Epidemiology
Dupuytren disease is a benign fibroproliferative disorder of unclear etiology and pathogenesis. It occurs primarily in people of Northern European descent, specifically, from the Scandinavian countries and the United Kingdom.1,2 This condition is rare in Asian and American Indian individuals and very rare in Africans.3 A US study attempted to determine the racial distribution of Dupuytren disease; of the 9938 Veterans Affairs patients with Dupuytren disease, 9071 were white, 412 were black, 234 were Hispanic, 11 were Native American, 8 were Asian, and the remaining 202 had unknown ethnicities.4 Manifestations of the disease were similar in each group except in black patients, in whom bilateral disease rarely occurred.
Men are more commonly affected than women; the male-to-female ratio ranges from 3:1 to 9.5:1 in Europe and Australia, respectively.5,6,7,8 A study conducted in Boston, Massachusetts, reported a ratio of 4:1 for patients younger than 54 years; this ratio approached 1:1 with advancing patient age.8 In Australia, as many as 20% of men older than 60 years are affected. Dupuytren disease is very rare in childhood, but cases of patients younger than 16 years have been reported. Usually, both hands are involved to a variable degree; strictly unilateral disease is uncommon.
Plantar fibromatosis (Lederhose disease) and Peyronie disease are often associated with Dupuytren disease; 10% of patients with Dupuytren disease also have Peyronie disease.9 Fibromatosis of the dorsum of the proximal interphalangeal (PIP) joints (known as Garrod nodes or knuckle pads) are also frequently observed in this condition.
Evidence for heritability of a disease can be found in study of populations, ie, prevalence and geographic variation and studies of families(eg, concordance in twins, family clustering).10 In addition to the well-known racial predilection for fair-skinned persons of Northern European descent, one third of patients with Dupuytren disease have a positive family history.
Autosomal dominant inheritance with incomplete penetrance is favored by several authors.11 Six pairs of identical twins appear in reports dating from 1937, with similar Dupuytren disease observed in 4. However, Lyall reported only 1 twin affected in each of 2 pairs.12 In 2006, Hindocha et al found that a greater severity and lower age of onset of Dupuytren disease had a significant association with positive family history of this condition.13 They found a significantly increased risk for recurrent Dupuytren disease in siblings. Burge suggests that data regarding Dupuytren disease could be explained by autosomal dominant or autosomal recessive inheritance, or Dupuytren disease could be a complex trait.10 A study using DNA analysis found a positive association between human leukocyte antigen-DRB1*15 in white persons with advanced stages of this condition compared to disease-free control subjects.14
The term Dupuytren diathesis was first used by Hueston to describe a group of patients with aggressive disease, young age of onset, and high incidence of early recurrence.15 The presence of bilateral disease, positive family history, and ectopic lesions (eg, knuckle pads, penile or plantar fibrosis) completed his criteria for the diathesis. Hindocha et al studied 322 patients with Dupuytren disease for diathesis and added male gender and age (onset <50 y) to Hueston’s original factors.16 They also defined family history as one or more affected siblings or parents and limited ectopic lesions to knuckle pads alone. They concluded that the familial clustering they observed strongly suggests genetic influence in the development of Dupuytren disease.
Historically, a number of retrospective studies have consistently associated various environmental factors with Dupuytren disease. Dupuytren disease is statistically associated with diabetes.17,18 The incidence rises with the duration of diabetes; up to 80% of patients who have had diabetes for more than 20 years also have Dupuytren disease.19,20 These authors believe that microangiopathy in diabetes could induce ischemia, resulting in palmar fascial thickening.19,20
Heavy smoking21,22 and epilepsy23 have been linked to Dupuytren disease. Alcoholism (but not liver disease) has also been associated with Dupuytren disease.22 The studies of Hindocha confirmed association with heavy alcohol intake but could not confirm association with any other of these environmental factors.16
Dupuytren postulated in his original presentation that trauma to the hands, possibly related to occupation, was a cause for the disease.24 Numerous population-based studies have failed to conclusively link Dupuytren disease to trauma. In reviewing available studies on the question of the work-relatedness of Dupuytren disease, Liss stated "No controlled studies of acute trauma and Dupuytren’s contracture were identified."25 Liss did find acceptable studies linking occupational exposure to vibration with a higher incidence of Dupuytren disease.26,27,28,29,30 Notably, the exposure in one study was severe enough to cause persistent symptomatic circulatory disturbance ("vibration white finger"); in another, the exposure was associated with other soft tissue "wasting" and peripheral nerve damage.
In their discussion of Dupuytren disease and occupational exposure, Melhorn and Ackerman reviewed 46 available studies, including those cited by Liss.31 They concluded that evidence associated Dupuytren disease with vibration but not with highly repetitive or forceful work generally. The debate continues, with recent reports of Lucas finding increased Dupuytren disease in a group of French male civil servants with greater occupational exposure to vibration and manual work.32 Case reports of Dupuytren disease occurring after surgical injury to the hand also appear, with the authors suggesting that injury can trigger the onset of Dupuytren disease.33,34
History
Descriptions of Dupuytren disease first appeared in the 16th century. It was described by Henry Cline in 1808, and more completely characterized by French surgeon Guillaume Dupuytren (1777-1835) in 1834.24
Pathology
The fibromatoses are classified as an intermediate group between benign fibrous lesions and fibrosarcoma;35 examples include Dupuytren disease (palmar fibromatosis), Peyronie disease (penile fibromatosis), and plantar fibromatosis (Lederhose disease). On histopathologic evaluation, Dupuytren disease is characterized by poorly defined broad fascicles or nodules of abundant dense collagen surrounding fibroblasts.35
A 1962 discussion of the pathology of Dupuytren disease by MacCallum and Hueston states that "the palmar nodule formed by progressive perivascular spindle cell proliferation becomes the center of a centripetally contracting field of newly formed collagen."36 They referred to the process of contracture as "collagen shrinkage." Almost immediately after their description of the myofibroblast in 1971, Gabbiani and Majno determined the presence of these cells in active palmar nodules of Dupuytren disease (and in plantar fibrosis) and suggested their probable role in contracture.37
The myofibroblast is a metabolically active cell that not only synthesizes collagen but also contains various isoforms of actin and myosin similar to those in smooth muscle. Myofibroblasts can generate contractile force38 and possess specialized cytoskeletal structures, including microfilaments, which allow strong attachment of the myofibroblast to the extracellular matrix (fibronexus) and to other cells. Transmembrane proteins (integrins) and fibronectin are also critical to this linkage.39,40
The origin of the myofibroblast in Dupuytren disease is debated. As in other granulating wounds that contract, myofibroblasts may differentiate from pluripotential cells in the perivascular zone. Myofibroblasts do share some specialized protein expression in common with vascular smooth muscle.39 However, cytokine growth factors can also induce mature fibroblasts to develop characteristics of the myofibroblast cell, including production of contractile proteins.40,41 Hypoxic stimuli also appear to stimulate the formation of myofibroblasts. Other immunohistochemical studies and studies of protein expression suggest the existence of different fibroblast cell populations in different stages of Dupuytren disease.42,43
A host of different tissue factors have been shown to modify myofibroblast activity. These include several prostaglandins, fibronectin, plasminogen-activating enzymes and thrombin, angiotensin-II, serotonin, interleukin-1alpha, interleukin-1beta, and several cytokine growth factors including platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF).44,23,45,46,40 However, transformation growth factor beta 1 (TGF-b1 has emerged as a prime stimulator of myofibroblast production and activity.47 TGF-beta is upregulated in Dupuytren disease.48 Other recent studies have shown type 1 collagen to be a regulator of TGF-b1 signaling in Dupuytren disease.49
In a small pilot study, Pettet demonstrated inhibition of myofibroblast activity in vivo by gamma interferon that acts to block TGF-beta.50 This was an initial attempt at pharmacologic manipulation of myofibroblast activity in vivo. Although direct delivery of this agent into tissue affected by Dupuytren disease showed some local effect, systemic adverse effects were also noted.50
Pilcher et al described unique in vitro models that allow quantitative measurement of myofibroblast contractility in tissue culture.51 These models have been used to test the effect of various pharmacologic agents on myofibroblast activity.51 Changes in myofibroblast morphology and physical orientation in response to mechanical stress have also been demonstrated.52
Rayan et al demonstrated that a phospholipid, lysophosphatidic acid (LPA), was a potent stimulator of myofibroblast contraction.45 Upon binding with a cell surface receptor, LPA appears to exert its effects, in part, by modulation of cyclic adenosine monophosphate (AMP) levels and by increasing intracellular calcium. These, in turn, increase the activity of enzymes producing phosphorylated myosin, a prerequisite for actin-myosin interaction. The authors were able to reduce LPA-promoted myofibroblast contraction using available calcium channel blockers nifedipine and verapamil. This observation provided a rationale for off-label use of these agents to treat hypertrophic scars. More recent work has focused on the intracellular signaling pathways for production of contractile elements in fibroblast variant cells.43 Hopefully, improved understanding will lead to additional molecular targets for therapy.
Investigations of the biochemistry of the extracellular matrix in tissue from patients with Dupuytren disease have confirmed the presence of multiple "immature" collagen subtypes (predominantly type III collagen), a 4-fold increase in hexosamine, and that presence of galactosamine, suggesting the presence of chondroitin sulfate (glycosaminoglycan).40,53 Some have suggested this synthetic activity parallels that in early wound healing or tissue repair.
Townley has demonstrated increased metalloproteinase activity in Dupuytren disease; this is a characteristic shared with chronic wounds.54 Bickley-Parsons et al described biochemical changes in extracellular collagen in Dupuytren disease.53 They found extracellular collagen cross-linking and other organization typical for rapidly synthesized new collagen in normal connective tissue repair. They found no evidence that "… contracture of the palmar fascia in Dupuytren’s disease is due to shortening, plication, or contraction of the collagen fibrils or fibers…."53
Similarities exist between biochemical activity in the extracellular matrix in Dupuytren disease and early wound repair. Myofibroblasts exhibit response to stress or tension in tissue culture, and both cellular elements and extracellular collagen tend to reorient longitudinally along lines of stress in the forming cords of Dupuytren disease. Taken together, these observations have suggested to some that mechanical loading may contribute to the progress of contracture in Dupuytren disease.
Pathogenesis
The pathognomonic lesion in Dupuytren disease is the fibrous nodule, which is usually adjacent to the distal palmar crease and may be multiple. It is the initial site of the contractile process. Nodules may also form near the metacarpophalangeal (MP) and PIP joints of the thumb and digits. Four clinical stages in Dupuytren disease were described by McIndoe and Beare;3 however, Luck's55 description of 3 clinical stages of Dupuytren disease has gained popularity.
Three clinical stages of Dupuytren disease.
Proliferative (early) stage
This stage involves thickening and local nodularity of the fascia with blanching of palmar skin on finger extension. In early disease, some patients may report tenderness and discomfort associated with the nodules. Proliferating myofibroblasts and type III collagen are noted in the involved tissue.
Involutional (active) stage
This stage is marked by the appearance of contracture. The first clinical sign is a palpable cord proximal to a nodule with limited extension of the adjacent affected digit. Cords are relatively acellular and collagenous and are responsible for joint flexion contractures.56 The observed number of myofibroblasts is greatly diminished. Grooves and pits demonstrate attachment of palmar dermis to fascia. Joint involvement and secondary changes in periarticular structures follow. Functional limitation results from decreased range of motion in the hand.
Residual (advanced) stage
In this stage, nodules have disappeared, leaving joint flexion contracture and firm, thickened, fibrous (pretendinous) cords. In the digits, nerve compression can cause distal sensory disturbance. Ultimately, type I collagen is dominant in the fibrous cords and only occasional mature fibrocytes are observed.
Hueston advanced the extrinsic theory, suggesting that Dupuytren’s nodules arise de novo and progress to cords.36 Vasomotor disturbance and neurovascular mediation by the skin were suggested by Hueston as possible contributors to the development of Dupuytren disease. In contrast, McFarlane postulated the intrinsic theory, that the cords of more advanced Dupuytren disease are derived from normal fascia.57 A combination of these ideas forms the synthesis theory, which states that the nodules and pretendinous cords represent different forms of the disease.56
Etiology
Although the understanding of this condition has advanced, no hypothesis or model of Dupuytren disease has provided a complete explanation of the process at the molecular level.
Flint focused on the fibrous replacement of subdermal fat in Dupuytren disease as the primary abnormality.58 He believed that loss of the cushioning fatty tissue resulted in damage to the longitudinal fibers of the dermal fascia and that fibrosis in the palmar fascia represents a reparative response.
The Murrell hypothesis states that localized fat hypoxia in the palmar tissue results in the release of oxygen free radicals by the reaction of xanthine oxidase and oxygen.59,60 Myofibroblasts have been demonstrated to proliferate and contract after stimulation by oxygen free radicals in a positive feedback loop.
Pathologic Anatomy
In the normal hand, the palmar aponeurosis runs longitudinally from the wrist, crosses over the superficial transverse palmar ligament, and splits into pretendinous bands to each digit.
Normal anatomy of digital ligaments.
In the distal palm and fingers, the following superficial facial components are typically involved in Dupuytren disease:
- Pretendinous band
- Spiral band
- Lateral digital sheet
- Grayson ligament
- Natatory ligament
The extension of a palmar fascial band to the index finger frequently ends in the skin on the radial side of the hand. The band to the thumb is inconsistent. The insertion of the pretendinous bands to the skin distal to the distal palmar crease is by means of a bifurcate insertion into the side of the finger dorsal to the neurovascular bundle. A natatory ligament runs transversely across each webspace distal to the metacarpophalangeal (MP) joint, giving fibers that blend with each lateral digital sheet and to the superficial aspect of the flexor tendon sheath. The superficial transverse ligament lies deep to the pretendinous bands, proximal to the MP joints and the natatory ligament. In the fingers, the Cleland ligament Landsmeer ligaments (oblique retinacular ligaments), and other deeper fascial layers are usually spared in Dupuytren disease.56,61
According to Luck, normal longitudinal components of the superficial palmar aponeurosis are referred to as bands; diseased tissue is referred to as cords.55 Cardinal features of Dupuytren disease are the nodule, the cord, and the digital flexion contracture.
Parts of the palmar and digital fascia that become diseased in Dupuytren disease (left). Diseased fascia that is associated with the pretendinous cord (center). Diseased fascia that is not associated with the pretendinous cord (right).
Normal parts of the fascia that produce the spiral cord (left). The spiral cord demonstrating medial displacement of the neurovascular bundle in Dupuytren disease (right).
- The pretendinous cord is formed from pretendinous bands.
- The spiral cord comprises the pretendinous band, spiral band, lateral digital sheet, and Grayson ligament. This often occurs in the ring and small fingers and winds around the neurovascular bundle.
- The lateral cord is formed from the lateral digital band and is rarely observed, except on the ulnar aspect of the small finger.
- The central cord has no defined fascial precursor; it is the most common cause of proximal interphalangeal (PIP) contracture.
- The natatory cord contributes to web space contractures and passes superficial to neurovascular bundles.
Spiral and lateral cords displace the neurovascular bundle toward the digital midline, while a central cord may encase the neurovascular bundle and usually is directed toward one side of the finger. The central, lateral, and spiral cords terminate on the tendon sheath of the adjacent middle phalanx. One or more may be found in any individual patient, but they seldom occur on both sides of the same finger. McFarlane describes displacement of the neurovascular bundle superficially and toward the digital midline by a spiral cord, which makes it more vulnerable to injury during surgery.57 With increasing degrees of flexion contracture, nerve compression and vascular embarrassment may also occur.
In the thumb, 3 fascial structures may be involved: the natatory ligament, the pretendinous band, and the superficial transverse ligament of the palm. Knuckle pads may develop with fibrosis in the dorsal subcutaneous wrinkle ligaments (of McGrouther) dorsally at the PIP joints. These often indicate progressive disease.
Clinical Presentation
Dupuytren disease is usually bilateral. In unilateral disease, the right hand is more frequently affected. The small and ring fingers are the most commonly affected.8 Typically, one or more nodules develop at the base of the volar ulnar digits in the earliest stage of the disease. Nodules are typically small and tender. Longitudinal cords gradually form proximal to these nodules. Flexion contractures start in the metacarpophalangeal (MP) joint and may progress to the proximal interphalangeal (PIP) joints. Skin overlying the cords adheres to the diseased palmar fascia by vertical fibrous connections, creating pits adjacent to the cords.62
Visible cord characteristic of Dupuytren disease with planned markings for surgical release.
Treatment
The goals of treatment are to improve function, reduce deformity, and prevent recurrence or extension of the disease. Both surgical and nonsurgical treatments have been described. Incision or excision of diseased palmar fascia is the most common treatment to correct joint contracture.
Indications
Indications for surgery depend on the patient’s requirement for hand function, the patient’s age, the severity of the contracture, and the joint or joints involved. Generally, surgery is not necessary until contracture occurs.63 Indications include the following:- Metacarpophalangeal (MP) flexion contracture of 30° or more is an accepted criterion for surgical correction.63,64 At this point, flexion becomes functionally significant for most people; even in the ulnar digits where there is some carpometacarpal (CMC) extension range. MP joint flexion contracture of up to 60o has been easily correctable.62
- Proximal interphalangeal (PIP) flexion contracture of any degree constitutes an indication for operation. A flexion contracture of the PIP joint quickly becomes more difficult to correct because of shortening of collateral ligaments and fibrosis and adherence of periarticular structures such as the volar plate. Adequate correction may require joint release after the resection of contracted diseased tissue. Shortening of neurovascular bundles can also limit extension after release in long-standing PIP contracture. Because of these technical challenges, complete correction is less common, and persistence of joint flexion contracture is more likely.62,65
- Neurovascular compromise due to Dupuytren disease is an indication for intervention.
- Secondary involvement of periarticular structures may also require correction.
Types of Surgery
Some believe that early surgical intervention is more likely than delayed operation to yield excellent results, while others believe radical prophylactic palmar clearance potentiates need for revisions with the natural disease progression.3,15 Surgical techniques for Dupuytren disease include closed and open fasciotomy, regional or limited palmar fasciectomy, and extended or total fasciectomy.Dissection of the spiral cord in a patient with Dupuytren disease. Image courtesy of Lawrence Yeung, MD.
Dissection of a diseased cord.
Two important considerations are adequate release of longitudinal tension and the management of involved skin. Other important decisions involve selection of the incisions required and any special method of wound closure employed. The patient’s age and functional requirements, and the potential for recurrent disease, also impact decisions on the extent of surgery.
Fasciotomy
Sir Astley Cooper described a technique of closed fasciotomy in 1822 for the release of contracted digits. In closed fasciotomy for Dupuytren disease, a limiting cord of diseased superficial fascia is incised via an overlying skin incision. This technique can be successful in MP contractures but is not as useful for PIP contracture, since more than one cord is usually present. Closed fasciotomy presents some risk of neurovascular injury. One indication described is to facilitate hygiene in a debilitated elderly patient who has contractures that keep the fingernails in contact with the palmar skin or produce secondary wounds. Closed fasciotomy has also been used as an initial stage in very severe contracture to facilitate further release.
Open fasciotomy allows direct visualization of neurovascular structures. The offending cord is divided at a point not immediately underlying the skin incision. Fasciotomies are usually most successful for MP flexion contracture. This procedure can be performed under local anesthesia and recovery is rapid; the recurrence rate is also high. Open fasciotomy is usually reserved for patients who cannot tolerate a more extensive procedure.
Segmental aponeurectomy of Moermans66,67 is a procedure intermediately between simple fasciotomy and limited fasciectomy. Segments (1 cm in length) of fascia are excised through C-shaped incisions. Moermans claims that a Dupuytren cord can resolve once the tension across it is diminished. A prospective study performed by Andrew demonstrated a recurrence rate comparable to other techniques with fewer complications.68 This is also an outpatient procedure.
Duthie and Chesney reported a nonselected series of 160 patients treated by percutaneous (closed) fasciotomy with follow-up for 10 y for the 51% of patients remaining alive.69 Although contracture progressed in most patients, 34% required no further surgery, while the mean time to fasciectomy for the remaining 66% was 5 y. A 4% complication rate is described for this outpatient surgery, performed under local anesthesia or nerve block. They conclude that this is a useful procedure for patients who may be "unsuitable for local fasciectomy."69 Other modern reports of fasciotomy include those of Denkler.70
A more recent variation is percutaneous needle fasciotomy (PNF), adopted by a group of French rheumatologists and repopularized by Foucher and other European surgeons. This minimally invasive procedure is usually performed as an office procedure under local anesthesia. It involves multiple puncture sites and sectioning of the Dupuytren cord using the bevel of a needle. In study of 211 older patients, (average age 65 y), one digital nerve injury, no infections, and no tendon injuries were found with needle "aponeurotomy."71 However, recurrence (58%) and disease activity (69%) were high at the 3-y follow-up.
Foucher et al believed this technique was ideal for the elderly patient with a bowing cord and a predominant MP joint contracture.71 Limitations of fasciotomy in treating digital disease and PIP contracture were again noted. Contraindications to PNF include infiltrating disease, rapid recurrence in a young patient, inaccessible multiple cords, chronic digital disease, and postsurgical recurrence in the digits.71
More recently, van Rijssen et al72 reported a comparison of PNF and limited fasciectomy with short-term follow up. PNF demonstrated an improvement of 63% in passive extension deficit and no significant complications. While fasciectomy produced more improvement in contracture, particularly in more advanced cases, the major complication rate was 5%. The authors emphasize less discomfort, quick recovery, and better immediate hand function in the PNF group. They also noted the need to avoid applying PNF in a zone at the junction of the palm and the base of the finger where the neurovascular bundle may be displaced superficially and toward the midline and more vulnerable to injury. The authors concluded from another study that PNF was a good treatment alternative to limited fasciectomy in patients with a total passive extension deficit of 90o or less.
Regional (limited) palmar fasciectomy
In regional or limited fasciectomy, only the diseased parts of the superficial fascial aponeurosis are excised; eg, in the palm, pretendinous cords and involved natatory ligaments; in the fingers, only those structures visibly affected. Although Dupuytren disease may reoccur or progress by extension in the nonoperated areas of the hand, good results have been obtained with a acceptable complication rates.73,15 Limited palmar fasciectomy is the most commonly performed procedure for Dupuytren disease.
Hueston more carefully described the complications in 96 operated hands, finding hematoma in 7.5%, problematic or persistent edema in 15.5%, digital nerve injury in 2 %, skin necrosis in 2%, and wound infection in 1%.15 "Functional recovery" was delayed beyond 6 weeks in 15.5%. He found the lower rate of hematomas to be less than half of that reported in radical fasciectomy. At 2-y follow-up in this series, 27 patients were found to have "extension" and 12 patients had true recurrence of diseased tissue. These results led Hueston to conclude that this limited fasciectomy does not prevent recurrence but did allow correction of deformity with more rapid recovery of hand function.
Radical (total) fasciectomy
Radical surgery was thought by McIndoe and Beare to "cure" Dupuytren disease.3 They sought to eliminate recurrent Dupuytren disease through complete removal of the palmar aponeurosis and natatory ligaments, based on the idea that Dupuytren nodules cannot form if no remnant of palmar fascia is present. In the digits, all diseased cords and tissue that may be affected are excised. McIndoe and Beare3 reported satisfactory results in over 200 cases with an extended or total palmar fasciectomy utilizing a transverse palmar incision with separate Z-plasty incisions used, when necessary, in the digits. They also employed hypotensive anesthesia and drains. They reported that skin grafting was practically never necessary. They reported satisfactory results in more than 200 cases without specific data on complications.
While McIndoe and Beare believed that small hematomas would drain spontaneously, others report hematoma formation with subsequent swelling and stiffness (as well as infection) to be a formidable problem with this procedure.15 Unfortunately, recurrent disease was not eliminated by the more extensive surgery. Hueston found a nearly equal recurrence rate at 5- to 15-y follow-up in a comparison of limited fasciectomy and more radical procedures.15 He reserved radical fasciectomy for those few patients with extensive and diffuse involvement of the entire palm in Dupuytren disease. He found this approach to be necessary in roughly 10 % of his patients.
McCash reduced the incidence of hematoma by leaving his transverse palmar incision open for closure by secondary intention (open palm technique).74 The McCash technique is most often used when diffuse involvement of the entire palm dictates extended or radical fasciectomy. A delayed skin graft can be employed for closure of the palmar wound.
Dermofasciectomy
Hueston encountered a 28% overall rate of recurrence following surgical treatment of Dupuytren disease. Early and aggressive (or repeated) recurrence was seen in younger patients. Hueston found that full-thickness skin grafts appeared to "arrest" this process. He theorized that the skin flaps overlying fasciectomy were the (extrinsic) source of recurrent Dupuytren tissue rather than unresected elements of palmar fascia left after fasciectomy.75,76 These observations led him to employ dermofasciectomy for recurrent disease, particularly in the digits. In dermofasciectomy, diseased fascia and the overlying skin are excised completely, and full-thickness skin grafting is applied for closure. Later reports of McCann and Logan suggested the dermis as a possible source for myofibroblasts causing recurrent disease.77
Tonkin reported that dermofasciectomy with skin grafting prevented recurrent Dupuytren disease without compromising hand function, suggesting it as a prophylactic approach in young patients with Dupuytren diathesis.78 Logan recommended dermofasciectomy as the first line of treatment for recurrent digital Dupuytren disease but found that it did not prevent recurrence in all cases.79 He also noted that the immobilization required for the associated skin grafts interfered with early postoperative rehabilitation. McFarlane has criticized this approach because it may not address the presence of diseased retrovascular tissue and suggests that the exposed flexor tendon sheath is unfavorable as a graft bed. He felt that it was usually possible to separate the diseased fascia from the overlying skin.
Other authors have confirmed recurrent Dupuytren disease following this procedure.80,81 Subsequently, Armstrong et al found a recurrence rate of 11.6% in 103 patients undergoing dermofasciectomy, but they still advanced it as the best method for control of "diffuse Dupuytren disease with involvement of the skin."82 They stated the possibility that dermofasciectomy was not popular because of concerns about the success of the skin grafting required.
Skin grafting
Excision of skin (and fascia) leaves a wound that requires additional coverage. Although McIndoe and Beare believed that grafts were practically unnecessary,3,83 they reported a lower recurrence rate of Dupuytren disease when grafts or flaps were placed in flexion creases. Generally, the latter believes that skin replacement should be reserved for young patients who have an active diathesis, postfasciectomy recurrence, or a rapid progression of skin fixation and deformity.84 Skin grafting has also been used in conjunction with the open-palm technique of McCash. Good results with a technique of limited palmar fasciectomy with skin grafting have been reported.85 More recent reports have not confirmed either lower rate of recurrence or better functional results when skin grafting is combined with other procedures.86
Generally, authors recommending digital dermofasciectomy prefer full-thickness skin grafting to split-thickness skin grafting because of increased wound contraction beneath the latter. Ipsilateral inner arm donor sites can be used for skin grafting, while distant donor sites including the distal lower extremity have been suggested for improved cosmesis.82 Successful use of skin grafts require a protective dressing and preclude early or vigorous interphalangeal joint movement.87
Flaps
Local flap wound closure (beyond Z-plasty) has rarely been used. An L-shaped skin flap, called the Jacobsen flap, was developed as a modification of the McCash technique by Tripoli and Merle.88 Upon flap transposition, a more limited 15-mm palmar skin defect is left to heal by secondary intention. The authors report satisfactory correction of contracture and a low complication rate in 98 cases using this technique.
Free microvascular transfer of a circumflex scapular artery perforator flap was reported for coverage of a very large palmar defect after radical dermofasciectomy for disabling recurrent Dupuytren disease.89 Following multiple revisions and extensive hand rehabilitation, flexion deformities were significantly improved and satisfactory function was obtained.
PIP joint contracture
Correction of the PIP joint is a more difficult technical problem in Dupuytren disease. If complete extension is not obtained by careful digital fasciectomy, the options are either to rely on postoperative therapy and splinting or to perform some form of volar PIP joint release. PIP joint release is usually employed when the flexion contracture is greater than 30o. The flexor sheath can be incised, and the lateral proximal attachment of the volar plate (so-called checkrein ligaments) released, as necessary.
However, if these maneuvers do not achieve full PIP extension, some recommend further joint capsulotomy, as described by Curtis.90 His stepwise approach involved sequential release of accessory collateral ligaments followed by release of the proper collateral ligaments on one side of the joint at a time until full joint extension was achieved or all structures had been released. Others have cautioned that the correction achieved at surgery would not be maintained and that aggressive capsulotomy of the PIP joint is likely to result in permanent loss of flexion range, which is more limiting than a mild flexion contracture.91
In 1979, Watson and associates examined 115 checkrein releases and found full intraoperative extension in 110 joints with additional release necessary in only 5 joints.92 They concluded that releasing the accessory collateral or proper collateral ligaments is almost never required with successful checkrein excision. McFarlane and Botz discouraged the use of capsulotomy in patients with chronic PIP contracture, if correction to 40ºof flexion or less could be obtained.91
A study of 48 involved PIP joints in 28 patients demonstrated no advantage to capsuloligamentous release compared with fasciectomy alone.93 The authors also felt that stretching or adherence of the extensor mechanism with prolonged flexion contracture could render it ineffective, contributing to late return of flexion deformity.
Alternatives for severe PIP joint contracture include arthroplasty (including implant arthroplasty), and arthrodesis. The shortening concomitant with arthroplasty (or arthrodesis) results in improvement of the contracture. While PIP arthrodesis establishes a desired functional angle at the joint, it further limits function. Amputation is rarely necessary in digital disease. It is usually performed in elderly patients with a severely contracted fifth digit following thorough surgeon-patient discussion and realistic analysis of attainable function.
Distal interphalangeal joint hyperextension
Hyperextension of the distal interphalangeal (DIP) joint usually occurs secondary to long-standing PIP joint contracture with foreshortening of the Landsmeer ligament (oblique retinacular ligament); the DIP joint itself remains normal. If DIP joint deformity is passively correctable, it usually resolves with correction of PIP contracture. If it is not passively correctable, division of Landsmeer ligaments usually corrects the deformity. Severe fibrosis of dorsal skin related to knuckle pads can also limit DIP joint flexion.
Technical Points
Incision typesVarious incisions can facilitate exposure during surgery for Dupuytren disease.94 Incisions can be transverse, longitudinal, or combined, depending on the pattern of involvement.
- For a single digit, a midline volar incision closed with multiple Z-plasties can be employed. Some authors believe that a midline digital incision is least likely to expose a neurovascular bundle to injury. Alternatively, a volar zig-zag incision or V-Y plasty can be used.95 Overall, digital Z-plasty incisions have been shown to give excellent exposure and functionally stable scars.3
- For palmar disease with multiple MP flexion contractures, a transverse incision at the level of distal palmar crease can be made. This can be joined to longitudinal digital incisions if necessary. Part of the palmar incision(s) can be left open as in McCash’s open technique.
- Alternatives for palmar disease include palmar V-Y plasty.
Other technical points
Safe dissection during surgery for Dupuytren disease is enhanced by use of loupe magnification. Sharp dissection is usually employed in separation of skin from the underlying diseased fascia. Dissection of the skin from the underlying fascia may leave very thin skin flaps, particularly in the digits. If skin grafts are employed in the digits, they should extend from midlateral line to midlateral line across the digit.
In a severely involved digit, the neurovascular bundle may be most easily located distally. Dissecting retrovascular disease is important. Awareness of possible displacement of the neurovascular structures is essential. Proximal division of the pretendinous cord may facilitate dissection by allowing finger extension and abduction.
In planning reoperative surgery for Dupuytren disease, if clinical evaluation suggests that the digital nerve has been severed, one should assume that the related digital artery has also been severed and should confirm adequate contralateral circulation to that digit.
Postoperative Management
Most surgeons employ similar methods in postoperative care with the common goals of protecting the operative site for uncomplicated wound healing and preserving active motion, while maintaining the digital extension range gained at surgery. Carefully applied bulky dressings, appropriate splinting, and consistent effective elevation of the hand can help to prevent hematoma formation and skin loss while reducing edema and stiffness.
Since surgery for Dupuytren disease is most often performed on an outpatient basis, close follow-up in the early postoperative period is recommended. Early motion is encouraged. Some surgeons feel that routine formal supervised hand therapy at an early stage of healing is important for functional rehabilitation. Many use intermittent static extension splinting for more resistant contractures. As wound healing progresses, the patient can be encouraged to use the hand in activities of daily living and more vigorous passive range of motion exercises can be employed.
Complications
A significant complication rate with surgical treatment of Dupuytren disease remains. An overall surgical complication rate near 20% is reported.91
Early complications
- Hematoma: Tourniquet release and meticulous hemostasis prior to wound closure is recommended. Adequate drainage, such as an open area in a palmar surgical site, has been beneficial.
- Skin loss: Skin flaps can fail for many reasons, but underlying hematoma is a frequent problem. The skin may be very thin after dissection from the underlying fascia. In this situation, if skin viability is in doubt, a preemptive skin graft may be a better option. Potential donor sites can be identified preoperatively.
- Infection: Infection usually follows hematoma, skin loss, or both. If contracture prevents adequate skin preparation, a fasciotomy can be performed as a preliminary measure before definitive fasciectomy.
- Division of the digital nerve or artery: Dissection in a fasciectomy is similar to neurolysis, ie, the involved neurovascular bundles must be dissected free along the entire course of the surgical wound. The area of greatest risk is adjacent to the web space over the base of the proximal phalanx. Awareness of the displacement of the neurovascular bundle to the midline by a spiral cord is important. Surgeons should be prepared for appropriate repair of divided nerves and arteries.
Later complications
- Loss of flexion range: This is a common late complication. Active and passive preoperative range of motion should be recorded. Active flexion exercises should be part of early postoperative care. Maintenance of flexion range is often neglected in the effort to regain full extension. Schneider reported a 41% loss of flexion range after surgery for palmar disease.63
- Reflex sympathetic dystrophy (RSD) or chronic regional pain syndrome (CRPS type 1): Several authors have warned that RSD is a significant problem following surgery for Dupuytren disease.96,97,98 Luck reported that features of RSD were observed with increased frequency after surgery for Dupuytren disease.55 It is at least 5 times more common in women than in men with Dupuytren disease.
- Other postoperative pain: Local hyperalgesia, possibly due to digital nerve injury and neuroma formation, can be problematic.55
- Recurrence: Recurrence (ie, Dupuytren tissue forming in the area of resection) and recurrence of flexion deformity with disease extension (ie, Dupuytren tissue appearing outside the area of resection) are believed to be separate entities. Recurrence is much more likely in a young patient with a strong family history and knuckle pads.15 A recurrence rate ranging between 26% and 80% has been reported. In his evaluation of 224 patients post-fasciectomy, Hueston concluded that recurrence is rare after 2 years postoperatively and occurs less frequently in older patients but is an early postoperative event in younger patients with Dupuytren diathesis, with some patients requiring multiple reoperations.75,76 The incidence of recurrence has been decreased but not completely eliminated with skin replacement techniques.
The patient will likely judge his or her own result subjectively, with the perception of functional improvement as an endpoint. Andrew found that MP contracture invariably was corrected (86% excellent), while good results for PIP contracture were less frequent (40% excellent result in middle, ring fingers; 20% in small fingers).65 Secondary contracture in the DIP joint was corrected with approximately 50% excellent results.
Other Treatments for Dupuytren Disease
Distraction and passive extension techniques
Successful use of bone distraction and tissue expansion techniques led to the use of distraction devices in conjunction with fasciectomies. According to Messina, this technique of gradual passive extension has allowed salvage of severely contracted digits.99,100,101,102 The application of continuous passive extension was used to elongate the contracted palmar fascia. Authors described reorganization of the once densely packed collagen fibers in the cords of Dupuytren disease into a parallel, "ribbon-like" appearance.100 In 1994, another device for PIP extension, referred to as the Proximal Interphalangeal Skeletal Traction Extender, was introduced by Hodgkinson for preoperative outpatient use.103 Authors believe this device makes adjacent tissues more available and decreases PIP flexion contracture, facilitating successful surgery.
Nonoperative treatment
5-fluorouracil has been used to treat other fibroproliferative disorders. 5-flourouracil was found to inhibit collagen production by Dupuytren fibroblasts in vitro.104 This effect was dose-dependent, selective, and specific. From their results, Bulstrode et al concluded that 5-fluorouracil could potentially reduce extracellular matrix production, thereby reducing recurrent Dupuytren disease.104
Rayan and associates performed in vitro tests of various agents on fibroblast explant cell cultures from patients with Dupuytren disease.45 Nifedipine and verapamil were tested to partially block lysophosphatidic acid (LPA)-contraction of fibroblasts, suggesting that these pharmacologic agents may have therapeutic potential.
Local steroid injections in Dupuytren disease were explored by Ketchum with limited results.80 Radiation therapy, gamma-interferon, systemic vitamin E, dimethylsulfoxide, splinting, and standalone physical therapy have been briefly or anecdotally reported as treatment options but have been without the convincing efficacy to supplant surgical treatment.105
"Enzymatic fasciotomy" using nonspecific proteolytic enzymes was associated with local complications.106 Badalamente107 demonstrated that injection of a specific collagenase derived from Clostridium histolyticum into the cords of Dupuytren disease could significantly improve digital extension, sometimes postponing the need for surgery even in late stage disease.
Several interesting studies were been presented at the 2009 Annual Meeting of the American Society for Surgery of the Hand (ASSH) and American Society of Hand Therapists (ASHT). Hurst et al have recently presented results from a randomized, multicenter, double–blinded, placebo-controlled trial, confirming safety and efficacy of this C histolyticum treatment, with significant improvement in metacarpophalangeal (MP) and proximal interphalangeal (PIP) joint contracture.108 Despite a high recurrence rate, in this group, recurrent Dupuytren disease was not as severe as the initial contracture, and patient acceptance is very high. Watt has presented a subset of patients from this phase III study demonstrating that although Dupuytren contracture progressed or recurred over time, significant improvement persisted at 5 years posttreatment.109 At the time of this writing, the US FDA is considering release of Clostridial collagenase for treatment of Dupuytren disease.
Multimedia
 | Media file 1: Dissection of spiral cord in the hand of a patient with Dupuytren disease. Image courtesy of Lawrence Yeung, MD. |
 | Media file 2: Dissection of the spiral cord in a patient with Dupuytren disease. Image courtesy of Lawrence Yeung, MD. |
 | Media file 3: Visible cord characteristic of Dupuytren disease with planned markings for surgical release. |
 | Media file 4: Dissection of a diseased cord. |
 | Media file 5: Normal anatomy of digital ligaments. |
 | Media file 6: Three clinical stages of Dupuytren disease. |
 | Media file 7: Parts of the palmar and digital fascia that become diseased in Dupuytren disease (left). Diseased fascia that is associated with the pretendinous cord (center). Diseased fascia that is not associated with the pretendinous cord (right). |
 | Media file 8: Normal parts of the fascia that produce the spiral cord (left). The spiral cord demonstrating medial displacement of the neurovascular bundle in Dupuytren disease (right). |
Keywords
Dupuytren, Dupuytren’s disease, Dupuytren’s contracture, fibroproliferative disorder, joint contracture, proximal interphalangeal joint contracture, PIP joint contracture, metacarpophalangeal joint contracture, MP joint contracture, knuckle pads, Garrod nodes, palmar fibromatosis, plantar fibromatosis, Lederhose’s disease, Peyronie’s disease
The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, D Glynn Bolitho, MD, PhD, FACS, FRCSC, FCS(SA), to the development and writing of this article.
More on Hand, Dupuytren Disease |
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Further Reading
Keywords
Dupuytren, Dupuytren’s disease, Dupuytren’s contracture, fibroproliferative disorder, joint contracture, proximal interphalangeal joint contracture, PIP joint contracture, metacarpophalangeal joint contracture, MP joint contracture, knuckle pads, Garrod nodes, palmar fibromatosis, plantar fibromatosis, Lederhose’s disease, Peyronie’s disease
