AAOS Comprehensive Orthopaedic Review

Section 9 - Hand and Wrist

Chapter 88. Dupuytren Contracture

I. Relevant Anatomy and Disease Patterns

A. Fibers/pretendinous bands (

Figure 1)

 

1. In the proximal palm, fibers of the palmar fascia are contiguous with the palmaris longus or deep fascia of the forearm and continue distally toward the digits as pretendinous bands; each band lies superficial to the corresponding flexor tendon sheath for that digit.

 

2. At the level of the distal palmar crease (DPC), transverse fibers of the palmar fascia run just dorsal to the pretendinous bands and are not involved in the contractile process seen in Dupuytren contracture; the disease affects structures along longitudinal lines of tension.

 

3. Beyond the DPC, the pretendinous band fibers divide into three layers, along which the disease process also follows.

 

a. Layer 1—The pretendinous band sends off skin attachment fibers between the DPC and metacarpophalangeal (MCP) crease; when these fibers become diseased, nodules and skin pits form at this level.

 

b. Layer 2—Spiral bands emerge from either side of the pretendinous band to descend along either side of the flexor sheath, passing underneath the neurovascular bundle (relationship becomes important when the spiral band becomes involved in the contracture) to merge with the lateral digital sheet.

 

c. Layer 3—Flimsy perforating fibers from the pretendinous band pass dorsally around either side of the MCP joint, merging with the extensor tendons.

 

B. Natatory ligament—This transverse structure resides just under the skin at each commissure, sending fibers distally along the lateral border of each digit to merge with the lateral digital sheet.

 

C. Lateral digital sheet—Running lateral to and alongside the neurovascular bundles, the lateral digital sheet is formed by merging fibers of the spiral band and natatory ligament.

 

D. Grayson and Cleland ligaments

 

1. Maintain digital skin position relative to deeper structures

 

2. The Grayson ligament is palmar to the neurovascular bundle and passes from the flexor sheath to the skin.

 

3. The Cleland ligament is dorsal to the bundle and arises from the phalanges.

 

4. The Cleland ligament is relatively uninvolved in Dupuytren contracture.

 

5. The Grayson ligament can become part of a lateral cord when it joins the diseased lateral digital sheet.

 

E. Bands and cords—Normal anatomic structures are called bands; diseased or contracted structures are referred to as cords (

Figure 2).

 

1. Central cord

 

a. Results from disease involvement of the pretendinous bands

 

[Figure 1. Normal fascial anatomy of the palm and digits, illustrating relationships to the tendon sheath and neurovascular bundles.]

[Figure 2. Patterns of diseased cords. The spiral cord (derived from the pretendinous band, spiral band, Grayson ligament, and lateral digital sheet) displaces the neurovascular bundle toward the midline. The Grayson ligment is seen as an isolated thickened structure. The lateral cord comes off the natatory cord to merge with the lateral digital sheet along the midaxial line.]

b. Palmar nodules and pits form beyond the DPC.

 

c. Fibers from the cord extend and insert along the flexor sheath around the proximal interphalangeal (PIP) joint level; this usually results in MCP joint contracture.

 

d. The central cord is not involved with the neurovascular bundle.

 

2. Spiral cord

 

a. The spiral cord results from contracture of the spiral bands that pass dorsal to the neurovascular bundle to merge with the lateral digital sheet and the Grayson ligament; this generally results in contracture of the PIP joint.

 

b. The term "spiral cord" may be a misnomer because the structure actually becomes thickened and straight as it becomes diseased; as this occurs, it displaces the neurovascular bundle superficially and at the midline, rendering the bundle vulnerable to injury during disease resection.

 

[

Figure 3. The retrovascular cord arises from the preaxial phalanx and courses dorsal to the neurovascular bundle to insert in the side of the distal phalanx. It is the usual cause of DIP joint contractures.]

c. The components forming the spiral cord are the pretendinous band, spiral band, lateral digital sheet, and Grayson ligament.

 

3. Natatory cord

 

a. The natatory cord develops from the distal fibers of the natatory ligament, just under the commissure skin.

 

b. It results in a web space contracture.

 

4. Retrovascular cord (Figure 3)

 

a. The retrovascular cord can arise dorsal to the neurovascular bundle, taking origin from the proximal phalanx and inserting onto the distal phalanx.

 

b. It is the usual cause for a distal interphalangeal (DIP) joint contracture.

 

5. Nodules often appear before actual contractile cords.



II. Pathology

A. Origin and progression

 

1. The disease originates in longitudinally oriented fascial structures.

 

2. The early proliferative phase is characterized by high cell concentrations of immature fibroblasts and myofibroblasts in a whorled pattern; this early hypercellular structure is often referred to as a histologic nodule.

 

3. In the involutional phase, fibroblasts align along tension lines and produce more collagen.

 

4. The final residual phase is relatively acellular and features contracted, collagen-laden tissue more characteristic of scar formation.

 

B. Myofibroblast—The cellular contractile culprit of Dupuytren contracture.

 

1. The myofibroblast differs from the fibroblast in that it has actual bundles of contractile actin microfilaments arranged parallel to the long axis of the cell.

 

2. Adjacent myofibroblasts connect via extracellular fibrils of fibronectin and act together to generate the contracted tissue seen in Dupuytren contracture.

 

C. Type III collagen is more prevalent in the extracellular matrix in Dupuytren disease.

 

D. Other factors

 

1. Transforming growth factor-β1 (TGF-β1), TGF-β2, epidermal growth factor, platelet-derived growth factor, and connective tissue growth factor all have been suggested to play a role in initiating abnormal cellular proliferation.

 

2. Increasing levels of mechanical tension have also been shown to influence fibroblast differentiation into myofibroblasts.



III. Epidemiology

A. Race/geography—Dupuytren disease is seen more frequently in Caucasians and in individuals of northern European ancestry.

 

B. Autosomal dominant inheritance pattern

 

C. Links to other comorbidities remain incompletely understood.

 

1. Dupuytren disease appears to be linked to diabetes mellitus.

 

2. Associations with seizure disorders may be the result of antiseizure medications, but this remains unknown.

 

3. Links with alcoholism and HIV are also suggested.

 

D. Occupational/activity factors—No evidence currently exists to suggest that any occupation or activity plays any role in the development of Dupuytren contracture.



IV. Treatment

A. Nonsurgical

 

1. Clinical trials are underway regarding injection of clostridial collagenase into Dupuytren cords to produce lysis and rupture.

 

2. Although early results have been encouraging, definitive word on the efficacy of this method is still pending.

 

B. Surgical

 

1. Severity—Some patients clearly have more aggressive forms of the condition (relatively young age, rapid recurrence following surgery, rapid progression, multifocal disease in other sites such as plantar feet, penis, and knuckle pads), representing a true Dupuytren diathesis.

 

2. Indications

 

a. The mere presence of a nodule, cord, or mild joint contracture does not guarantee that the condition will progress to greater degrees of contracture and functional impairment.

 

b. If findings are mild without significant difficulty with daily activities, it is reasonable to follow the patient at repeated intervals to check for progression.

 

c. MCP joint contractures are easier to correct (and more likely to stay corrected) than are PIP joint contractures.

 

i. Prolonged contractures of the MCP joint can usually be fully corrected with excision of diseased Dupuytren tissue alone.

 

ii. PIP joints develop contracture of secondary palmar structures after prolonged disease and may require a more comprehensive release of the volar plate, accessory collateral ligaments, and flexor sheath to restore extension.

 

iii. PIP joint stiffness, flexion contracture, and instability are recognized undesirable outcomes following attempts at release of severe or prolonged contracture.

 

3. Technical points/issues

 

a. If patients are in poor medical condition and may not tolerate a general anesthetic, limited fasciotomy of diseased cords can be considered; this is more effective and safe for contracted cords in the palm.

 

b. Limited fasciectomy entails removal of all diseased tissue in a ray (or rays), with dissection generally proceeding in a proximal-to-distal direction; despite the term "limited," accomplishing this may require a great deal of dissection in a given ray. Dermofasciectomy, arthrodesis, or amputation may be required in recurrent, advanced disease.

 

c. Radical fasciectomy involves release of all palmar fascia, even that which does not appear to be diseased.

 

d. A variety of skin incisions can be used and should be individualized for the location of diseased tissue, presence of recurrence or diseased skin, and need for potential lengthening of skin lines.

 

e. Brunner zigzag incisions, multiple V-to-Y incisions, or sequential z-plasties can be used to lengthen skin.

 

f. In recurrent disease with skin involvement, resection of skin with subsequent full-thickness skin grafting can help minimize recurrence.

 

g. The "open palm technique," which involves leaving a transverse skin incision open at the level of the distal palmar crease, avoids postoperative hematoma formation and may help minimize stiffness in recovery (McCash technique).

 

h. PIP joint contracture with a nodule or tuft of diseased tissue just beyond the MCP joint should alert the surgeon to the strong possibility of a spiral cord with midline superficial and proximal displacement of the digital nerve.



V. Complications

A. Wound complications

 

1. Wound edge necrosis and slough of devascularized skin flaps occur frequently.

 

2. Hematoma formation contributes to flap necrosis and can be avoided by tourniquet deflation and hemostasis measures before closure.

 

B. Nerve injury

 

1. A spiral cord displaces the digital nerve to a superficial and midline position, placing it at risk for transection.

 

2. Finding the nerve both proximally and distally before proceeding into the zone of densely en-twined diseased fascia and nerve is recommended.

 

3. Treatment of nerve laceration is immediate primary neurorrhaphy.

 

C. Digital ischemia

 

1. Digital ischemia may occur as a result of either iatrogenic arterial transaction or vessel traction injury in the form of spasm, intimal hemorrhage, or actual rupture.

 

2. In Dupuytren disease, digital ischemia usually is a result of correction of long-standing joint contracture with vessels that have inadequate elasticity.

 

3. Initial measures include allowing the joint to return to relaxed posture and warming the patient and digit.

 

4. Topical lidocaine or papaverine can also relieve spasm.

 

5. If a thrombosed segment of vessel is identified in an ischemic digit, an interpositional vein graft may be needed.

 

D. Postoperative swelling—Often difficult to foresee, this swelling contributes to prolonged stiffness and early wound healing difficulties.

 

E. Postoperative "flare" reaction

 

1. Pain syndrome with features of diffuse swelling, hyperesthesia, redness, and stiffness.

 

2. Early treatment in the form of cervical sympathetic blockade, progressive stress-loading under supervision of a therapist, and oral medications helps to diminish pain, swelling, and inflammation enough to allow for needed digit mobilization.

 

3. Some clinicians recommend A1 pulley release for treatment.

 

F. Infection

 

1. Infection is usually superficial and can be treated with oral antibiotics.

 

2. Deep infection is relatively uncommon but does occur and requires prompt surgical drainage.

 

3. Patients with peripheral vascular disease or diabetes mellitus are at greater risk.

 

G. Recurrence

 

1. Recurrence of the contracture is always a possibility.

 

2. Early age, Dupuytren diathesis, multifocal disease, PIP disease, and little finger contracture may have some predictive value in identifying those at risk for recurrence.



Top Testing Facts

1. The Cleland ligament is not involved in Dupuytren contracture.

 

2. The spiral cord is formed by the pretendinous band, spiral band, lateral digital sheet, and Grayson ligament.

 

3. Key associations with Dupuytren contracture are type III collagen, myofibroblast, and intercellular fibronectin.

 

4. Conditions and factors that may be associated with Dupuytren contracture include diabetes mellitus, alcoholism, and the use of antiseizure medications.

 

5. Dermofasciectomy, arthrodesis, or amputation may be required in recurrent, advanced disease.



Bibliography

Boyer MI, Gelberman RH: Complications of the operative treatment of Dupuytren's disease. Hand Clin 1999;15:161-166.

McFarlane RM: Patterns of the diseased fascia in the fingers in Dupuytren's contracture: Displacement of the neurovascular bundle. Plast Reconstr Surg 1974;54:31-44.

Meunier M, von Schroeder HP, Boyer MI: Subtotal palmar and digital fasciectomy for Dupuytren's contracture. Atlas of Hand Clinics 2000;2:1-18.

Skoog T: Dupuytren's contracture: Pathogenesis and surgical treatment. Surg Clin North Am 1967;47:433-444.

Strickland JW, Bassett RL: The isolated digital cord in Dupuytren's contracture: Anatomy and clinical significance. J Hand Surg [Am] 1985;10:118-124.

Strickland JW, Leibovic SJ: Anatomy and pathogenesis of the digital cords and nodules. Hand Clin 1991;7:645-657.



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