AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Dupuytren contracture is a benign, slowly progressive fibroproliferative disease of the palmar fascia that has no clear etiology or pathogenesis. Plater first described this condition in 1614, but Dupuytren presented a meticulous anatomical study in 1831 that established the palmar fascia as the site of origin, which distinguishes it from other causes of finger contracture. Dupuytren also devised an effective surgical approach through palmar fasciotomy.

Dupuytren contracture is most commonly observed in persons of northern European descent and may be severe enough to result in debilitating finger contractures. Most patients are affected bilaterally (65%); in unilateral cases, the right side is affected more often than the left. The most commonly involved digit is the ring finger, followed by the small finger, and then the middle fingers. The index finger and thumb are typically spared.

Although the etiology is unclear, 27-68% of patients report a positive family history, which provides strong evidence for a genetic influence. Males are more likely to be affected than females, and the symptoms of the disease are more severe in males. In some studies, manual laborers have a slight predominance of disease (45%) compared with non–manual laborers (41%). Risk factors include prior hand trauma (13%), alcoholism (10%), diabetes mellitus (8%), epilepsy (2%), cigarette smoking, myocardial infarction, and HIV infection.¹

Pathophysiology

The basic pathophysiology of Dupuytren contracture is fibroblast proliferation and collagen deposition. Why this uncontrolled proliferation of palmar fascia begins and why it continues to the point of debilitating flexion contractures remain unknown. Studies implicate growth factors, including basic fibroblast growth factor, platelet-derived growth factor, and transforming growth factor-beta.² These factors show increased expression within the diseased fascia.

The disease progresses in several stages. The proliferative stage is characterized by the development of a nodule or nodules, the pathognomonic lesion of Dupuytren contracture. Nodules are composed of fibroblasts and type III collagen. The proliferative stage is the most biologically active phase of disease. Multiple nodules are common and may be tender to palpation. They are often located near the distal palmar crease but may be found throughout the palm and even in the digits.

Once the nodules are well-established, the active contractile, or involutional, stage begins. This phase is a more advanced disease state, but it is somewhat less biologically active than the proliferative stage. Cords begin to develop proximal to the nodules, and grooves or pits in the skin denote skin fixation to the underlying fascia. During this phase, myofibroblasts replace fibroblasts as the predominant cell type; they show morphologic similarities to fibroblasts and smooth muscle cells. Myofibroblasts are capable of manufacturing collagen and causing contraction because they contain myofibrils within the cells. Myofibroblasts also have intercellular connections to each other, permitting the generation of synchronized contractile forces. These cells are found not only within palpable nodules and cords but also as individual cells or groups of cells throughout the entire palmar fascia.

Histologically, the involutional stage demonstrates a predominance of collagen types III and V and an accompanying expansion of extracellular matrix, particularly glycosaminoglycans. Collagen and glycosaminoglycan deposition is similar to that seen in healing wounds. Occurring throughout the palmar fascia, these changes mirror those observed in the active stages of tissue repair and remodeling and are not isolated in the cords and nodules. Whether the changes are partly responsible for the resulting contractures or are merely the result of the physical forces being applied to the palmar fascia is unknown.

Advanced disease is referred to as the residual stage, which is the most biologically quiescent phase. Nodules regress and metacarpophalangeal (MCP) joint or proximal interphalangeal (PIP) joint contractures become most severe. Tendonlike cords are visible and contain densely packed, inelastic, longitudinally oriented collagen fibers, predominantly type I. At this stage, relatively few cells remain.

Frequency

United States

Dupuytren contracture is common, reflecting immigration from northern Europe. Approximately 5-15% of males older than 50 years are affected.

International

In Norway, approximately 5.6% of individuals older than 60 years are affected. In Australia, 26% of males and 20% of females older than 60 years are affected.

Mortality/Morbidity

Morbidity is limited to lifestyle changes. MCP joint and PIP joint contractures may interfere with daily living activities, and lesions may be tender. Occasionally, Dupuytren contracture is associated with plantar fasciitis or Peyronie disease.

Race

Dupuytren contracture is very common in northern Europe and the United Kingdom and in countries inhabited by immigrants from these areas (eg, Australia, Canada, United States).

• It is less common in individuals of southern European descent.
• Dupuytren contracture is less common in blacks and Asians. Incidence in these populations is less than 3%. Disease in these individuals more often involves the palm rather than the digits; therefore, it is less likely to be clinically significant or to cause the patient to seek medical attention. Consequently, incidence in these populations may be underreported.
• Dupuytren contracture is least common (incidence <1%) among Indians, Native Americans, and individuals of Hispanic descent.

Sex

Approximately 80% of affected individuals are male. This male predisposition is consistent throughout all countries and races studied.

Age

Incidence increases with age. See Frequency for related statistics.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

Obtain a thorough medical history when evaluating a patient thought to have Dupuytren contracture. Conditions possibly related to this disease include the following:

• Diabetes mellitus
• Alcoholism
• HIV infection
• Epilepsy
• Trauma
• Manual labor
• Cigarette smoking
• Previous myocardial infarction

Physical

Perform a thorough physical examination before focusing on the involved hand or hands. Important points to assess during physical examination of involved extremities include the following:

• Firm nodules that may be tender to palpation
• Cords proximal to the nodules that are usually painless
• Skin blanching upon active finger extension
• Atrophic grooves or pits in the skin, denoting adherence to the underlying fascia
• Tender knuckle pads over the dorsal aspect of the PIP joints: If present, aggressive disease is indicated.
• Presence of MCP or PIP joint contractures: Objectively measure and record degree of flexion contracture to investigate possible compensatory distal interphalangeal (DIP) joint hyperextension or DIP joint contracture.

Causes

• Dupuytren contracture is probably genetic in origin. Several studies suggest an autosomal dominant pattern of inheritance with variable penetrance.^{3, 4}
• HLA-B7 and HLA-DR3 have been identified in a number of patients, suggesting a possible immunologic influence as well.
• Other authors suggest that Dupuytren contracture may result from an error in growth and regulation of the fibroblast, resulting from chromosomal changes similar to those seen in cells undergoing neoplastic change. Trisomy 8 abnormality has been identified in the fibroblasts excised from some patients. Nodules certainly display some features of a benign neoplasm.
• Because the changes occurring in the palmar fascia approximate the normal stages of wound repair and remodeling, but to an excessive and detrimental extent, another theory holds that this disease is a response to trauma. One observation suggests that the subdermal fat pads in the palm gradually disappear with age in the races most affected by this process. This regression may expose the underlying fascia to trauma. Repeated exposure to compression, stress, and other mechanical forces may trigger a reparative process in the palmar fascia. The reason for the progression to severe joint contractures remains unknown.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Palmar tendinitis

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• No routine diagnostic laboratory studies apply to this disorder.

Histologic Findings

Early disease shows nodules with a predominance of fibroblasts and type III collagen. In the active contractile phase, fibroblasts are replaced by myofibroblasts, and collagen types III and V predominate. During this stage, glycosaminoglycans increase 11-fold and dermatan sulfate increases 4-fold. Advanced disease is relatively acellular with a predominance of type I collagen in tendonlike cords.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

No medical treatment has long-term value in halting or reversing the progression of contracture.

Surgical Care

The goal of surgical care is to excise or incise the diseased fascia. This treatment does not cure the disease but is meant to prevent progression to severe debilitating joint contractures.

• Indications for surgery
• • Surgery is indicated with MCP joint contracture of 30° or more. When the MCP joint is involved, surgical intervention is not urgent because even long-standing and severe contractures of the MCP joint are usually corrected readily after surgery and usually do not recur.
  • PIP joint contractures do not carry the same prognosis. Excising or incising involved fascia may not correct the joint contracture, particularly those of long duration. Proceed with surgery as soon as PIP joint contractures are observed.
  • Functional disability is a subjective symptom that may be an indication for surgery, but only if the patient clearly understands the potential morbidity and that the process is occasionally exacerbated by the operation.
  • In bilateral cases, the worst or dominant hand should be operated on first, allowing an interim healing period of 6-8 weeks before proceeding with surgery on the contralateral hand.
• Choice of operation
• • Fasciotomy involves incising the involved fascia and may provide short-term relief but is also associated with a very high recurrence rate. This procedure may correct an MCP joint contracture but almost certainly will not correct a PIP joint deformity. Reserve fasciotomy for elderly or debilitated patients who are unable to tolerate a more lengthy procedure.
  • Extensive fasciectomy involves removing as much fascia as possible, including that which is grossly normal. Today, this procedure is not commonly performed because of the increased associated morbidity, including hematoma risk and prolonged postoperative edema and stiffness. Some authors prefer to leave the skin wound open to heal by secondary intention as a means of decreasing hematoma risk.
  • Dermofasciectomy removes the diseased fascia and the overlying skin. Resurface the wound with a full-thickness skin graft. Recurrence rates are quite low with this approach. Because of the radical nature of this procedure, it is usually reserved for patients with recurrent or severe disease.
  • Regional fasciectomy involves excising only grossly involved fascia. Although the disease process clearly extends into clinically normal palmar fascia, this approach has proven successful in correcting MCP joint contractures and some PIP joint contractures and carries an acceptably low morbidity rate.
  • • Use loupe magnification during the procedure to help identify and preserve delicate structures. Use general, axillary block, or Bier block anesthesia. Place a pneumatic tourniquet on the operative extremity. Insufflate the tourniquet after the arm has been exsanguinated with elastic wrap or elevation.
    • Incisions vary and may be transverse, zigzag, or longitudinal, depending on the region involved. Elevate the skin off the underlying diseased palmar fascia. Identify all the neurovascular bundles that may be in jeopardy during dissection and subsequent excision. Each involved finger has a radial and ulnar neurovascular bundle that must be identified. Identify the bundles from proximal to distal, or vice versa, depending on surgeon preference and ease of dissection. The neurovascular bundles may be displaced, distorted, or centralized by the contraction of the components of the palmar fascia. Usually, a plane of dissection between the diseased palmar fascia and neurovascular bundles can be developed with careful blunt dissection. Immediately repair any inadvertent injury to the neurovascular bundle under surgical microscope.
    • After the full course of each neurovascular bundle has been identified and dissected away from the diseased palmar fascia, excise the diseased fascia. The MCP joint is usually fully corrected with this maneuver. Manage PIP joints that have residual flexion of less than 30° with postoperative splinting and hand therapy.
    • If PIP joint flexion is still greater than 30° following fasciectomy, consider whether further procedures would improve function. The initial step should be to release the flexor tendon sheath because the flexor tendon may become foreshortened secondary to the prolonged contracture and may be causing the residual deficit. If this fails to improve PIP extension, consider releasing the accessory collateral ligaments from the volar plate. Alternatively, consider releasing the checkrein ligaments or proximal attachment of the volar plate to the proximal phalanx. If these maneuvers fail to improve the flexion contracture, proceed to closure and use an aggressive course of postoperative splinting and hand therapy to improve function.
    • Release the pneumatic tourniquet and cauterize the bleeding sites with bipolar cautery. Use meticulous hemostasis to prevent postoperative hematoma. Close the skin with interrupted or running absorbable or nonabsorbable suture material. Consider modifying skin closure with a Z-plasty or V-Y advancement to 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, dress the hand and place it in a splint. Immobilize the wrist in neutral or slight flexion to relax the palmar skin and to allow MCP and PIP joint extension.

Consultations

• Hand surgeon
• Occupational therapist

Activity

Postoperatively, maintain the hand in the original dressing and splint and strictly elevate for 2 days. At this time, follow-up care with the hand surgeon and referral to an occupational therapist is required; ideally, the patient should see both simultaneously. After removing the initial surgical dressing, fit the patient with a comfortable Thermoplast splint, which should be worn throughout the rehabilitative process. A static dorsal forearm splint with the wrist in neutral or slight flexion that permits the use of uninvolved fingers is recommended. This splint counteracts the natural tendency of scars to contract and helps overcome any residual PIP joint contracture.

• Rehabilitation is a gradual process of increasing activity and decreased splinting to achieve optimal restoration of movement. Frequent visits to the occupational therapist help to restore preoperative flexion and to maintain extension gained at the time of surgery. Patient motivation and severity of disease dictate the intensity and duration of therapy.
• The splint may be removed several times daily beginning on postoperative day 2 to allow active and passive range of motion of the digits. Provide adequate oral analgesics to promote patient comfort and therapy compliance. Activity may be increased as tolerated, and heat applied prior to therapy may improve tissue elasticity and patient comfort.
• Request the occupational therapist to regularly record objective measurements of function to monitor progress, facilitate communication with the hand surgeon, and encourage patient compliance. The patient should perform simple exercises at regular intervals every day.
• Final results are realized in approximately 6 weeks. Following this period, patients should wear the splint nightly for an additional 3-6 months, at the discretion of the occupational therapist and hand surgeon, to maintain extension and prevent scar contracture. Silastic pads, stretching, and scar massage are useful adjuncts to promote scar softening and maturation. The patient can expect to return to normal activities within 2-3 months.

MEDICATION

Section 7 of 11  

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• References

Proposed medications have included allopurinol, colchicine, calcium channel blockers, interferon-gamma, vitamin E, intralesional steroids, and intralesional enzymes; however, none has long-term efficacy in the treatment or recurrence of this disease.

FOLLOW-UP

Section 8 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• See the Activity section for details on postoperative therapy.

Further Outpatient Care

• See the Activity section for details on postoperative therapy.

Complications

• The overall incidence of complications following surgery is 20%.
• The most common complications include postoperative joint stiffness and loss of preoperative flexion, further emphasizing the importance of a postoperative rehabilitation program.
• Significant hand arthritis is a relative contraindication to surgery because these patients are at an extremely high risk of worsened hand function after surgery.
• Other complications may include hematoma, skin loss, infection, nerve injury, vascular injury, prolonged edema, and reflex sympathetic dystrophy.

Prognosis

• Long-term overall recurrence is approximately 50% and can be in the same area of the hand or in a new area.
• MCP joint contractures are readily corrected with surgery (80-96%) and usually do not recur.
• PIP joint contractures are usually not completely corrected (20-56% are corrected) and are occasionally exacerbated by surgery (25%).

MISCELLANEOUS

Section 9 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Patients must understand that surgery is not a cure; it is only a means of relieving some disability. Furthermore, patients should have realistic expectations of results. Emphasize that hand function may actually be worsened with surgery. Explain that reflex sympathetic dystrophy is a possible complication.
• Explain that intense rehabilitation must be undertaken following surgery.
• With realistic expectations, clear documentation, meticulous surgical technique, and attention to postoperative rehabilitation, a mutually beneficial outcome can usually be achieved.

MULTIMEDIA

Section 10 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Typical appearance of Dupuytren contracture of the small finger.
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Media file 2:  Arrow denotes the typical cords of Dupuytren contracture. These cords are usually painless. Note the metacarpophalangeal joint contracture.
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Media file 3:  Arrow denotes the cord often present in Dupuytren contracture. Metacarpophalangeal joint and proximal interphalangeal joint contractures are also present.
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Media file 4:  Arrows denote the firm nodules that may be the initial physical finding in Dupuytren contracture. These nodules may be tender upon palpation or painful with extension of the corresponding digit.
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Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

1. Ross DC. Epidemiology of Dupuytren's disease. Hand Clin. Feb 1999;15(1):53-62, vi. [Medline].
2. Badalamente MA, Hurst LC. The biochemistry of Dupuytren's disease. Hand Clin. Feb 1999;15(1):35-42, v-vi. [Medline].
3. Benson LS, Williams CS, Kahle M. Dupuytren's contracture. J Am Acad Orthop Surg. Jan-Feb 1998;6(1):24-35. [Medline].
4. Burge P. Genetics of Dupuytren's disease. Hand Clin. Feb 1999;15(1):63-71. [Medline].
5. Boyer MI, Gelberman RH. Complications of the operative treatment of Dupuytren's disease. Hand Clin. Feb 1999;15(1):161-6, viii. [Medline].
6. Dupuytren G. De la retraction des doigts par suite d'une affection de l'apponeurose palmaire. J Univ Med Chir Paris. 1831;5:352.
7. Elliot D. The early history of Dupuytren's disease. Hand Clin. Feb 1999;15(1):1-19, v. [Medline].
8. Fitzgerald AM, Kirkpatrick JJ, Naylor IL. Dupuytren's disease. The way forward?. J Hand Surg [Br]. Aug 1999;24(4):395-9. [Medline].
9. Hurst LC, Badalamente MA. Nonoperative treatment of Dupuytren's disease. Hand Clin. Feb 1999;15(1):97-107, vii. [Medline].
10. Jabaley ME. Surgical treatment of Dupuytren's disease. Hand Clin. Feb 1999;15(1):109-26, vii. [Medline].
11. Lubahn JD. Open-palm technique and soft-tissue coverage in Dupuytren's disease. Hand Clin. Feb 1999;15(1):127-36. [Medline].
12. Meek RM, McLellan S, Crossan JF. Dupuytren's disease. A model for the mechanism of fibrosis and its modulation by steroids. J Bone Joint Surg Br. Jul 1999;81(4):732-8. [Medline].
13. Mullins PA. Postsurgical rehabilitation of Dupuytren's disease. Hand Clin. Feb 1999;15(1):167-74, viii. [Medline].
14. Rayan GM. Clinical presentation and types of Dupuytren's disease. Hand Clin. Feb 1999;15(1):87-96, vii. [Medline].
15. Tomasek JJ, Vaughan MB, Haaksma CJ. Cellular structure and biology of Dupuytren's disease. Hand Clin. Feb 1999;15(1):21-34. [Medline].
16. Tubiana R. Dupuytren's disease of the radial side of the hand. Hand Clin. Feb 1999;15(1):149-59. [Medline].
17. Yi IS, Johnson G, Moneim MS. Etiology of Dupuytren's disease. Hand Clin. Feb 1999;15(1):43-51, vi. [Medline].

Article Last Updated: Nov 30, 2007