Needle Aponeurotomy and Collagenase Injection for Treatment of Dupuytren Disease

 

 

 

DEFINITION

Dupuytren disease (DD) is a benign, generally painless, fibroproliferative disorder affecting the palmar fascia that often leads to progressive contractures of the fingers and thumb (FIG 1).

These contractures can be severe having a significant impact on hand function.

Although most estimates give the incidence of DD as 3% to 6% of Caucasians, some studies have

reported rates as high as 42%.46 This would mean that as many as 13.5 to 27 million people in the United States and Europe could be affected.

 

 

ANATOMY

 

For a detailed description of normal and pathologic anatomy, please see the excellent description in Dr. Rayan's chapter 143, Surgical Treatment of Dupuytren's Disease.

 

A particular concern is the location of the digital nerve when there is a spiral cord. The presence of a spiral nerve can be predicted if the patient has a soft, fatty mass lying between the distal palmar flexion crease and the proximal finger flexion crease. In 44 dissections, if a patient had this mass, there was a spiral nerve 90% of

the time.60

 

The neurovascular bundle usually makes a straight line in the digit. When the pretendinous band, the spiral band, and the lateral digital sheet become involved in DD, they contract and become straight displacing the

neurovascular bundle centrally and palmarly (FIG 2).44

 

 

 

FIG 1 • Surgical dissection showing a pretendinous Dupuytren cord (arrow) affecting the palm and finger.

 

 

When the spiral cord contracts, it causes the neurovascular bundle and fibrofatty tissue to become more superficial. This causes redundant skin and fibrofatty tissue to become a soft, pliable mass in the palm that measures approximately 2 cm in diameter.

 

The spiral nerve occurs most commonly in the ring and small fingers when there is a proximal interphalangeal (PIP) joint contracture of 30 degrees.60

PATHOGENESIS

 

DD is believed to be inherited as an autosomal dominant trait with incomplete penetrance. Hu et al32 was able to identify an autosomal dominant gene for DD on chromosome 16q in a Swedish family.

 

The progression of DD is not uniform. Cords can be nodular or nonnodular based on the number of localized cellular nodules in a cord. Nodular cords are hypercellular, the majority of which are alpha smooth muscle actin (α-SMA) positive cells. Nonnodular cords are the most contracted. Cells in nodular cords are responsible for cord contraction. Stress shielding leads to myofibroblast apoptosis that results in cords becoming less

cellular.69

 

Normal palmar fascia is composed largely of type I collagen. DD cords are largely composed of type III collagen.10

 

DD has been staged histologically7,58:

 

Type I (proliferative stage): All lesions show mitotic figures. Mitotic figures are regular in shape and are rare. Cells have round nuclei.

 

Type II (fibrocellular stage): There is high cellularity but no mitotic figures. Cell nuclei are elongated with abundant wavy collagen fibers. Silver stain shows a dense reticulin network in the more cellular areas.

 

Type III (fibrotic stage): There are dense fibrous cords that rarely contain cells with elongated nuclei.

 

The highest incidence of recurrence is in patients with the type I histologic group at 54%. By 8 to 9 years postoperatively, the recurrence rate increases to 71%.

 

The major source of contraction in DD is the myofibroblast. This cell can generate significant contractile forces and has characteristics of both smooth muscle and fibroblasts.5,23

 

Prostaglandin F2α stimulates significant contracture of myofibroblasts, whereas prostaglandin E2 causes relaxation.5,35

 

DD tissue contains large amounts of transforming growth factor beta (TGF-β1 and TGF-β2) that has a significant effect on myofibroblast proliferation.6

 

TGF-β1 is a mechanotransduction cytokine that causes increased contractile force of myofibroblasts during the early phase of attachment and contractions as well as an increased contractile response to mechanical stimuli.9

 

P.1209

 

 

 

 

FIG 2 • The formation of a spiral cord showing displacement of the neurovascular bundle.

 

 

Z19 transcription factor gene increases the potency of TGF-β1.

 

Multiple other proteins influence differentiation, growth, and contractility of myofibroblasts. These include platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), epidermal growth factor (EGF), interleukin-1 (IL-1) tenascin and periostin (Tables 1 and 2).10,49

NATURAL HISTORY

 

DD progresses through three clinical stages15,42:

 

Stage I: the proliferative or nodular stage. In this stage, patients have a nodule or nodules within the palmar fascia. The nodules are predominantly cellular, composed of peripheral, perivascular spindle-shaped hyperplastic fibroblasts with irregular hyperchromatic nuclei. The nodules tend to be vascular with reactive

 

tissue around the periphery. There is no increase in collagen deposition. The hyperplastic cells disrupt the continuity of the normal palmar fascia.

 

 

Table 1 Selected Genes and Proteins Upregulated in Dupuytren Disease

 

From Black EM, Blazar PE. Dupuytren disease: an evolving understanding of an age-old disease. J Am Acad Orthop Surg 2011;19(12):746-757.

 

A disintegrin and metalloproteinase domain (ADAM) 12 Alpha smooth muscle actin (α-SMA)

β-1 integrin

Cadherin 11 (CDH11)

Collagen I, collagen V, collagen VIII Contactin 1 (CNTN1)

Fibronectin

Heat shock protein 47 (HSP47) Laminin

Leucine-rich repeat (LRR) domain-containing 17

V-maf musculoaponeurotic fibrosarcoma oncogene homolog B (MafB) Periostin, osteoblast specific factor (POSTN)

Postsynaptic density protein-95 (PSD-95) Tenascin C

Tissue inhibitor of metalloproteinase (TIMP-1) Transforming growth factor-β2 (TGF-β2) Zonula occludens-1 protein (ZO-1)

 

 

Stage II: the involutional or active disease stage. In this stage, there is nodular thickening of the palmar fascia with the beginning of joint contracture. Fibroblasts align themselves along lines of stress. They become more mature and decrease in size and number. The predominate cell type is myofibroblast. There are definite cords composed of well-aligned, mature collagen fibers and few scattered cells.

 

Stage III: the residual or advanced disease stage. In this stage, there are diffuse, thick fibrotic cords that become more contracted. The cords are predominantly collagen with few cells that are elongated and compressed by the collagen fibers. Cell types are both fibroblasts and myofibroblasts.

 

 

Table 2 Selected Genes and Proteins Downregulated in Dupuytren Disease

 

Chitinase 3-like protein 2 Collagen XV

Cornea-derived transcript 6 (CDT6) Cysteine dioxygenase 1 (CDO1) Matrix metallopeptidase 27 (MMP27) Matrix metalloproteinase-3 (MMP3) Superoxide dismutase (SOD) Superoxide dismutase 2 (SOD2)

 

From Black EM, Blazar PE. Dupuytren disease: an evolving understanding of an age-old disease. J Am Acad Orthop Surg 2011;19(12):746-757.

 

 

 

P.1210

 

The progression of DD is unpredictable. Nodules may lay dormant for years without progression or can

progress rapidly over a matter of months.42 Reilly et al57 reported on 59 patients with Dupuytren nodules. Thirty of the 59 patients had developed a cord at an average of 8.7 years (range 6 to 15 years). However, by

8.7 years only, 5 patients met the criteria for surgery and 7 patients had regressed.57

 

PATIENT HISTORY AND PHYSICAL FINDINGS

 

DD predominantly affects Caucasian males of northern European descent. It has been reported in all races, however.

 

The peak incidence occurs in the 50s for men and the 60s for women. The literature reports that it is more

common in men than women with ratios ranging from 7.5:1 to 5.4:1.42 Other studies report ratios ranging from

9.5:1 to 3:1. These studies have largely looked at populations in Europe and Australia, however. In a more

recent study, Anthony et al1 looked at the incidence in the U.S. population and found the male-to-female ratio to be 1.7:1 and noted with advancing age, the ratio approached 1:1.

 

DD interferes with activities of daily living and work including hair brushing, face washing, holding hands, putting hands in pockets, holding tools, and wearing gloves.

 

 

 

 

FIG 3 • A. Dupuytren cord affecting the ring finger. B. Pitting and dimpling associated with Dupuytren contracture. C. Multiple Dupuytren cords involving all fingers and the thumb.

 

DD is associated with a number of medical conditions including diabetes mellitus,3,13 HIV11 frozen shoulder, a high lipid profile,29 and epilepsy.2

 

It has also been associated with lifestyle risk factors including smoking, alcoholism,12,24,25 manual labor,41 hand and wrist trauma,40 and the use of vibratory tools.64

 

DD usually begins as painless nodules in the palm. The most common finger involved is the ring finger (60.7%), followed by the small finger (51%), the middle finger (22.5%), the thumb (7.0%), and the index finger

(5.8%). The thumb web can also be involved resulting in an adduction contracture (FIG 3A).55

 

Early in the disease, patients may note thickening of the skin with pitting or dimpling. This may progress to cords that can ultimately lead to contracture of the metacarpophalangeal (MP) and PIP joints (FIG 3B).

 

DD usually begins with one finger but often progresses to others (FIG 3C).

 

DD can also occur in ectopic locations such as over the dorsum of the PIP joints (Garrod nodes), in the feet (Lederhose disease), and in the penis (Peyronie disease).30

 

Five factors have been identified that indicate a DD diathesis. They include onset younger than age 50 years, bilateral involvement, ectopic lesions, male gender, and a positive family history.30,33

 

P.1211

 

Patients with a DD diathesis have a more aggressive disease with higher rates of recurrence.

 

 

The “fasciodesis” maneuver is useful for predicting minimum gain in PIP motion after percutaneous needle fasciotomy (PNF).

 

 

Flex the MP joint to 90 degrees.

 

 

Measure the extension gain at the PIP joint.20

 

Tubiana classified DD based on total passive extension deficit (TPED) of the MP, PIP, and distal interphalangeal (DIP) joints (Table 3).65

IMAGING AND OTHER DIAGNOSTIC STUDIES

 

In most instances, radiographic imaging is not necessary to adequately evaluate DD. The only time one might consider imaging is if there is a concern for some other pathology such as significant osteoarthritis or neoplasm. If these are suspected, then appropriate imaging studies could be ordered.

 

DIFFERENTIAL DIAGNOSIS

The differential diagnosis of DD is well covered in the chapter on Surgical Treatment of Dupuytren's Disease.

 

 

NONOPERATIVE MANAGEMENT

 

In the past, a number of nonoperative treatments for DD have met with limited success. These include physical therapy, splinting, dimethylsulfoxide injections, topical vitamins A and E, gamma interferon injections,

radiation, and the calcium channel blockers such as nifedipine and verapamil.56

 

In 1971, Hueston33 performed what he referred to as enzymatic fasciotomy. He injected patients with a mixture of trypsin, hyaluronidase, and lidocaine, followed by a forcible extension maneuver. He was able to

obtain full extension of all fingers 15 minutes following injection.33

 

Table 3 Tubiana Grades of Dupuytren Disease Based on Total Passive Extension Deficit

Grade I

0-45 degrees

Grade II

45-90 degrees

Grade III

90-135 degrees

Grade IV ≥135 degrees

 

 

When McCarthy43 studied the long-term results, however, he found that seven of nine patients had developed recurrence within 2 to 3 years.

Injection of triamcinolone acetonide directly into the DD nodules resulted in regression in 97% of patients. The average number of injections was 3.2. There was a 50% recurrence rate between 1 and 3 years after the last injection, however.38

COLLAGENASE CLOSTRIDIUM HISTOLYTICUM (XIAFLEX)

In 2009, Hurst et al34 reported the results of the multicenter collagenase option for reduction of Dupuytren (CORD) I study. This was a double blind, placebo-controlled study in which they injected Dupuytren cords with

0.58 mg collagenase Clostridium histolyticum (CCH) (Xiaflex).34

Xiaflex is a mixture of two synergistic collagenases that tend to rapidly degrade type I and type III collagens.61

 

Indications for Treatment

A palpable cord with an MP or PIP joint contracture of 20 degrees or more

 

 

Contraindications

Patients who are intolerant of pain are poor candidates.

The drug is expensive and patients with multiple cords may face months of treatment and a great deal of expense.

A history of sensitivity to CCH.

Patients who have been on anticoagulants other than low-dose aspirin within 7 days of CCH injection Contractures associated with huge nodules are not good candidates for collagenase.

 

 

Preoperative Planning

 

 

Give the patient take-home information describing common side effects and risks. Be sure to obtain insurance preauthorization if required.

 

Identify the primary cord for treatment.

 

Identify secondary and tertiary joints for later treatment.

 

TECHNIQUE

  • Injection28

 

CCH comes as a lyophilized powder containing 0.9 mg of the drug. It is reconstituted with 0.39 mL of sterile diluent for MP joint contractures and 0.31 mL for PIP joint contractures.

 

Once reconstituted, the drug should sit for 15 minutes, but if not, refrigerated should be used within 1 hour. Refrigerated CCH may be stored up to 4 hours.

 

The dosage for all injections is 0.58 mg.

 

The use of local anesthesia prior to injection is not recommended.

 

The injection is performed with a 1 mL syringe and a 0.5-inch 27-gauge needle. It is best to use the syringes supplied by the company.

 

Gently extend the involved finger to put the cord under tension, displacing it away from the underlying flexor tendon (TECH FIG 1).

 

 

Inject a cord where it bowstrings the most and is displaced furthest from the underlying flexor tendon. Insert the needle through the skin into the underlying cord. This should feel firm.

 

 

Passively manipulate the PIP or DIP joint to be certain the needle is not in the flexor tendon. Inject one-third of the volume. Resistance to injection indicates the needle is in the cord.

 

The cord is injected in three different locations. The needle can either be redirected or removed and reintroduced into two other locations 2 to 3 mm away. One-third of the volume is injected in each location (TECH FIG 2).

 

P.1212

 

 

 

TECH FIG 1 • CCH injection technique.

 

 

 

TECH FIG 2 • A. Inject by redirecting the needle. B. The preferred injection technique is to remove and reinsert the needle.

 

 

P.1213

 

 

MP joint cords are injected with 0.25 mL of CCH. PIP joint cords are injected with 0.20 mL of CCH

 

Cords causing PIP joint contractures should not be injected more than 4 mm distal to the proximal finger flexion crease (TECH FIG 3).

 

Insert the needle no more than 2 to 3 mm.

 

Currently, the manufacturer recommends injecting only one cord at a time.

 

 

 

TECH FIG 3 • Do not inject a PIP joint more than 4 mm distal to the proximal finger flexion crease.

 

 

Coleman et al16 reported on injecting cords affecting two joints in the same hand at one sitting. Although there was an increased incidence of some adverse events, few were serious and the authors concluded it was safe to perform.16

 

Each cord can be injected up to three times at 30-day intervals.

  • Manipulation

 

The day following the injection, patients return for manipulation. Manipulation may be safely performed up to 7 days following injection without negatively affecting the results (TECH FIG 4).28,37

 

Prior to manipulation, perform a wrist or digital nerve block with 1% lidocaine.

 

 

The wrist is flexed and moderate passive extension is applied to the involved digit for 10 to 20 seconds. If manipulating the PIP joint, the MP joint is flexed.

 

 

Often, a “pop” or tearing noise is heard as the cord breaks. Some cords rupture spontaneously.

 

Up to three attempts at 5- to 10-minute intervals can be made.

 

If unsuccessful after three attempts, the patient should be instructed to return in 30 days for another injection.

 

TECH FIG 4 • Manipulation of the finger 2 days following injection with CCH. Note the local reaction at the injection site.

 

 

P.1214

 

PEARLS AND PITFALLS

There is significant resistance when injecting into a cord. Sudden loss of resistance may mean the cord has been penetrated. It is safer to remove the needle and inject in another location rather than to try to redirect the needle.

When injecting, it is best to have the patient or an assistant hold the finger, so two hands can be used to prevent inadvertent advancement of the needle through the cord.

When injecting a spiral cord, lateral cord, or abductor digiti minimi cord, it is often safer to inject from the side with the needle pointing away from the flexor tendons.

If there is both a radial and ulnar cord in the same digit, consider splitting the dose and injecting both cords. On occasion, I have used the full vial to do this. This is technically off-label.

If the patient gets paresthesias during the injection, remove the needle and inject in another location.

If there is a Y-shaped cord, injecting at the apex of the Y often allows correction of both involved digits.

Periarticular fibrosis can cause joint contractures that do not respond to collagenase injections. Dynamic splinting following injection may be helpful, but on two occasions, I have had to surgically release the volar plate in order to release the PIP joint contracture.

Skin tears can be alarming and some authors have reported repairing them with split-thickness skin grafts. However, even dramatic tears heal quickly with simple wound care within 10 days to 3 weeks (FIG 4A-C).

First web contractures can have mixed results because of difficulty applying enough pressure on the cord

 

 

during manipulation.

The safety of CCH in patients receiving anticoagulant medications other than low-dose aspirin (150 mg per day) has not been established so it should be used with caution in patients on anticoagulants or with coagulation disorders.

Although there have been no reports of severe allergic reactions to CCH, it does contain foreign proteins and patients do develop anti-AUX-I and AUX-II antibodies. Therefore, physicians should be prepared to address severe allergic reactions following injections.

 

FIG 4 • A. There is a large skin tear following the manipulation of a PIP cord. The distal portion of the Dupuytren cord (arrow) can be visualized in the wound. B. Despite the large tear, the patient still has full ROM. C. Two weeks following the tear, it is almost completely healed with simple wound care.

 

 

 

POSTOPERATIVE CARE

 

Following the injection of CCH, a light compressive dressing is applied. Patients are told to remove the dressing either that evening or the next day.

 

Although some authors do not prescribe pain medication, I prefer to give patients a prescription for a few narcotic pain pills for the first few days.

 

Patients are advised to avoid heavy use of their hand until the next day.

 

Following manipulation, patients are given a home exercise program and a night splint that holds the fingers in extension. They are told to wear the splint at night for 3 to 4 months.

 

For severe PIP joint contractures (≥40 degrees), patients are given a dynamic extension splint and told to wear it full time for 3 to 4 months except for bathing and exercise.

 

Patients are advised to avoid heavy use of their hand until pain-free.

OUTCOMES

In the CORD I study, authors report getting 64% of digits to within 5 degrees of full extension with an average of 1.7 injections given at monthly intervals. Results were better for MP joints (76.7%) than PIP joints (40%) and in mild (MP <50 degrees = 88.9% and PIP <40 degrees = 80.9%) versus severe

disease (MP 57.7% and PIP 22.4%) (FIG 5A-C).34

Average improvement in range of motion (ROM) for all patients was: From 43.9 to 80.7 degrees (mean improvement 36.7 degrees)

MP joint motion improved from 42.6 to 83.7 degrees (mean improvement 40.6 degrees)

 

 

PIP joint motion improved from 46.6 to 74.9 degrees (mean improvement 29.0 degrees)

 

More recent data has shown similar outcomes from an academic and community-based experience with CCH. In this study, patients received an average of 1.08 injections.53

 

P.1215

 

 

 

FIG 5 • A. CORD I study: overall percentage of results for patients treated with an average of 1.7 injections of CCH. B. Percentage of results for patients treated with CCH by joint involved. C. Outcomes compared by degree of severity for MP joints (severe = >50 degrees) and for PIP joints (severe = >40 degrees).

 

 

Most patients (≥85.8%) developed antibodies to either type 1 (AUX-I) or type II (AUX-II) CCH or both within 30 days after the first injection. All patients developed antibodies to both AUX-I and AUX-II by the third injection.

 

However, there were no meaningful systemic allergic reactions.

 

Some patients ultimately require fasciectomy. Unlike surgery following previous limited fasciectomy, there is no significant distortion of anatomy or increased difficulty in dissection in patients previously treated

with CCH (FIG 6).26

 

In fingers with both MP and PIP joint contractures, the PIP joint will often correct with treatment of the MP joint cord alone.27

 

Recurrence rates are difficult to evaluate because there is no agreed definition of what constitutes

recurrence. Peimer et al50 reported on 3-year recurrence rates where he defined recurrence as a contracture of greater than or equal to 20 degrees with a palpable cord or as the need to have further surgical or medical treatment. Of the 1080 CCH treated joints, 35% had recurred. The MP joint had a recurrence rate of 27% and the PIP joint 56%. Only 7% of patients with recurrence received further treatment, however.

 

 

 

FIG 6 • A patient with a previous CCH injection who ultimately requested surgery. The arrow points to the previous site of injection. There is minimal scarring and distortion from the previous treatment.

 

 

Four-year recurrence data was recently reported. The overall recurrence rate was 42.1%. MP joint recurrence was 34.6% and PIP joint recurrence was 61.6%.31

 

Some authors have suggested using 30 degrees rather than 20 degrees as the indication of a

recurrence.67,68 If 30 degrees is used, the recurrence rate was 27.9% overall with a 22.2% recurrence at the MP joint and a 43% recurrence at the PIP joint (FIG 7).

 

P.1216

 

FIG 7 • Four-year recurrence data presented at the 2013 American Society for Surgery of the Hand (ASSH) Annual Meeting by Hotchkiss et al.31

87.2% of joints successfully treated with CCH did not require further treatment. However, patients treated with fasciectomy had a lower incidence of retreatment.

 

 

 

COMPLICATIONS4,51,52

The most recent data reported 1732 adverse events from 49,078 injections on 846 patients.

The majority of these adverse events were mild injection site reactions that resolved rapidly. These include the following:

Skin tear (13.2%)

Ecchymosis (9.7%) (FIG 8)

Hand and finger edema (9.5%) (FIG 9)

 

 

 

 

FIG 8 • Ecchymosis of the hand 2 days following a CCH injection.

 

 

 

FIG 9 • Swelling and ecchymosis of the hand and finger 2 days following a CCH injection.

 

 

Drug ineffective (6.1%)

 

Extremity pain (4.6)%

 

 

Lymphadenopathy (elbow/axilla) (3.1%) (FIG 10A,B) Hematoma (2.8%)

 

Injection site pain (2.7%)

 

 

Injection site hematoma (2.8%) (FIG 11A,B) Flexor tendon rupture (0.05%)

 

 

 

Ring finger MP joint (four reports) Little finger MP joint (five reports) Little finger PIP joint (eight reports)

 

 

Complex regional pain syndrome (CRPS) (two reports) A2 pulley injury (one report)

 

 

Stretch neurapraxia (one report) Flexor pulley injury (one report)

 

 

Loss of a well-established skin graft (one report)62 Pruritus or localized rash

 

SURGICAL MANAGEMENT

 

Sir Astley Cooper originally performed percutaneous fasciotomy in 1822 using a bistoury later known as a

Cooper knife. The procedure came to be known as Cooper fasciotomy.18,36,66

 

In 1979, two French rheumatologists, Lermusiaux and Debeyre,39 popularized using a 25-gauge needle to perform PNF.

 

Indications for Treatment18,20

 

MP joint contracture of 30 degrees or greater

 

 

PIP joint contracture of any degree that results in functional impairment A discreet, palpable cord

 

 

An elderly, medically frail patient A compliant patient

 

 

 

Early Tubiana stage I disease with a moderate MP flexion contracture PNF can be used to treat recurrent DD.68

P.1217

 

 

 

FIG 11 • A. Injection site hematoma. These usually resolve rapidly. B. Despite the large injection site hematoma, the patient is able to make a complete fist immediately following manipulation.

 

FIG 10 • A. Swelling of the arm with epitrochlear lymphadenopathy. B. Forearm pain and swelling following an injection of CCH.

 

 

P.1218

Contraindications20

Large, bulky ill-defined cord (relative) Patients without a distinct, palpable cord19 Recurrent cord after surgery (relative)

Patients unable to tolerate local procedures

A cord that allows for full passive finger extension Uncooperative or mentally impaired patients Nodules without cords

Long-standing PIP flexion contractures (relative) Deep lateral cords

Contractures resulting from insufficient skin or postsurgical scarring

 

 

Preoperative Planning

 

Perform a detailed history and physical examination.

 

 

 

 

Measure and document the degree of flexion contracture. Note the character of the cord or nodules.

 

Document preoperative sensation and flexor tendon function.

 

Counsel the patient to inform you immediately if they feel electric shocks in the finger.

 

Warn the patient of potential complications including skin tears, nerve injury, flexor tendon damage, and recurrence.

 

Positioning

 

The patient is supine with the hand resting on a hand table.

 

 

 

A 2-inch thick pad of folded towels is placed behind the hand to facilitate MP extension.19 The hand is draped with sterile drapes.

Approach

 

 

The procedure can be performed in either an office setting or an outpatient surgery suite. A tourniquet may be used but is usually not necessary.

 

The cord is marked on the skin where it is most prominent (FIG 12).

 

 

 

 

FIG 12 • The skin is marked outlining the cord.

 

 

 

FIG 13 • The figure shows an ideal cord for PNF. The arrow points to an ideal position to place a portal.

 

 

 

Portals are usually placed directly over the cord a minimum of 5 mm apart. Dual side-by-side portals maybe used with wide cords (>5 mm in width).

 

Plan portals on the convex side of skin creases.

 

 

Whenever possible, place portals in areas where the cord bowstrings maximally (FIG 13). Avoid nodules and skin creases for portals.

 

Beware of skin dimples.

 

Doppler examination may help elucidate the location of a suspected spiral cord.

 

Look for blanching when tension is applied. No blanching indicates the cord is tighter than the skin and this is a good location for a portal. Once the cord is released, the skin should blanch with tension (FIG 14).

 

A small amount of 1% plain lidocaine is used to infiltrate the overlying skin (0.1 to 0.2 mL).

 

 

 

FIG 14 • Skin blanching (arrow) with traction on the finger indicates the skin is tighter than the underlying cord.

 

 

P.1219

 

TECHNIQUE

  • Collagenase Injection

Pull the finger into extension, making the cord more palpable and hold it under tension (TECH FIG 5A). Use a 25-gauge needle to perforate the cord in the area of anesthesia (TECH FIG 5B).

Some authors prefer to use a 19-gauge needle.20 Check fingertip sensation repeatedly during procedure.

Monitor tendon involvement by asking the patient to flex and extend the DIP and PIP joints during the procedure. The needle should not move with the tendon.

Begin perforations distally and progress proximally along the cord for approximately 1 cm. Initially, use the needle to develop a plane between the skin and the cord.

Orient the needle to use as a probe to define the width of the cord. Perforations should not go completely through the cord.

 

 

 

 

TECH FIG 5 • A. A patient with a large Dupuytren cord causing contracture of both the MP and PIP joints. B. A 25-gauge needle is used to inject 0.1 to 0.2 mL of 1% lidocaine immediately under the skin. The needle is then used to release the cord as described. C. The ring finger is gently manipulated into extension releasing the contracture at both the MP and PIP joints.

 

 

Alternately, use the needle in a sawing motion.

 

With either technique, there should be a grating feeling. If a grating is not felt, change the needle and move to another portal.

 

Following the perforations, the finger is firmly but gently extended while stabilizing the hand. Frequently, a pop is heard as the cord breaks (TECH FIG 5C).

 

 

Flex the wrist and ask the patient to actively extend the finger during the manipulation maneuver. Extend the finger and palpate for a residual cord.

 

Repeat the procedure as necessary until full extension is achieved, the remaining cord is no longer palpable, or further treatment would put the neurovascular bundles at risk.

 

A local or wrist block may be helpful if the manipulation is too painful.

 

Injecting triamcinolone acetonide (TA) into the portals and nodules following release may be helpful.

McMillan and Bidhammer45 reported significantly improved correction of deformity at 6 months in patients who received TA injection postoperatively.

 

 

 

P.1220

 

PEARLS AND PITFALLS

A spiral nerve can be predicted with 90% reliability if there is a soft, pulpy mass of skin lying between the distal palmar crease and the proximal finger crease.60

If this soft, pulpy mass is present, perform the fasciotomy proximally at the level of the transverse fibers only.20

Patients will report a strong electrical shock sensation if the nerve is touched.

If the fingertip becomes numb from the use of local anesthetic, move to a more proximal portal.19

Traction on the skin or nodule is safer than pulling on the fingertips. The flexor tendons should remain relaxed.

Repeatedly check for nerve or tendon involvement during the procedure.

Change to a fresh needle and new portal if you no longer feel a grating sensation.

 

 

POSTOPERATIVE CARE

 

 

A Band-Aid or light dressing covers the wound for 24 hours. Ice and elevate the hand for 48 hours.

 

Avoid strenuous gripping for 1 week.

 

 

Skin tears are treated with a light dressing and local wound care until healed. Patients are instructed to avoid painful activity.

 

 

 

Postoperative therapy is rarely necessary. A night splint is worn for 1 month.47

 

OUTCOMES

Patients with diseases such as rheumatoid arthritis, and diabetes, anticoagulant therapy or a history of previous CRPS are bad prognostic factors for treatment.

Foucher reported follow-up at 3.2 years.21,22 MP joint motion improved by 79%

PIP motion improved by 65%

Recurrence of DD occurred in 58% of patients and 24% required additional treatment.

 

PNF has been compared to limited fasciectomy (LF).66

TPED improved 63% in the PNF group and 79% in the LF group.

LF recovery took from 21 to 58 days. Most PNF patients are using their hands optimally within 1 week. Poor outcomes are reported in patients with Tubiana stage III and IV DD.

Pess et al54 reported initial correction of contractures of 99% at the MP joint and 89% at the PIP joint with PNF. Final follow-up was a minimum of 3 years and the correction was maintained in 72% of the MP

joints and 31% of the PIP joints.54

Five-year follow-up recurrence rates have been reported to be 84.9% for PNF compared to 20.9% for LF.67

Comparison of PNF and collagenase demonstrate similar clinical outcomes in the short term.48

Cost analysis comparing LF, PNF, and CCH demonstrate LF is not cost effective. PNF is cost effective if the success rate is high. CCH is cost effective if the cost per injection is significantly less than currently priced in the United States.8,14,17,59

 

 

COMPLICATIONS

Vascular injury Nerve laceration Infection

Skin tears Paresthesias CRPS type I

Increased postoperative pain requiring analgesics False aneurysm63

FDP injury (0.05%)63

 

 

REFERENCES

  1. Anthony SG, Lozano-Calderon SA, Simmons BP, et al. Gender ratio of Dupuytren's disease in the modern

    U.S. population. Hand 2008; 3(2):87-90.

     

     

  2. Arafa M, Noble J, Royle SG, et al. Dupuytren's and epilepsy revisited. J Hand Surg Br 1992;17(2):221-224.

     

     

  3. Arkkila PE, Koskinen PJ, Kantola IM, et al. Dupuytren's disease in type I diabetic subjects: investigation of biochemical markers of type III and I collagen. Clin Exp Rheumatol 2000;18(2):215-219.

     

     

  4. Badalamente MA, Hurst LC. Efficacy and safety of injectable mixed collagenase subtypes in the treatment of Dupuytren's contracture. J Hand Surg Am 2007;32(6):767-774.

     

     

  5. Badalamente MA, Hurst LC, Sampson SP. Prostaglandins influence myofibroblast contractility in Dupuytren's disease. J Hand Surg Am 1988;13(6):867-871.

     

     

  6. Badalamente MA, Sampson SP, Hurst LC, et al. The role of transforming growth factor beta in Dupuytren's disease. J Hand Surg Am 1996; 21(2):210-215.

     

     

  7. Balaguer T, David S, Ihrai T, et al. Histological staging and Dupuytren's disease recurrence or extension

    after surgical treatment: a retrospective study of 124 patients. J Hand Surg Eur Vol 2009;34(4): 493-496.

     

     

  8. Baltzer H, Binhammer PA. Cost-effectiveness in the management of Dupuytren's contracture. A Canadian cost-utility analysis of current and future management strategies. Bone Joint J 2013;95-B(8): 1094-1100.

     

     

  9. Bisson MA, Beckett KS, McGrouther DA, et al. Transforming growth factor-beta1 stimulation enhances Dupuytren's fibroblast contraction in response to uniaxial mechanical load within a 3-dimensional collagen gel. J Hand Surg Am 2009;34(6):1102-1110.

     

     

  10. Black EM, Blazar PE. Dupuytren disease: an evolving understanding of an age-old disease. J Am Acad Orthop Surg 2011;19(12): 746-757.

     

     

  11. Bower M, Nelson M, Gazzard BG. Dupuytren's contractures in patients infected with HIV. BMJ 1990;300(6718):164-165.

     

     

  12. Burge P, Hoy G, Regan P, et al. Smoking, alcohol and the risk of Dupuytren's contracture. J Bone Joint Surg Br 1997;79(2):206-210.

     

     

  13. Cagliero E, Apruzzese W, Perlmutter GS, et al. Musculoskeletal disorders of the hand and shoulder in patients with diabetes mellitus. Am J Med 2002;112(6):487-490.

     

     

  14. Chen NC, Shauver MJ, Chung KC. Cost-effectiveness of open partial fasciectomy, needle aponeurotomy, and collagenase injection for dupuytren contracture. J Hand Surg Am 2011;36(11):1826-1834.e1832.

     

     

  15. Chiu HF, McFarlane RM. Pathogenesis of Dupuytren's contracture: a correlative clinical-pathological study. J Hand Surg Am 1978;3(1): 1-10.

     

     

  16. Coleman S, Gilpin D, Kaplan FT, et al. Efficacy and safety of concurrent collagenase clostridium histolyticum injections for multiple Dupuytren contractures. J Hand Surg Am 2014;39(1):57-64.

     

     

    P.1221

     

  17. De Salas-Cansado M, Cuadros M, Del Cerro M, et al. Budget impact analysis in Spanish patients with Dupuytren's contracture: fasciectomy vs. collagenase Clostridium histolyticum. Chir Main 2013;32(2): 68-73.

     

     

  18. Diaz R, Curtin C. Needle aponeurotomy for the treatment of Dupuytren's disease. Hand Clin 2014;30(1):33-38.

     

     

  19. Eaton C. Percutaneous fasciotomy for Dupuytren's contracture. J Hand Surg Am 2011;36(5):910-915.

     

     

  20. Foucher G, Medina J, Malizos K. Percutaneous needle fasciotomy in dupuytren disease. Tech Hand Up Extrem Surg 2001;5(3):161-164.

     

     

  21. Foucher G, Medina J, Navarro R. Percutaneous needle aponeurotomy. Complications and results [in French]. Chir Main 2001;20(3): 206-211.

     

     

  22. Foucher G, Medina J, Navarro R. Percutaneous needle aponeurotomy: complications and results. J Hand Surg Br 2003;28(5):427-431.

     

     

  23. Gabbiani G, Majino G. Dupuytren's contracture: fibroblast contraction? An ultrastructural study. Am J Pathol 1972;66:131-138.

     

     

  24. Godtfredsen NS, Lucht H, Prescott E, et al. A prospective study linked both alcohol and tobacco to Dupuytren's disease. J Clin Epidemiol 2004;57(8):858-863.

     

     

  25. Gudmundsson KG, Arngrimsson R, Jonsson T. Dupuytren's disease, alcohol consumption and alcoholism. Scand J Prim Health Care 2001; 19(3):186-190.

     

     

  26. Hay DC, Louie DL, Earp BE, et al. Surgical findings in the treatment of Dupuytren's disease after initial treatment with clostridial collagenase (Xiaflex). J Hand Surg Eur Vol 2013;39(5):463-465.

     

     

  27. Hayton MJ, Bayat A, Chapman DS, et al. Isolated and spontaneous correction of proximal interphalangeal joint contractures in Dupuytren's disease: an exploratory analysis of the efficacy and safety of collagenase collagenase Clostridium histolyticum. Clin Drug Investig 2013;33(12):905-912.

     

     

  28. Hentz VR. Collagenase injections for treatment of Dupuytren disease. Hand Clin 2014;30(1):25-32.

     

     

  29. Hindocha S, John S, Stanley JK, et al. The heritability of Dupuytren's disease: familial aggregation and its clinical significance. J Hand Surg Am 2006;31(2):204-210.

     

     

  30. Hindocha S, Stanley JK, Watson S, et al. Dupuytren's diathesis revisited: evaluation of prognostic indicators for risk of disease recurrence. J Hand Surg Am 2006;31(10):1626-1634.

     

     

  31. Hotchkiss RN, Peimer CA, Coleman SG, et al. Recurrence of Dupuytren contracture after nonsurgical treatment with collagenase Clostridium histolyticum: summary of 4-year CORDLESS data. Presented at the 68th Annual Meeting of the American Society for Surgery of the Hand, October 3-5, 2010, San Francisco, CA.

     

     

  32. Hu FZ, Nystrom A, Ahmed A, et al. Mapping of an autosomal dominant gene for Dupuytren's contracture to chromosome 16q in a Swedish family. Clin Genet 2005;68(5):424-429.

     

     

  33. Hueston JT. Enzymatic fasciotomy. Hand 1971;3(1):38-40.

     

     

  34. Hurst LC, Badalamente MA, Hentz VR, et al. Injectable collagenase clostridium histolyticum for Dupuytren's contracture. N Engl J Med 2009;361(10):968-979.

     

     

  35. Hurst LC, Badalamente MA, Makowski J. The pathobiology of Dupuytren's contracture: effects of prostaglandins on myofibroblasts. J Hand Surg Am 1986;11(1):18-23.

     

     

  36. Hutchison RL, Rayan GM. Astley Cooper: his life and surgical contributions. J Hand Surg Am

    2011;36(2):316-320.

     

     

  37. Kaplan FT, Badalemente M, Hurst L, et al. Delayed manipulation following clostridial collagenase histolyticum injection for Dupuytren contracture. Presented at the 68th Annual Meeting of the American Society for Surgery of the Hand, October 3-5, 2013, San Francisco, CA.

     

     

  38. Ketchum LD, Donahue TK. The injection of nodules of Dupuytren's disease with triamcinolone acetonide. J Hand Surg Am 2000; 25(6):1157-1162.

     

     

  39. Lermusiaux J, Debeyre N. Le traitement médical de la maladie de Dupuytren. In: De Seze S, Ryckewaert A, Kahn MF, et al, eds. L' Actualité Rhumatologique. Paris, France: Expansion Scientifique, 1979: 338-343.

     

     

  40. Logan AJ, Mason G, Dias J, et al. Can rock climbing lead to Dupuytren's disease? Br J Sports Med 2005;39(9):639-644.

     

     

  41. Lucas G, Brichet A, Roquelaure Y, et al. Dupuytren's disease: personal factors and occupational exposure. Am J Ind Med 2008;51(1):9-15.

     

     

  42. Luck JV. Dupuytren's contracture; a new concept of the pathogenesis correlated with surgical management. J Bone Joint Surg Am 1959; 41-A(4):635-664.

     

     

  43. McCarthy DM. The long-term results of enzymic fasciotomy. J Hand Surg Br 1992;17(3):356.

     

     

  44. McFarlane RM. Patterns of the diseased fascia in the fingers in Dupuytren's contracture. Displacement of the neurovascular bundle. Plast Reconstr Surg 1974;54(1):31-44.

     

     

  45. McMillan C, Binhammer P. Steroid injection and needle aponeurotomy for Dupuytren contracture: a randomized, controlled study. J Hand Surg Am 2012;37(7):1307-1312.

     

     

  46. Medjoub K, Jawad A. The use of multiple needle fasciotomy in Dupuytren disease: retrospective observational study of outcome and patient satisfaction. Ann Plast Surg 2014;72(4):417-422.

     

     

  47. Meinel A. Long-term static overnight extension splinting following percutaneous needle fasciotomy [in German]. Handchir Mikrochir Plast Chir 2011;43(5):286-288.

     

     

  48. Nydick JA, Olliff BW, Garcia MJ, et al. A comparison of percutaneous needle fasciotomy and collagenase injection for dupuytren disease. J Hand Surg Am 2013;38(12):2377-2380.

     

     

  49. O'Gorman DB, Vi L, Gan BS. Molecular mechanisms and treatment strategies for Dupuytren's disease. Ther Clin Risk Manag 2010;6: 383-390.

     

     

  50. Peimer CA, Blazar P, Coleman S, et al. Dupuytren contracture recurrence following treatment with collagenase clostridium histolyticum (CORDLESS study): 3-year data. J Hand Surg Am 2013;38(1): 12-22.

     

     

  51. Peimer CA, McGoldrick CA, Fiore GJ. Nonsurgical treatment of Dupuytren's contracture: 1-year US post-

    marketing safety data for collagenase clostridium histolyticum. Hand 2012;7(2):143-146.

     

     

  52. Peimer CA, McGoldrick CA, Kaufman G. Nonsurgical treatment of dupuytren contracture: 3-year safety results using collagenase Clostridium histolyticum. Presented at the 68th Annual Meeting of the American Society for Surgery of the Hand, October 3-5, 2013, San Francisco, CA.

     

     

  53. Peimer CA, Skodny P, Mackowiak JI. Collagenase clostridium histolyticum for dupuytren contracture: patterns of use and effectiveness in clinical practice. J Hand Surg Am 2013;38(12):2370-2376.

     

     

  54. Pess GM, Pess RM, Pess RA. Results of needle aponeurotomy for Dupuytren contracture in over 1,000 fingers. J Hand Surg Am 2012; 37(4):651-656.

     

     

  55. Rayan GM. Clinical presentation and types of Dupuytren's disease. Hand Clin 1999;15(1):87-96, vii.

     

     

  56. Rayan GM, Parizi M, Tomasek JJ. Pharmacologic regulation of Dupuytren's fibroblast contraction in vitro. J Hand Surg Am 1996; 21(6):1065-1070.

     

     

  57. Reilly RM, Stern PJ, Goldfarb CA. A retrospective review of the management of Dupuytren's nodules. J Hand Surg Am 2005;30(5): 1014-1018.

     

     

  58. Rombouts JJ, Noel H, Legrain Y, et al. Prediction of recurrence in the treatment of Dupuytren's disease: evaluation of a histologic classification. J Hand Surg Am 1989;14(4):644-652.

     

     

  59. Sanjuan Cerveró R, Franco Ferrando N, Poquet Jornet J. Use of resources and costs associated with the treatment of Dupuytren's contracture at an orthopedics and traumatology surgery department in Denia (Spain): collagenase clostridium hystolyticum versus subtotal fasciectomy. BMC Musculoskelet Disord 2013;14:293.

     

     

  60. Short WH, Watson HK. Prediction of the spiral nerve in Dupuytren's contracture. J Hand Surg Am 1982;7(1):84-86.

     

     

  61. Starkweather KD, Lattuga S, Hurst LC, et al. Collagenase in the treatment of Dupuytren's disease: an in vitro study. J Hand Surg Am 1996;21(3):490-495.

     

     

  62. Swanson JW, Watt AJ, Vedder NB. Skin graft loss resulting from collagenase clostridium histolyticum treatment of Dupuytren contracture: case report and review of the literature. J Hand Surg Am 2013;38(3):548-551.

     

     

  63. Symes T, Stothard J. Two significant complications following percutaneous needle fasciotomy in a patient on anticoagulants. J Hand Surg Br 2006;31(6):606-607.

     

     

  64. Thomas PR, Clarke D. Vibration white finger and Dupuytren's contracture: are they related? Occup Med 1992;42(3):155-158.

     

     

    P.1222

  65. Tubiana R. Surgical management. In: Tubiana R, ed. The Hand. Philadelphia: WB Saunders Company, 1999:480.

     

     

  66. van Rijssen AL, Gerbrandy FS, Ter Linden H, et al. A comparison of the direct outcomes of percutaneous needle fasciotomy and limited fasciectomy for Dupuytren's disease: a 6-week follow-up study. J Hand Surg Am 2006;31(5):717-725.

     

     

  67. van Rijssen AL, ter Linden H, Werker PM. Five-year results of a randomized clinical trial on treatment in Dupuytren's disease: percutaneous needle fasciotomy versus limited fasciectomy. Plast Reconstr Surg 2012;129(2):469-477.

     

     

  68. van Rijssen AL, Werker PM. Percutaneous needle fasciotomy for recurrent Dupuytren disease. J Hand Surg Am 2012;37(9): 1820-1823.

     

     

  69. Verjee LS, Midwood K, Davidson D, et al. Myofibroblast distribution in Dupuytren's cords: correlation with digital contracture. J Hand Surg Am 2009;34(10):1785-1794.