A 70-year-old right-hand-dominant man presents for evaluation of a left small finger contracture. He was diagnosed with Dupuytren’s disease of the bilateral hands 30 years ago, and his left hand has always been more severely affected than the right. Shortly following his diagnosis, he underwent partial palmar fasciectomy of the bilateral long, ring, and small fingers with good correction of metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joint contractures. Twenty-five years later, he developed recurrent contracture of the left small finger PIP joint, which was treated with needle aponeurotomy with good correction. He presents now, 5 years following the needle aponeurotomy, with progressive flexion contractures of the small finger PIP and distal interphalangeal (DIP) joints, impairing his ability to golf, garden, and wear gloves (▶Fig. 7.1).
On clinical evaluation, the patient has full composite flexion and extension of all digits of the left hand, except the small finger, which has full MCP joint motion, a fixed 90-degree flexion contracture of the PIP joint, and 40-degree contracture of the DIP joint. He has full abduction of his digits without web-space adduction contractures. In addition to the pits and nodules in the palm, there is a palpable cord along the ulnar aspect of the small finger, extending distally from the MCP to the DIP joint. All digits are neurovascularly intact with brisk capillary refill and two-point discrimination to 5 mm in all digits.
Dupuytren’s contractures result from proliferation of fibroblasts in the palmar and digital fascia, which then differentiate into myofibroblasts and cause normal fascial bands to involute into nodules and cords. The specific components of the palmar and digital fascia affected by this process determine which digits and joints become contracted (▶Table 7.1).
When Dupuytren’s contractures recur following treatment, multiple anatomic structures are often responsible, including continued proliferation of pathologic palmar fascia, secondary contractures of adjacent skin and joint capsules, and scar formation resulting from the prior intervention. Although it is often difficult to differentiate which of these elements is responsible for the contracture recurrence, ideally all pathologic structures are addressed to achieve maximum correction and minimize the risk of recurrence. Occasionally, full correction of the contracture cannot be achieved due to contracted neurovascular structures limiting full extension.
Although recurrent contractures may occur in any patient following treatment of Dupuytren’s disease, several risk factors have been identified. Patients meeting the modified Dupuytren’s diathesis criteria of male gender, age of onset younger than 50 years, bilateral hand involvement, family history of at least one parent or sibling affected, or presence of Garrod’s pad (thickenings on dorsum of MCP joints) are at increased risk in a dose-dependent fashion. Presence of all five diathesis factors increases the risk of recurrence by 71% compared to a baseline risk of 23% in Dupuytren’s patients without these risk factors (▶Fig. 7.2).
Fig. 7.1 (a, b) The patient presented for evaluation of a contracture of the small finger on his left hand.
Fig. 7.2 Influence of number of Dupuytren’s diathesis risk factor on contracture recurrence. (Adapted from Hindocha S, Stanley JK, Watson S, Bayat A. Dupuytren’s diathesis revisited: evaluation of prognostic indicators for risk of disease recurrence. J Hand Surg Am 2006;31(10):1626–1634.)
Risk of recurrent contracture may also be influenced by the previous treatment. The rate of contracture recurrence appears to be greatest in patients undergoing needle aponeurotomy, with 85% of patients developing recontracture at 4 years and 50% requiring repeat intervention. The risk of recontracture is less with collagenase clostridium histolyticum (CCH) injection and open fasciectomy, but these too have substantial recurrence rates (▶Table 7.2).
Finally, Dias et al evaluated patterns of recurrent contracture specifically at the PIP joint and identified four patterns of recontracture: (1) minimal recontracture, (2) mild early recontracture, (3) severe early recontracture, and (4) progressive recontracture. The authors reported that worsening of contractures of more than 6 degrees between 3 and 6 months after surgery was predictive of progressive recontracture at 5 years.
The literature does not provide clear guidance for the management of recurrent Dupuytren’s contracture, as no one treatment has demonstrated superiority over another.
Given this lack of consensus regarding the optimal treatment of recurrent Dupuytren’s contracture, we recommend presenting all treatment options to the patient (observation, CCH injection, needle aponeurotomy, and open palmar fasciectomy) and allow their preferences of the risk–benefit profiles of the various interventions to determine the treatment.
We tend to favor either CCH injection or open partial fasciectomy. CCH injection is recommended in patients with contractures resulting principally from a discrete, palpable cord of pathologic fascia in the palm. The benefits of CCH injection include that it is minimally invasive with a shorter recovery time compared to open fasciectomy; however, it is associated with substantial edema, hemorrhage, and ecchymosis; carries a small risk of flexor tendon injury; and has a higher recurrence rate than open surgery. In patients with less well-defined cords who are likely to have multiple structures contributing to contracture recurrence, we recommend open fasciectomy with joint contracture release, and possible local skin flaps as this allows all pathologic structures to be addressed and has the lowest recurrence rate. The limitations of open fasciectomy include the higher risk of neurovascular injury, wound complications, infection, and longer duration of recovery.