. 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 affects a large area of the palm, leading to diffuse thickening of many components of the palmar fascial complex including 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 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 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 phalanx on one side of the digit. The central 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 ligament. The lateral cord leads to contracture of the proximal interphalangeal joint but can cause a flexion contracture of 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 insertion 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 retrovascular 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 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 joint⁵⁹, which is uncommon.

Diagnosis and Classification

Anatomy | Pathophysiology | Diagnosis and Classification | Treatment | References

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 fibrosing lesions over the proximal interphalangeal joints. They are prevalent in patients with bilateral disease and in those with ectopic disease, such as in the feet and genitals⁶³. 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 produces a pseudocallus or thickening of the skin and underlying subcutaneous tissue. These vertical bands are probably the first anatomic structures to become 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 other conditions and therefore it is a reliable 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, localized, 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. Nodules have an abundance of myofibro-blasts 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 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 consistency 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 meta-carpophalangeal 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 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 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 commonly involved digit, followed in order of frequency by the small, long, and index fingers and lastly by the thumb. The anatomy of the neurovascular bundle can be distorted as the spiral cord contracts. 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 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 almost 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 extremity^72,73. 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 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 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, including surgery. Patients with this disease rarely need surgical treatment, and the condition can spontaneously improve. Confusing these two conditions can produce contrasting epidemio-logical 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 disease. Epithelioid sarcoma has masqueraded as Dupuytren disease^77,78. Also, skin changes and nodules in Dupuytren disease should be distinguished from occupational thickening, hyperkeratosis, and callus formation that are caused by chronic friction and pressure on a working person's hand⁶¹. McGrouther described 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 appearance 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 ganglions, and inclusion cysts. Stenosing tenosynovitis without triggering can be associated with thickening and adherence of the skin to the underlying flexor tendon sheath. Prominence of flexor ten-dons due to attenuation of anular pulleys, as is found in rheumatoid arthritis, can be confused with pretendinous cords⁷⁹. Digital joint flexion deformity such as that seen following ulnar nerve lesions and posttraumatic contracture also should be differentiated from longstanding Dupuytren disease. The presence of other manifestations in the typical 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

Anatomy | Pathophysiology | Diagnosis and Classification | Treatment | References

Observation is indicated for a patient who has static Dupuytren disease with minimal contracture and without compromise 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 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. Intralesional injections of gamma-interferon⁸³ decrease the symptoms and the size of the lesions in both Dupuytren disease and hypertrophic scars, probably by decreasing expression of alpha-smooth muscle actin and production of collagen. There is no consensus regarding local injection for the treatment of Dupuytren disease.

Surgery is the most widely used treatment for advanced Dupuytren disease. 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 inter-phalangeal joint contractures.

Percutaneous fasciotomy was first used by Astley Cooper and has been advocated for palmar cords in older patients^84,85. In severe cases, this technique may be useful as a preliminary procedure⁸⁶. 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 fasciotomy (15% compared with 43%). Partial, 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 only and was first described by Goyrand in 1834. Freehafer and Strong recommended 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 removal of all tissue. Russ first described this minimally invasive technique, and the results are comparable with those of other methods of treatment, with a recurrence 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 1958⁹¹. Zachariae compared this procedure with a limited fasciectomy and found nearly equal functional results, but other authors reported a higher incidence of complications with total fasciectomy⁹².

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 technique 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 arthrodesis⁹⁷. An attempt should always be made to dissect 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 of the central slip of the extensor tendon, 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 contracted 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 fixation device has been utilized to improve 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 orientation 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 excess of 70°) and especially for recurrent cases with an exuberant amount of scarring. Dorsal wedge osteotomy of the proximal phalanx is a method to prevent amputation¹⁰³. Another option is arthrodesis of the proximal interphalangeal 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 proximal 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 illustrated about sixty diagrams in the literature of surgical incisions used for the treatment of Dupuytren disease⁶². However, 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 satisfactory results of this method, with less pain, better motion, and low complication 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 postoperative, and late postoperative¹⁰⁹. 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 on the basis of knowledge of the pathologic anatomy. The dissection is carried out in a proximal-to-distal direction, sometimes in combination with a distal-to-proximal approach, prior to removal 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 resulting from vigorous correction of a severe digital joint contracture. Arterial laceration that results in vascular compromise requires immediate repair or placement of an interposition vein graft. Arterial spasm and intimal hemorrhage are treated first by repositioning 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 of the skin allows visualization of the thickness of the flap and can alert the surgeon when the dissection is becoming too superficial.

Hematoma is prevented by tourniquet deflation and then achievement of adequate hemostasis prior to wound closure. Deflating the tourniquet and assessing the skin vascularity prior to closure to ensure adequate circulation 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, excision 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 excessive 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 technique and gentle handling of nerves and other tissues during surgery should minimize the development of this complication. 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 of 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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Topics

dupuytren's contracture ; contracture ; fascia

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Ghazi M. Rayan; Dupuytren Disease: Anatomy, Pathology, Presentation, and Treatment. The Journal of Bone & Joint Surgery. 2007 Jan;89(1):189-198.

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