Dupuytren Contracture 

Updated: Nov 20, 2018
Author: Eva Kovacs, MD; Chief Editor: Herbert S Diamond, MD 

Overview

Practice Essentials

Dupuytren disease (DD) is a fibrosing disorder that results in slowly progressive thickening and shorting of the palmar fascia and leads to debilitating digital contractures, particularly of the metacarpophalangeal (MCP) joints or the proximal interphalangeal (PIP) joints. This condition usually affects the fourth and fifth digits (the ring and small fingers). See the images below.

Arrow denotes the cord often present in Dupuytren Arrow denotes the cord often present in Dupuytren contracture. Metacarpophalangeal joint and proximal interphalangeal joint contractures are also present.
This photo shows a patient with an inability to ex This photo shows a patient with an inability to extend the fourth and fifth digits. The differential diagnosis includes Dupuytren contracture, which is a flexion contracture most commonly involving digits 4 and/or 5.

Dupuytren contracture belongs to the group of fibromatoses that include plantar fibromatosis (Ledderhose disease), penile fibromatosis (Peyronie disease), and fibromatosis of the dorsal PIP joints (Garrod nodes or knuckle pads).[1] Although many cases appear to be idiopathic, various associated diseases have been reported. See Pathogenesis/Etiology.

Dupuytren contracture is most commonly observed in persons of Northern European descent and affects 4-6% of Caucasians worldwide.[2] Many individuals have bilateral disease (45%); in unilateral cases, the right side is more often affected.[3] The ring finger is most commonly involved, followed by the fifth digit and then the middle finger. The index finger and the thumb are typically spared. See Epidemiology and Presentation.

Although the cause of Dupuytren disease is unknown, a family history is often present. Males are three times as likely to develop disease and are more likely to have higher disease severity.[4, 5] Male predominance may be related to expression of androgen receptors in Dupuytren fascia. See Etiology and Epidemiology.[6]

Other potential risk factors include manual labor with vibration exposure, prior hand trauma, alcoholism, smoking, diabetes mellitus, hyperlipidemia, Peyronie disease, and complex regional pain syndrome.[7] Rheumatoid arthritis seems to protect against the development of Dupuytren disease. See Etiology.

Therapies include conservative medical and surgical modalities. Although the condition is not fatal, significant morbidity can occur if patients are untreated. See Treatment.

Stages of Dupuytren disease

Dupuytren disease occurs in the following three stages:

  • Proliferative phase - During this phase, myofibroblasts proliferate and a nodule develops. In early disease, some patients may report tenderness and discomfort associated with the nodules. The associated pain is thought to be due to nerve fibers embedded in the fibrous tissue or compression of local nerves.[8] On physical examination, palmar skin blanching is seen with finger extension.

  • Involutional phase - In this phase the disease, spreads along the fascia and into the fingers resulting in the development of a cord. Myofibroblasts are the predominant cell type during this phase and align themselves along tension lines within the nodule

  • Residual phase – During the residual phase, the disease continues to spread into the fingers and the cord tightens creating a contracture. The nodular tissue disappears as do the myofibroblasts and acellular tissue with thick bands of collagen remain.

Dupuytren disease is not always progressive, however. A prospective study in 247 Dutch participants with primary Dupuytren disease with follow-up at intervals of 3 to 6 months found that in up to 75% of patients, the disease stabilizes or even regresses.[9]

Grades of severity

The grading system for Dupuytren disease severity is as follows (see the images below)[10] :

  • Grade 1 - Thickened nodule and band in the palmar aponeurosis; may have associated skin abnormalities

  • Grade 2 - Development of pretendinous and digital cords with limitation of finger extension

  • Grade 3 - Presence of flexion contracture

See the images below.

Arrow denotes the cord often present in Dupuytren Arrow denotes the cord often present in Dupuytren contracture. Metacarpophalangeal joint and proximal interphalangeal joint contractures are also present.
Arrow denotes the typical cords of Dupuytren contr Arrow denotes the typical cords of Dupuytren contracture. These cords are usually painless. Note the metacarpophalangeal joint contracture.
This photo demonstrates the presence of a nodule a This photo demonstrates the presence of a nodule as well as skin blanching with extension of the affected digits.
Three clinical grades of Dupuytren disease. Three clinical grades of Dupuytren disease.

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. See the image below.

Normal anatomy of digital ligaments. Normal anatomy of digital ligaments.

In the distal palm and fingers, the following superficial fascial 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 web space distal to the MCP 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 MCP 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.[11, 12, 13]

According to Luck, normal longitudinal components of the superficial palmar aponeurosis are referred to as bands; diseased tissue is referred to as cords.[14] Cardinal features of Dupuytren disease are the nodule, the cord, and the digital flexion contracture. The bands and cords are characterized as follows:

  • The pretendinous cord is formed from pretendinous bands.

  • The spiral cord is made up of 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 PIP contracture.

  • The natatory cord contributes to web space contractures and passes superficial to neurovascular bundles.

See the images below.

Visible cord characteristic of Dupuytren disease w Visible cord characteristic of Dupuytren disease with planned markings for surgical release.
Dissection of a diseased cord. Dissection of a diseased cord.
Parts of the palmar and digital fascia that become 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 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).

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.[13] 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.

Pathogenesis/Etiology

Although the underlying etiology for the development of Dupuytren disease is uncertain, the basic pathophysiology involves fibroblast proliferation, and collagen deposition leading to contractures of the palmar fascia. Investigators have proposed several hypotheses for the pathogenesis of Dupuytren disease. Al-Qattan hypothesizes that an individual with a genetic predisposition to develop Dupuytren disease experiences a second inciting event (ie, smoking, diabetes, trauma, alcoholism), resulting in microvascular ischemia.[6] The localized ischemia causes two events to take place in the palmar fascia: (1) the conversion of adenosine triphosphate to hypoxanthine and (2) the conversion of xanthine dehydrogenase to xanthine oxidase.

Xanthine oxidase acts as a catalyst for the oxidation of hypoxanthine to xanthine and uric acid; this conversion results in the production of free radicals. Free radicals result in fibroblast proliferation and the production of numerous cytokines. Interleukin 1 (IL-1) is the most abundant cytokine in Dupuytren disease and, via its receptor, upregulates the production of transforming growth factor beta (TGF-beta), fibroblast growth factor, epidermal-derived growth factor, and platelet-derived growth factor.[15, 16] This milieu of cytokines and growth factors results in the proliferation of fibroblasts and their differentiation into myofibroblasts (the primary cell type in Dupuytren disease).[17]

Increased levels of nerve growth factor are present, which induce fibroblast transformation to myofibroblasts, especially during stages II-III. The splicing of fibronectin affects collagen binding. Platelet activation produces lysophosphatidic acid (LPA). LPA is a signaling molecule for cell proliferation and myofibroblast contraction. After binding to its receptor on myofibroblasts, LPA leads to a decrease in cyclic adenosine monophosphate and an increase in intracellular calcium levels. These events mediate smooth muscle contraction of the myofibrils within the myofibroblast. Normal palmar fascia is primarily composed of type I collagen; Dupuytren disease is associated with an increase in type III collagen.

The ratio of type III collagen to type I collagen increases, the reverse of the normal pattern, in the palmar fascia.[10] Excess type III collagen production occurs from an increased density of fibroblasts secondary to enhanced stimulation and diminished apoptosis, as well as an imbalance between the collagenases and their endogenous inhibitors. Dupuytren fascia exhibits an increased ratio of tissue inhibitors of metalloproteinases (TIMP) to matrix metalloproteinases (MMP).[18, 19, 20]

The myofibroblasts are indirectly connected to collagen, and the contractile force is transmitted from the intracellular actin microfilaments to the collagen bundles. Ultimately, the end result is contracture from excess deposition of type III collagen and the formation of cross-links between myofibroblasts and collagen. Another hypothesis by Vi et al suggests an up regulation of the gene transcript POSTN mRNA that encodes the protein periostin. Periostin is secreted by diseased cord myofibroblasts into the extracellular matrix. It promotes the transition of palmar fascia fibroblasts into a myofibroblast phenotype, thereby enhancing disease progression.[21]

Additionally, periostin is prevalent during the early stages of bone fracture repair and vascular injury. Hueston advanced the extrinsic theory, suggesting that Dupuytren nodules arise de novo and progress to cords.[22] Vasomotor disturbance and neurovascular mediation by the skin are 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.[13] A combination of these ideas forms the synthesis theory, which states that the nodules and pretendinous cords represent different forms of the disease.[23]

Genetic factors

Though the cause of Dupuytren contracture remains unknown, genetic factors are thought to play a role.[24] One study derived a sibling recurrence-risk ratio of 2.9 (range, 2.6-3.3).[25]

Furthermore, DNA microarray analysis has demonstrated that the gene MafB is up-regulated in Dupuytren cord tissue. MafB is involved in tissue development and cellular differentiation.[26, 25] Further support for a genetic link was provided by Al-Qattan, who described a maternally transmitted inheritance within the mitochondrial genome in 90% of patients. The defective mitochondria generate high levels of free radicals and defective apoptosis and are therefore directly related to disease pathogenesis.[6]

Another study of 20 patients with apparent maternal inheritance identified a polymorphism in the mitochondrial 16s rRNA region present in 90% of their DNA.[27] Other studies suggest an autosomal dominant pattern of inheritance with variable penetrance.[28] One such study analyzed 5 generations of a Swedish family and mapped the affected gene (not yet identified) to 16q.[29] Some authors suggest an error in growth and regulation of the fibroblast resulting from chromosomal abnormalities, similar to those seen in cells undergoing neoplastic changes. Trisomy 7 and 8 have been identified in the fibroblasts excised from some patients.[30] Nodules may display features of a benign neoplasm.[31]

Others believe that Dupuytren contracture has a multifactorial inheritance, similar to diabetes or hypertension.

Additional risk factors

Whether certain conditions represent independent risk factors for the development of Dupuytren contracture is unclear. A large, retrospective study by Loos and colleagues on 2919 hands on which surgery had been performed revealed no statistically significant evidence that the occurrence of Dupuytren contracture could be correlated with the presence of diabetes, with alcoholism, or with smoking.[31]

Another report, however, found different results, noting an association between Dupuytren contracture and several conditions (eg, alcoholism, diabetes, epilepsy, pulmonary disease), as well as a link with smoking.[32] Nonetheless, even if such associations exist, no clear causal relationship has been established in the literature.

HLA-DRB1*15 and HLA-DR3 have been identified in numerous patients, suggesting an immunologic influence. Each confers about a 2-3 times relative risk for the development of Dupuytren disease.[33, 34] Most likely, an inciting disease or event in a genetically predisposed individual causes a cascade of events that may include processes that promote the formation of growth factors and free radicals that ultimately leads to abnormal fibroproliferation and the appearance of the characteristic Garrod nodule. Even when homeostasis is ultimately achieved and fibroblastic growth lessens, the pathologic nodule and cord remain.

Many hand surgeons believe that trauma to the hand or the distal part of the forearm, such as falling on an outstretched hand, may precipitate the onset.[35] (A positive family history may play a role in occupational and traumatic cases of Dupuytren disease.) However, numerous population-based studies have failed to conclusively link Dupuytren disease to trauma,[36] although case reports have suggested a possible association. Reports by Lucas et al found increased Dupuytren disease in a group of French male civil servants with occupational exposure to vibration and manual work.[37]

Case reports of Dupuytren disease occurring after surgical injury to the hand have been identified, with the authors suggesting that injury can trigger the onset of Dupuytren disease.[38] A history of manual labor with vibration exposure or recurrent trauma has been found to result in a 5-fold increase in the incidence of Dupuytren disease.[39, 40, 41] Liss performed a systemic review of the literature regarding occupation and Dupuytren disease. Although he failed to identify a link between trauma and development of disease, he did find an association between occupational exposure to vibration and Dupuytren disease.[36]

Notably, the exposure in one study was severe enough to cause persistent symptomatic circulatory disturbance ("vibration white finger")[39] ; in another, the exposure was associated with other soft tissue "wasting" and peripheral nerve damage. In a review of 46 available studies, Melhom and Ackerman concluded evidence suggests an association between Dupuytren disease and vibration but not with highly repetitive or forceful work.[42]

Diabetes mellitus has been identified as a risk factor.[43] Dupuytren disease in patients with diabetes ranges from 1.6-32%, the prevalence of diabetes in patients with Dupuytren disease is 5%.[4] The use of insulin and oral hypoglycemics are strongly associated with Dupuytren disease. The disease seems to occur at a younger age and tends to be more severe in those with type 1 diabetes.[44]

Patients with diabetes mellitus and Dupuytren disease have a 4-fold increased risk of developing microalbuminuria than do persons with diabetes alone.[45] A higher incidence of retinopathy was identified in diabetics with Dupuytren contracture, likely attributable to microangiopathic changes. Alcoholic liver disease Individuals with alcohol-related liver disease have an increased prevalence of Dupuytren contracture (approximately 20%) compared with control populations. Patients with liver disease from other causes do not appear to be at increased risk. The reason for this is unknown, and some studies have disputed the association.[46]

A 3-fold increased risk for Dupuytren contracture is seen in individuals who smoke, even when studies control for alcohol use, perhaps due to microvascular impairment.[32] Autoantibodies to connective tissue Significant associations have been found with HLA-DRB1*15, HLA-DR3 and autoantibodies to collagen types I-IV have been reported.[47]

Two studies have shown increased sensitivity to androgens in the palmar fascia.[48, 49] This may account for the male predominance of the disease.

Although implicated in previous studies, little conclusive evidence has been reported to link epilepsy and antiepileptic medications to the development of Dupuytren contracture. Phenobarbitone, in particular, results in increased LPA levels. Although the incidence of Dupuytren disease is 2-3 times higher in individuals with epilepsy, opinions about the cause differ. One group of investigators concluded that electroencephalogram (EEG) abnormalities were more common in patients with Dupuytren disease than in persons with other clinical conditions.

Another study showed a correlation between increased barbiturate medication and a higher occurrence of Dupuytren disease, whereas other studies implicated a genetic link between the two diseases.[50]

Results are conflicting as to whether the human immunodeficiency virus (HIV) is implicated in some cases of Dupuytren disease.[51] Bower et al demonstrated an increased incidence in patients with both Dupuytren contracture and HIV infection, whereas a study by French et al showed no statistically significant difference in these patients compared with the general population.[52]

Epidemiology

Frequency

Dupuytren disease is common in the United States with a prevalence of 4%, reflecting immigration from Northern Europe.[10] In Northern Europe the prevalence ranges from 4-39%. In Norwegian populations, 30% of males over the age of 60 years are affected. The incidence of Dupuytren disease for the British population in 2004 was calculated at 34.4 per 100,000 for men aged 40-84 years.[10] Australia has a reported prevalence of 28%; Spain's reported prevalence is 19% prevalence in in men older than 60 years.[3] Sporadic cases are reported in Africa and Asia.[10]

Mortality/Morbidity

The effects of morbidity in Dupuytren contracture are generally limited to lifestyle changes. MCP and PIP joint contractures may interfere with activities of daily living and the nodules can be painful. Occasionally, Dupuytren contracture is associated with plantar fascial thickening (Ledderhose disease), involvement of the penis (Peyronie disease), or involvement of the knuckle pads (Garrod nodes). These associations tend to reflect more aggressive disease.[53] No mortality occurs from Dupuytren contracture.

Race

Racial variation in Dupuytren disease is as follows:

  • Dupuytren disease is most often found in Caucasians of Northern European descent.

  • The disease prevalence in Asians is 3% and usually involves the palm rather than the digits. Therefore, it is less likely to be clinically significant, and the incidence may be underreported.

  • Dupuytren disease has been reported in East Africa, Zimbabwe, and Tanzania.[7]

  • Dupuytren disease is uncommon among Indians (< 1%), Native Americans, and patients of Hispanic descent.[7]

Sex and age

Approximately 80% of affected individuals are male; this is consistent throughout all countries and races. The disease onset in males tends to occur in the fifth to sixth decade. Men tend to present a decade earlier than females. The disease course tends to be more rapid and severe in males and increases in incidence with advancing age.[45]

Dupuytren disease is rare in children younger than 10 years. Only eight histologically proven cases have been reported.[54]

Patient Education

Patients must have realistic expectations that surgery can relieve some disability but that it cannot cure Dupuytren disease. Discuss all potential complications of the procedure, including complex regional pain syndrome. In addition, intensive rehabilitation with an occupational therapist is necessary postoperatively for an optimal outcome.

 

Presentation

History

Obtain a thorough medical history when evaluating a patient thought to have Dupuytren contracture. Presenting symptoms typically include the following:

  • Decreased range of motion

  • Loss of dexterity

  • Getting the hand "caught" when trying to place it in a pocket

Conditions possibly related to Dupuytren contracture include the following:

  • Diabetes mellitus

  • Alcohol abuse

  • HIV infection

  • Epilepsy

  • Trauma

  • Manual labor with vibratory exposure

  • Cigarette smoking

Patients describe feeling a knot or thickening on the palmar surface or, less frequently, on the digits, typically the proximal palmar aspect. Often, the thickening has been present for many years and may be slowly progressive.

The fourth digit (ring finger) is most frequently affected, followed by the fifth digit. The disease can be bilateral but is generally not symmetric in severity. Hand dominance is not a factor. Nodules typically are painless, unless nerve compression or tenosynovitis is present. Tenosynovitis can develop and lead to pain when the nodules are large. With progressive disease, flexion deformity can develop and patients will report an inability to straighten the fingers.

Asking about functional disabilities may elicit a history of certain tasks that the individual can no longer perform, such as grasping objects and typing. No sensory deficits are reported unless there is a concomitant pathology. The condition is painless in its later stages.

Physical Examination

Perform a thorough physical examination focusing on the involved extremity. A careful physical examination often confirms the diagnosis without the need for further tests.[55]

Important points to assess include the following:

  • Firm nodules that may be tender to palpation: The nodules are closely adherent to the skin; movement of the nodule with finger motion suggests an association with the tendon and not Dupuytren contracture. See the image below.

    This photo demonstrates the presence of a nodule a This photo demonstrates the presence of a nodule as well as skin blanching with extension of the affected digits.
  • Painless cords proximal to the nodules

  • Skin blanching upon active finger extension

  • Atrophic grooves or pits in the skin: These represent adherence to the underlying fascia.

  • Tender knuckle pads over the dorsal aspect of the PIPs (Garrod nodes): These occur in 44-54% of patients and suggest more aggressive disease.[3]

  • Plantar fascia involvement, known as Ledderhose disease (6-31%): This can indicate more severe disease.[3]

  • Presence of MCP and PIP joint contractures: Objectively measure and record the degree of flexion contracture and assess for compensatory DIP joint hyperextension or contracture.

  • Hueston table top test: If the patient is unable to lay the palm flat on a tabletop, the findings are considered positive.

 

DDx

Diagnostic Considerations

Dupuytren disease must be distinguished from several other conditions that affect the hand, including trigger finger, stenosing tenosynovitis, a ganglion cyst, or a soft-tissue mass. Unlike Dupuytren contracture, trigger finger typically involves pain with flexion followed by the inability to extend the affected digit.

Stenosing tenosynovitis may be distinguished from Dupuytren disease by pain and a history of overuse or trauma. A small, movable nodule that is tender to palpation at the MCP joint is likely a ganglion cyst. A soft-tissue mass must also be excluded from the diagnosis, especially if the patient is significantly younger than the typical patient with Dupuytren disease and if he or she has no other risk factors.

A patient younger than age 40 years without involvement of the dorsal hand, foot, or penis is unlikely to have Dupuytren disease; however, the possibility of a sarcoma must be ruled out—although the pathologic findings of a biopsy will most likely reveal a benign etiology (eg, lipoma, inclusion cyst).

Conditions to consider in the differential diagnosis of Dupuytren contracture include the following:

  • Diabetic cheiropathy

  • Epithelioid sarcoma

  • Fibroma

  • Giant cell tumor

  • Intrinsic joint disease

  • Lipoma

  • Neurofibroma

  • Palmar fibromatosis

  • Palmar tendinitis

  • Retinacular ganglion of the A-1 pulley

  • Tendon nodule of stenosing tenosynovitis

  • Tophi

  • Traumatic scars

  • Callus

  • Ganglion cyst

  • Prolapsed flexor tendon

  • Ulnar nerve palsy

  • Camptodactyly

  • Changes secondary to rheumatoid arthritis

  • Hyperkeratosis

  • Non-Dupuytren disease

  • Palmar ganglion

Differential Diagnoses

 

Workup

Approach Considerations

No routine diagnostic laboratory studies apply to this disorder. However, diabetes mellitus has been associated with Dupuytren contracture. A fasting blood glucose level should be obtained if diabetes mellitus is suggested by the patient's clinical history and physical examination findings.

No routine radiographs are necessary, but ultrasonography can demonstrate thickening of the palmar fascia, as well as the presence of a nodule. In addition, ultrasonography of a thickened cord may be useful prior to intralesional injections so that the underlying tendon can be identified and avoided during the injection. (See the image below.)

Ultrasound of the palm in Dupuytren disease of the Ultrasound of the palm in Dupuytren disease of the fourth digit; the Dupuytren nodule and thickening of the palmar fascia with puckering of the skin is noted. Green arrow: Flexor tendon; Red arrow: Dupuytren nodule; Blue arrow: Thickened palmar fascia; Yellow arrow: Puckering of the skin.

Histologic Findings

Histologic analyses of lesions resulting from Dupuytren contractures indicate physiologic characteristics of hypertrophic scar formation, including the following: myofibroblastic proliferation with increased water levels, an increase in type III collagen, chondroitin sulfate, and reducible cross-linkages. In addition, surrounding tissue without clinical manifestations reveal newly formed type III collagen, reducible cross-links, and fibroblasts with myofibroblastic characteristics, such as intracellular microfilaments, as well as basement lamina-like condensation. This suggests that Dupuytren disease spreads by migrating along the altered collagen bundles and clinically silent areas are affected on a microscopic level.[56]

A histologic staging system was proposed by Luck in 1959. He described three progressive stages, as follows[14] :

  • Proliferative stage: This is characterized by intense cellularity with collagen fibrils randomly arranged and surrounded by proliferating fibroblasts

  • Involution stage: The collagen fibrils are organized along lines of tension; the myofibroblast is the predominant cell and aggregates near the collagen fibrils

  • Residual stage: Collagen is uniformly oriented, with few to no cells and fibrosis; this stage is analogous to that of wound healing

In all stages, a core of type I collagen is surrounded by type III collagen. Studies suggest that the percentage of type III collagen changes with the stage of the disease.[57]

 

Treatment

Approach Considerations

A variety of non-surgical and surgical options are available for management of Dupuytren disease (DD). The choice largely depends on the severity of disease, degree of deformity, limitations in function, and provider preference.  Although there is no consensus, it is generally accepted that surgical procedures are reserved for patients with contractures >30-40º or with significant disability.[58]  

A study by Stepic et al found that the degree of contracture may influence surgical outcomes with proximal interphalangeal (PIP) joint Dupuytren disease, but not metacarpophalangeal (MCP) joint Dupuytren disease. These researchers followed 60 patients (85 affected fingers) undergoing partial palmar fasciectomy with either PIP or MCP joint contracture of varying degrees (group 1: < 15º, group 2: 15-30º;  group 3: > 30º). Surgical success rates were the same across all MCP joint groups, with complete contracture resolution at 6 months. However, for PIP joint involvement, contractures of  > 30º had a statistically lower contracture reduction index compared with groups 1 and 2. This study suggests that optimal results for PIP joints are achieved when contractures are 15-30º.[59]

Observation

Observation is appropriate for patients with unchanging, painless Dupuytren disease who have minimal contracture and no functional impairment.[60] Patients with mild Dupuytren disease can be monitored on an infrequent basis via a brief follow-up visit every 6-12 months. In addition to accurate measurement of the progression of the contractures, the follow-up also provides an opportunity to elicit a history of any functional deficits. Further, these visits allow assessment and discussion of the need for surgical referral.

Physical and occupational therapy

Stretching with the application of heat and ultrasonographic waves may be helpful in the early stages of Dupuytren contracture. The physical therapist also may recommend that the patient wear a custom splint or brace to stretch the fingers further. Range of motion (ROM) exercises should be performed several times a day. If the patient undergoes surgical correction of the contracture, physical therapy often is involved following the procedure. The postsurgical program consists of the following:

  • Wound care
  • Massage
  • Passive stretching
  • Active ROM exercises
  • Splinting

Through a course of occupational therapy, the patient may learn adaptive techniques and begin to use assistive devices that enhance functional abilities. For example, adaptive equipment can help a patient to open jars, despite contractures.

Corticosteroid injection

Intralesional triamcinolone acetonide (Kenalog-40) injections of 40 mg/mL have yielded subjective improvement in the size of Dupuytren nodules in some patients. In one study by Ketchum et al, patients received 60-120 mg injections of triamcinolone acetonide directly into the nodule, resulting in nodule regression in 97% of the hands after an average of 3 injections. However, 50% of patients experienced recurrence of nodules 1 to 3 years after their last injection, and those with mild MCP contractures (< 15º) did not have improvement in their contractures.[61]  Ketchum argues that early treatment of a nodule with an intralesional steroid injection, before the development of joint contracture (particularly PIP joint involvement), can interrupt the inflammatory process and thus the progression of disease.[62]

However, corticosteroid injections are associated with a high risk of complications, including fat atrophy and skin discoloration,[60] although in Ketchum et al's study nearly all patients saw resolution of atrophy and depigmentation by 6 months after the last injection.[61]  In addition, intralesional injection of corticosteroids can result in tendon rupture.

Tamoxifen

Transforming growth factor (TGF)-beta is a key cytokine in myofibroblast activation. Tamoxifen is an anti-estrogen known to modulate the production of TGF-beta and thus affect the activity of myofibroblasts in vitro and in vivo. Degreef et al studied the effect of high- dose tamoxifen given 6 weeks before and 12 weeks after surgery in Dupuytren disease patients with a strong predisposition toward fibrosis. In the short term (3 months post operatively) the tamoxifen group showed favorable outcomes, with smaller passive extension deficits compared with placebo (surgery alone), but this effect was lost within 2 years, with worsening of contractures after the medication was discontinued.[63]

Anti-TNF

Tumor necrosis factor (TNF) promotes the development of myofibroblasts, the cells responsible for the fibrosing process that lead to the contractures seen in Dupuytren disease. Anti-TNF agents inhibit myofibroblasts in vitro. An ongoing phase II trial is studying the use of adalimumab injected directly into diseased tissue in early Dupuytren disease. This is a two-part study, with the first part looking on a molecular level at tissue excised from patients injected with varying doses of adalimumab prior to surgery. The second part is a  multi-center, prospective study following patients receiving adalimumab at 3-month intervals and measuring nodule size, hardness, and disease progression compared with placebo, over a 1-year period.[64]

Radiotherapy

Radiotherapy can be effective in slowing disease progression in the early stages of Dupuytren contracture but was not effective in advanced disease. Radiotherapy did not reduce the rate of surgical intervention and was associated with a high rate of adverse events.[65]

5-Fluorouracil

5-Fluoruracil has been shown to cause a dose-dependent, selective and specific decrease in collagen production by fibroblasts and to inhibit fibroblast proliferation and myofibroblast differentiation.[66, 67] However, TGF-beta1 gene expression and procollagen type I and III messenger ribonucleic acid (mRNA) are not affected. After undergoing clinical trials, this treatment may find use as an adjuvant therapy to surgery in reducing extracellular matrix production and recurrence of Dupuytren contracture.[16]

Imiquimod

Imiquimod is an immune modulator that downregulates TGF-beta and fibroblast growth factor-2, which are important cytokines in the pathogenesis of Dupuytren contracture. Immune modification of profibrotic cytokines may be an innovative way to control disease. Imiquimod cream has been proposed as a therapy.[68] However, no reports have described experimental use of imiquimod for Dupuytren contracture.

Botulinum toxin

This has also been proposed as an intralesional therapy for Dupuytren contracture, based on its inhibition of Rho GTPase, which is necessary for the activation of the interleukin-1 inflammation pathway.[69] As with imiquimod, no reports currently describe clinical use of botulinum toxin for this condition.

Hyperbaric oxygen

Hyperbaric oxygen is another theoretical therapeutic option. Fibroblast and myofibroblast production may cease if hypoxic conditions are reversed by high tissue oxygenation.[16, 70]

Collagenase injection

Prior to February 2010, surgical intervention was the mainstay of treatment for Dupuytren disease despite a high rate of recurrence and complications.[71] In February 2010, the US Food and Drug Administration (FDA) approved collagenase Clostridium histolyticum (CCH; Xiaflex) at a dose of 0.58 mg per injection for the treatment of Dupuytren contracture in a single digit during a 30-day treatment cycle. Injected collagenase extracted from C histolyticum weakens and dissolves the Dupuytren cord.[72, 73]  This is a minimally invasive procedure done in office where collagenase is injected locally into the cord, then the following day the pathologic cord through passive extension is ruptured.

Over the years, this has become a first-line treatments for Dupuytren contractures.[58] Although this procedure is typically done without local anesthesia, Nordenskjold et al found that a nerve block using local injection of 10 ml of mepivacaine 20 minutes prior to CCH injection significantly reduced pain levels.[74]

FDA approval of CCH for the management of Dupuytren contracture was based on the results of CORD I and CORD I Extension, which were prospective, randomized, double-blind, placebo-controlled trials by Hurst et al in 308 patients with contractures greater than 20º. Findings included a reduction in contractures to less than 5º in 64% of collagenase-injected patients compared with 6.8% of patients treated with placebo. Patients with MCP involvement tended to improve to a greater extent, as did those patients with less severe flexion contractures.[2]

Glipin et al performed a 90-day double-blind placebo-controlled study with a 9-month open label extension evaluating the efficacy of CCH in Dupuytren disease in Australia, termed CORD II. Sixty six patients were enrolled: 45 in the treatment group and 21 in the placebo arm. The primary end-point was reduction of the contracture to 0-5º of normal, 30 days after the last injection. A statistically significant reduction in contracture was reported in the treatment group, with 44% of patients meeting the primary endpoint with treatment versus 4.8% of controls.[73]

Witthaut et al reported on the efficacy and safety of CCH in 2 open-label trials (JOINT I in the United States and JOINT II in Australian and Europe). Patients with fixed-flexion contractures of the MCP or PIP could receive up to 3 0.58-mg CCH injections per cord, with finger extension procedures 24 hours later. Dupuytren cords affecting 879 joints in 587 patients were injected. Clinical success was achieved in 57% of joints (MCP 70% success rate, PIP 37% success rate). The mean change in contracture was 55º for MCP joints and 25º for PIP joints.[75]

Peimer et al evaluated the long-term safety and efficacy of CCH in the CORDLESS study, which enrolled 1080 patients from the original 5 clinical trials (JOINT I, JOINT II, CORD I, CORD I extension, and CORD II). Patients were evaluated beginning 2 years after their first injection and then annually for a total of 4 years. Recurrence rate was 35% (MCP, 27%; PIP, 56%). In the original studies 301 joints were partially corrected; 50% of these had a nondurable response (MCP, 38%; PIP, 62%).[76]

Two additional studies of efficacy with CCH 2 years after treatment found results comparable to the CORDLESS study (although the doses used and definition of recurrence were slightly different).  Beeck et al evaluated 87 patients (88 joints) treated with CCH and found a recurrence (as defined as increase in passive extension deficit of > 20º) in 28.2% of MCP and 62.1% of PIP joints after 2 years.[77]  Lauritzson et al found that in 57 patients (59 hands), at 2 years following their CCH injection, 28% of the treated hands had recurrence (defined as active extension deficit > 20º), in MCP and PIPs joints equally.[78]  In both studies, the rate of complete correction was much higher with contractures of MCP joints (>80%) than of PIP joints (48-61%).[77, 78]

Anticlostridial type I collagenase and/or anti-clostridial type II collagenase antibodies were reported in 96% or more of patients who had received 2 or more CCH injections and in 82% who received one injection. No correlation of antibody titer to adverse events was reported. No new or long-term serious adverse events were noted, although the recurrence rate was noted to be lower in fully corrected joints than in partially corrected ones.[76]

Coleman et al studied the efficacy of concurrent injection injection of CCH into two Dupuytren cords. The study treated 12 subjects with more than three joint contractures. During the first treatment session, all subjects were injected with single dose of CCH (0.58 mg) into a single cord. Thirty days later, the same patients were injected at two different cords concurrently in the same hand. A mean reduction in joint contracture of 30º was obtained. All patients were satisfied with the outcome, and the rate of adverse events was similar to a single injection. This study suggested that two cords can be treated concurrently with safety profile similar to that of sequential treatment of the individual cords.[79]

In October 2014, the FDA  approved an expanded indication for CCH for the treatment of up to two Dupuytren contracture joints in the same hand during a single treatment visit.[80] A finger extension procedure can be performed at 24, 48, or 72 hours after injection.

Complications associated with CCH are common. In the Hurst et al study, an adverse event occurred in 96% of patients, although only 3 serious reactions were reported. The most common complications included injection site reactions, peripheral edema, bruising, bleeding, and pain. More serious reactions included tendon rupture and complex regional pain syndrome. To date, tendon rupture has been described in 0.3% of 1080 patients.[72]  There has also been one case report of a proximal phalanx fracture that occurred during attempted release of the contracture following CCH injection.[81]  Although the incidence of mild adverse affects with CCH can be high, with reports of between 46%-100% of patients experiencing one; these complications tend to be self-limiting and resolve quickly without sequelae.[82]   

Bear et al reported that patients with recurrent contractures in joints previously successfully treated with CCH may be effectively re-treated with up to 3 injections of CCH. In their study, 43 (86%) of 50 patients had a 20° or greater increase in range of motion after re-treatment, and the adverse event profile was consistent with that in previous studies.[83]

Bronier et al looked at the safety and efficacy of CCH injections in the treatment of palmar Dupuytren nodules using three different doses (0.25, 0.40, and 0.60 mg) versus placebo in an 8-week, double-blinded study. Their results showed a sigificant reduction in nodule size at 8 weeks with the 0.40-mg and 0.60-mg single injection compared with placebo and reduction in nodular consistency and hardness at weeks 4 and 8. The most common adverse events included bruising, extremity pain, and local swelling, but no trends for increased events were noted with using the higher dose; most patients expressed a high degree of satisfaction with CCH treatment.[84]

Surgical therapy

The goal of surgical care is to excise the diseased fascia to help prevent progression of the disease.[85] A patient should be referred to a hand surgeon if the MCP contracture is more than 30º or if any contracture of the PIP is present. Functional disability may be an indication for surgery if the patient accepts the associated morbidity and understands that surgery may not be curative. As with all elective surgeries, the patient's age, comorbid conditions, and ability to comply with postoperative care and rehabilitation also determine whether surgery is appropriate.

Surgical interventions consist mostly of fasciectomy.[86] Complete extension of affected joints may be possible with earlier intervention. However, any degree of PIP contracture carries a poor prognosis, and excising the involved fascia may not correct the joint contracture, especially if it has been long standing. MCP involvement is more amenable to surgical correction than PIP involvement, even in more advanced or long-standing cases. Subsequently, surgery is recommended as soon as a PIP contracture is detected.

A study found that improvement in the PIP joint contracture has a greater correlation with hand function at 6 and 12 months after surgery than does improvement in the MCP joint contracture.The results of another study revealed the severity of contracture preoperatively had a significantly negative effect on hand power, and older patients experienced less functional benefit from selective fasciectomy.[87] In bilateral cases, the initial operation is on the worst or dominant hand. If indicated, the other hand can be operated on 6-8 weeks after healing of the first hand.

If a patient needs to undergo surgical fasciectomy for Dupuytren disease and also requires a carpal tunnel release for carpal tunnel syndrome, a study recommends that both procedures be done concomitantly, as the complication rate is not significantly increased.[88]

For more information, see Surgery for Dupuytren Contracture.

Surgery versus percutaneous needle fasciotomy versus collagenase injection

In a study that compared CCH injection with limited fasciectomy in 132 patients with Dupuytren contracture, Zhou and colleagues reported no significant difference in the degree of residual contracture of the MCP joint (13° with CCH versus 6° with surgery; P = 0.095). With PIP joint treatment, residual contracture was significantly worse with CCH (25° versus 15° with surgery; P = 0.010). However, patients treated with CCH had more rapid recovery of hand function and experienced fewer serious adverse events than did those treated with fasciectomy.[89]

A prospective, single-blinded, randomized study in patients with an MCP contracture of 20° or more in a single finger found no significant differences in outcome after 1 year between the 69 patients randomized to CCH treatment and the 71 patients randomized to needle fasciotomy. In both groups, 90% of patients had full extension of the treated MCP joint.[90]

A meta-analysis by Sanjuan-Cervero et al looked at the safety and efficacy of CCH compared with fasciectomy and percutaneous needle fasciotomy (PNF) in Dupuytren disease. This study found that short- and medium-term improvement to joint movement achieved with CCH were similar to those achieved with fasciectomy, although fasciectomy did outperform CCH with regard to treatment of PIP joint contractures. CCH was associated with higher odds of mild, moderate, or serious complications, but these effects disappeared when mild adverse effects were removed from the equation. Further, these complications were mild, self-limited and resolved without sequelae.[82]

Toftgaard et al compared treatment of Dupuytren contractures in PIP joints with CCH versus PNF in an open-label, randomized, controlled trial. After 30 days, all patients treated with PNF and 89% of those treated with CCH had clinical improvement. However, at 2 years, 32% of PNF patients maintained clinical improvement compared with only 8% of CCH patients. In contrast, a study by Nydick et al of patients with mixed PIP and MCP joint contractures reported clinical success in 50% of PNF patients and 42% of CCH patients after 3 to 28 months. It is well established that PIP joint involvement appears more resistant to treatment compared with, MCP joint disease, which may explain the lower maintenace rates found by Toftgaard.[91]

Although treatment outcomes with CCH are comparable to surgery and PNF in the short term, CCH is less expensive but associated with higher rates of recurrence. Leafblad et al found in a retrospective review that CCH treatment had the greatest rate of repeat intervention with the highest cumulative cost over time, particularly for large PIP contractures and younger age at time of initial intervention. Fasciectomy had the highest initial cost but long-term costs were significantly less.[92]  However, a cost-utility analysis by Chen et al, based on quality-adjusted life years, found that an open partial fasciectomy was not cost effective compared with CCH.[93]

Recurrrence of disease is problematic across all treatment options. CCH and PNF have higher recurrence rates than fasciectomy, but the recurrence rate after 5 years with limited fasciectomy was 20.9%.[94]  Thus, even surgery is not a definitive cure for the disease. With recurrence, re-treatment after CCH or PNF with CCH or PNF is possible and satisfactory, and surgery after CCH is usually not considered to be more challenging than primary surgery (although there is some debate about this.[95]  However, with recurrence following surgery, surgical revision is much more difficult than the primary surgery.[96, 95]

There is no general agreement on treatment recommendations regarding the choice between PNF/needle aponeurotomy, surger,y and CCH at this time among hand surgeons. McMillan et al surveyed 36 hand surgeons from 9 countries including North America based on case scenarios and found little agreement on treatment recommendations. Those in practice longer were significantly less likely to recommend surgery and more likely to recommend collagenase injections rather than multiple treatments, and those with more experience in collagenase injections recommended CCH more frequently.[97]

Consultations

Surgical intervention may be appropriate in more severe cases. Consider surgical consultation with one of the following specialists:

  • Plastic surgeon

  • Orthopedic hand surgeon

Rehabilitation

Physical therapy

Stretching with the application of heat and ultrasonographic waves may be helpful in the early stages of Dupuytren contracture. The physical therapist also may recommend that the patient wear a custom splint or brace to stretch the fingers further. ROM exercises should be performed several times a day. If the patient undergoes surgical correction of the contracture, physical therapy often is involved following the procedure. The postsurgical program consists of the following:

  • Wound care
  • Massage
  • Passive stretching
  • Active ROM exercises
  • Splinting

Occupational therapy

Through a course of occupational therapy, the patient may learn adaptive techniques and begin to use assistive devices that enhance functional abilities. For example, adaptive equipment can help a patient to open jars, despite contractures.

Fasciotomy

Percutaneous needle fasciotomy/closed fasciotomy

Percutaneous needle fasciotomy (PNF) is a minimally invasive treatment that 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.[98, 99, 100, 101]

Needle fasciotomy may be an effective initial intervention in the treatment of Dupuytren contracture, either alone or as a first step to subsequent procedures such as repeated fasciotomy, fasciectomy, or CCH injection.[102]  

A study by Skov et al found that CCH is not superior to PNF for the treatment of isolated PIP joint Dupuytren contracture. At 2 years, clinical improvement was maintained in 29% of PNF patients (6 of 21), versus 7% of CCH patients (2 of 29). Complications (mostly transient) occurred in in 93% of the patients treated with CCH, versus 24% of the patients treated with PNF.[103]

In a study of 211 older patients (average age 65 y), investigators found a single digital nerve injury, no infections, and no tendon injuries with needle aponeurotomy, although damage to the neurovascular bundle is a concern. Recurrence rates (58%) and disease activity (69%) were high at 3-year follow-up.[104]

Foucher et al believed this technique was ideal for the elderly patient with a bowing cord and a predominant MCP joint contracture. Needle fasciotomy may also facilitate hygiene in a debilitated elderly patient. Limitations of fasciotomy in treating PIP joint contracture were noted.[104]

More recently, fat grafting in conjunction with PNF/percutaneous aponeurotomy has been studied with promising short-term results.  In Dupuytren disease, subdermal fat is lost as it is displaced by fibrosis, often leading to adherence of the fibrosed tissue to the skin.  Further, lipoaspirate containing stem cells may have an inhibitory affect on myofibroblasts (key cells in the process of fibrosis). Kan et al used lipofilling together with percutaneous aponeurotomy and had similar contracture correction results at 12 months compared with selective fasciectomy, but shorter recovery times and lower complication rates.[105, 106]  

Contraindications to PNF include the following[104] :

  • Infiltrating disease
  • Rapid recurrence in a young patient
  • Inaccessible, multiple cords
  • Chronic digital disease
  • Postsurgical recurrence in the digits

Open fasciotomy

An open fasciotomy is sometimes used to manage more severe cases of Dupuytren contracture, and is more effective in the long term when compared with needle aponeurotomy. Open fasciotomy is still an outpatient procedure performed under local anesthesia. An incision is made over the diseased cord and direct visualization of the cord and neurovascular structures is possible. The offending cord is divided at a point immediately underlying the skin incision.

Fasciotomy is usually most successful for MCP flexion contracture. The recovery is rapid, but the recurrence rate is high. Open fasciotomy is usually reserved for patients who cannot tolerate a more extensive procedure.

Segmental aponeurectomy/fasciotomy

Segmental aponeurectomy of Moermans is a procedure that is intermediate between simple fasciotomy and limited fasciectomy. Segments (1 cm in length) of fascia are excised through C-shaped incisions.[107, 108]

Fasciectomy

Regional (or selective) fasciectomy

This involves excising only the fascia that is grossly affected (eg. in the palm, pretendinous cords and involved natatory ligaments; in the fingers, only those structures that are visibly affected). Although the disease process clearly extends into clinically normal palmar fascia, this approach has proven successful in correcting MCP joint contractures and some PIP contractures and carries an acceptably low morbidity rate.

Areas not treated may develop disease. This method is commonly used to treat primary and recurrent disease. Skin incisions may be transverse, longitudinal, or diagonal/zigzag (eg, Z-plasty, Y-V-plasty, Bruner-type zigzag incision). Local advancement flaps, including an ulnar-based skin flap[109] and palmar inter-metacarpal flap[110] have been described.

In a study of selective fasciectomy, Hueston concluded that this procedure does not prevent recurrence of Dupuytren disease but does allow correction of deformity with more rapid recovery of hand function.[111]

Extensive or radical fasciectomy

This involves excision of the entire palmar fascia, including tissue that appears grossly healthy (in an effort to prevent recurrence). Although this procedure is not commonly performed today, it results in a relatively low recurrence rate of about 11%.[112] It does have an increased risk of morbidity postoperatively, including hematoma in 14% of cases and nerve irritation or damage in 6%. Patients are also prone to prolonged postoperative edema and stiffness. One study concluded that total aponeurectomy was most appropriate for stage 2 disease.[112]

Dermofasciectomy

This removes the diseased fascia and the overlying skin. The wound is then resurfaced and a full thickness skin graft is applied. Recurrence rates are low, being similar to those of extensive fasciectomy.[112] Because of the radical nature of this procedure, it is usually reserved for patients with recurrent or severe disease.

In dermofasciectomy, two incisions are made, one from the distal interphalangeal joint of the affected digit to the distal palmar flexion crease, and a transverse palmar incision, to form an L shape. A selective fasciectomy is performed, with partial closure of the incision site. A full-thickness skin graft is harvested from the hypothenar eminence during this surgery. A portion of the palm is left open, and an extension splint is applied. After 4 days, the splint is removed, the wound is cleaned, and the skin graft is applied to the palm. The palm is splinted again for 1 week.

General recommendations for surgical intervention

A fasciotomy or regional fasciectomy is usually sufficient to establish normal function in the MCP joint. The procedure of choice for PIP joint involvement is either dermofasciectomy or extensive fasciectomy.

Amputation may be recommended if digital contracture is greater than 90º or if vascular compromise has developed. Some patients may prefer amputation to the postoperative care required for fascial surgery.

Surgical Considerations

The surgeon and the patient may choose general or regional anesthesia during the procedure. Loupe magnification is used to aid visualization and detection of the delicate structures, specifically the neurovascular bundle.

A pneumatic tourniquet is typically used on the operative extremity to control blood loss and assist with visualization.

Incisions vary and may be transverse, zigzag, or longitudinal, depending on the region involved. The skin is separated from the underlying diseased palmar fascia and all neurovascular bundles that may be jeopardized during dissection are identified. The neurovascular bundles are often displaced or distorted by the contraction of the components of the palmar fascia.

After each neurovascular bundle has been identified and dissected away from the diseased palmar fascia, the diseased fascia is excised. The MCP joint is often fully corrected with this maneuver. PIP joints may have residual flexion at this stage and may require release of the flexor tendon sheath, as it can become shortened with chronic contracture.

The skin is closed with running or interrupted absorbable or non-absorbable suture material. A modified skin closure with Z-plasty or V-Y advancement can provide additional length without undue tension. If skin grafting is necessary to close the wound, use a full-thickness graft to minimize wound contracture during healing. Postoperatively, bandage the hand and place it in a splint.

Wound Closure

Skin overlying the contracture is closed either primarily (using skin grafts) or by secondary intention.

Open-palm technique

The open-palm technique (McCash technique) involves a transverse skin incision and division of the aponeurosis; healing is by secondary intention.

Jacobsen flap

A modification of the McCash technique, called the Jacobsen flap, uses the L-shaped incision of dermofasciectomy, but healing is by secondary intention.[113]

Synthesis technique

The synthesis technique is a method of wound closure that incorporates the advantages of tissue rearrangement, the open-palm technique, and full-thickness skin grafting. One study showed a decreased healing time and recurrence rate using the synthesis technique versus the traditional open-palm technique.[114, 115, 116]

Postoperative Care

Routine postoperative care is essential for an optimal outcome. Immediately following the procedure, a splint should be applied dorsally to avoid excess pressure on the incision site. The hand should be placed in extension with flexion of the MCPs and extension of the PIPs. Initially, the splint is worn continuously, with removal only for dressing changes and exercise.[117] Patients who undergo PIP surgery should wear the brace for 6 weeks on a continual basis and may require 3 months of bracing to minimize scar contractures.

The overall goal of splinting is to provide a prolonged stretch to the tissues and prevent flexion contractures. Splinting is modified over the next 8-10 weeks to accommodate range of motion, with the splint worn primarily at night. However, studies investigating orthoses after surgery have not been high quality and are vulnerable to various sources of bias. Further, orthosis use is associated with potential adverse effects such as pain, slower return of function, joint stiffness and edema. A systematic review by Samargandi et al of night orthosis after surgery, which examined 3 randomized control trials and 4 observational trials, did not find a significant difference in total active extension or Disabilities of the Arm, Shoulder, and Hand (DASH) scores regardless of whether night orthotics were used or not.  Nonrandomized studies showed contrasting results;[118] thus, further research is needed to clarify the utility of post-surgical splinting.

A specific exercise regimen with an occupational therapist should be instituted with range-of-motion exercises 1 week postoperatively. A rehabilitation program is critical for successful management of these patients; it helps to reduce swelling, improve wound healing, and restore finger mobility and function.[119]

Rehabilitation following surgery is a gradual process of increasing activity and decreasing splinting to achieve increased range of motion. According to one study, therapy that avoids applied mechanical tension in the early postoperative phase results in fewer complications, with no digital motion lost to extension.[120]

The occupational therapist regularly records the patient’s degree of extension to assist in monitoring the patient’s progress. Maximal results are evident 6 weeks postoperatively. Return to normal activity is expected in 2-3 months.

 

Medication

Medication Summary

In February 2010, the US Food and Drug Administration (FDA) approved collagenase Clostridium histolyticum (Xiaflex) for the treatment of Dupuytren contracture. Injected collagenase extracted from C histolyticum weakens and dissolves the Dupuytren cords.[2, 121, 122, 123]

Complications associated with collagenase C histolyticum are common; they include injection site reactions, peripheral edema, bruising, bleeding, and pain. More serious reactions include tendon rupture and complex regional pain syndrome. (To date, tendon rupture has been described in 0.3% of 1082 patients.)[2]

Intermittent reports detail a decrease in the size of nodules with the use of corticosteroid injections. However, corticosteroids are associated with a high risk of complications, including fat atrophy and skin discoloration.[60] In addition, intralesional injection of corticosteroids can result in tendon rupture.

Because Dupuytren contracture is generally painless, analgesic medications usually are not required.

Enzymes

Class Summary

Collagenase Chistolyticum was approved in February 2010 for percutaneous fasciotomy. Collagenase Chistolyticum is a protease that hydrolyzes collagen and breaks down its triple helix conformation, thus disrupting the Dupuytren cord. It is composed of 2 purified microbial collagenases and is indicated only for those patients with a palpable cord.

Collagenase Clostridium histolyticum (Xiaflex)

This is a proteinase that hydrolyzes collagen in its native triple-helical conformation, resulting in lysis of collagen deposits. Injection into a Dupuytren cord (composed mostly of collagen) may result in enzymatic disruption of the cord. Injection is indicated for Dupuytren contracture with a palpable cord.

Corticosteroids

Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli.

Triamcinolone (Kenalog-40, Aristospan)

Triamcinolone is used in the treatment of inflammatory dermatosis responsive to steroids. It decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

 

Questions & Answers

Overview

What is Dupuytren contracture?

What are the stages of Dupuytren contracture?

How is Dupuytren contracture graded?

What is the anatomy of the hand relevant to Dupuytren contracture?

How are the cardinal features of Dupuytren contracture characterized?

What is the role of immunologic factors in the etiology of Dupuytren contracture?

What is the pathophysiology of Dupuytren contracture?

What is the role of genetics in the etiology of Dupuytren contracture?

What are the risk factors for Dupuytren contracture?

What is the role of trauma in the etiology of Dupuytren contracture?

What is the role of diabetes mellitus in the etiology of Dupuytren contracture?

What is the role of smoking in the etiology of Dupuytren contracture?

What is the role of androgens in the etiology of Dupuytren contracture?

What is the role of epilepsy and antiepileptic medications in the etiology of Dupuytren contracture?

What is the role of barbiturate medications in the etiology of Dupuytren contracture?

What is the role of HIV infection in the etiology of Dupuytren contracture?

What is the prevalence of Dupuytren contracture?

What is the morbidity associated with Dupuytren contracture?

What are the racial predilections of Dupuytren contracture?

What are the sexual predilections of Dupuytren contracture?

Which age groups have the highest prevalence of Dupuytren contracture?

What is included in the patient education about Dupuytren contracture?

Presentation

What are the signs and symptoms of Dupuytren contracture?

Which conditions may be associated with Dupuytren contracture?

Which clinical history findings are characteristic of Dupuytren contracture?

Which physical findings are characteristic of Dupuytren contracture?

DDX

How is trigger finger differentiated from Dupuytren contracture?

How is stenosing tenosynovitis and ganglion cyst differentiated from Dupuytren contracture?

How is sarcoma differentiated from Dupuytren contracture in younger patients?

Which conditions are included in the differential diagnoses of Dupuytren contracture?

What are the differential diagnoses for Dupuytren Contracture?

Workup

How is Dupuytren contracture diagnosed?

Which histologic findings are characteristic of Dupuytren contracture?

What are the histologic stages of Dupuytren contracture?

Treatment

How is Dupuytren contracture treated?

When is observation indicated for the treatment for Dupuytren contracture?

What is the role of rehabilitation therapies in the treatment of Dupuytren contracture?

What is the role of corticosteroid injection in the treatment of Dupuytren contracture?

What is the role of tamoxifen in the treatment of Dupuytren contracture?

What is the role of anti-tumor necrosis factor (TNF) in the treatment of Dupuytren contracture?

What is the role of radiotherapy in the treatment of Dupuytren contracture?

What is the role of 5-Fluorouracil in the treatment of Dupuytren contracture?

What is the role of imiquimod in the treatment of Dupuytren contracture?

What is the role of botulinum toxin in the treatment of Dupuytren contracture?

What is the role of hyperbaric oxygen in the treatment of Dupuytren contracture?

What is the role of collagenase injection in the treatment of Dupuytren contracture?

What is the role of surgery in the treatment of Dupuytren contracture?

What is the efficacy of collagenase Clostridium histolyticum (CCH; Xiaflex) injection in the treatment of Dupuytren contracture?

Which specialist consultations are beneficial to patients with Dupuytren contracture?

What is the role of physical therapy in the treatment of Dupuytren contracture?

What is the role of occupational therapy in the treatment of Dupuytren contracture?

What is the role of percutaneous needle fasciotomy (PNF) in the treatment of Dupuytren contracture?

What are the contraindications to percutaneous needle fasciotomy (PNF) to treat Dupuytren contracture?

What is the role of open fasciotomy in the treatment of Dupuytren contracture?

What is the role of segmental aponeurotomy in the treatment of Dupuytren contracture?

What is a regional (selective) fasciectomy in the treatment of Dupuytren contracture?

What is an extensive (radical) fasciectomy in the treatment of Dupuytren contracture?

What is a dermofasciectomy in the treatment of Dupuytren contracture?

How is surgery selected for Dupuytren contracture?

How is surgery performed for the treatment of Dupuytren contracture?

What are the options for wound closure following surgery for Dupuytren contracture?

What is included in postoperative care following fasciectomy for the treatment of Dupuytren contracture?

Medications

What is the role of medications in the treatment of Dupuytren contracture?

Which medications in the drug class Corticosteroids are used in the treatment of Dupuytren Contracture?

Which medications in the drug class Enzymes are used in the treatment of Dupuytren Contracture?