6 Acute Vascular Compromise after Dupuytren’s Fasciectomy
6.1 Patient History Leading to the Specific Problem
A 51-year-old man presented with Dupuytren’s contracture involving the right finger. This progressively worsened over the past 3 years and now limited his ability to perform manual labor. On examination, there were palpable cords and visible flexion contractures of 60 degrees at the metacarpophalangeal (MCP) joints and 40 degrees at the proximal interphalangeal (PIP) joint. The patient was deemed to be a candidate for surgical intervention with aggressive fasciectomy. He was brought back to the operating theater, placed in the supine position with the right arm abducted to 90 degrees, and sterile tourniquet inflated to 250 mm Hg. A longitudinal incision with designed 60-degree Z-plasty markings was utilized for access in the palm and Bruner-type incisions were designed in the finger. The neurovascular bundles were intimately involved with the cord and displaced medially. The digital nerves were easily identified and protected on either side of the cord. Palmar fasciectomy was performed with removal of pretendinous bands, digital cords, and tight spiral cords around the ring finger. The tourniquet was let down and the ring finger remained extremely white (▶Fig. 6.1). The fingers were placed back in slight flexion and warm saline-moistened laps were applied. The patient had been hemodynamically optimized to make sure hypotension was not a contributing factor. After 30 minutes of ischemia time, no change was identified in the finger. Papaverine was used to try to topically dilate the vessels and the microscope was prepped and draped to visualize each digital vessel.
Fig. 6.1 Vascular compromise observed following fasciectomy of the finger. The digital arteries were compromised during the dissection.
6.2 Anatomic Description of the Patient’s Current Status
The eponym Dupuytren’s contracture takes root from Baron Guillame Dupuytren’s 1831 lecture on the disease. However, Plater in 1614, Cline in 1777, and Cooper in 1822 previously described the disease process and fasciotomy. Dupuytren’s disease is thought to have a genetic predisposition, most commonly affecting people of Northern European descent and occurring later in life. Manual labor, trauma, alcoholism, epilepsy, and others have previously been implicated in the etiology, although conclusive evidence is lacking. Fibroblasts and myofibroblasts are thought to be the cells responsible for nodule formation, collagen deposition into cords, and progressive contracture of the digits.
A firm understanding of normal anatomical structures in the palm must first be understood to appreciate this disease process. The palmar skin and subcutaneous fat are separated from the flexor tendons by the palmar aponeurosis. This triangular-shaped fascial layer originates from the palmaris longus tendon and splits distally into pretendinous bands. The pretendinous bands further divide into three distinct layers: superficial, middle, and deep. The superficial layer attaches to the skin at the MCP crease. The deep layer extends dorsally attaching to the interosseous muscle fascia and deep transverse metacarpal ligament. The middle layer forms two spiral bands that contribute to the web-space coalescence. The natatory ligaments are transversely oriented and travel across all digits. The natatory ligaments have fibrous attachments to the flexor tendon sheath at the MCP joint and contribute to the web-space coalescence. The web-space coalescence continues distally into the finger to form the lateral digital sheet, which further splits volarly and dorsally into Grayson’s ligament and Cleland’s ligament, respectively. The neurovascular bundle lies deep to the palmar aponeurosis. The bundles run parallel to the flexor tendons, separated from the tendons by adipose and vertical fascial bands of Legueu and Juvara. At the palmar–digital junction, the neurovascular bundle becomes more superficial and midline, passing volar to the spiral bands. The bundle continues to travel distally in the finger encased by the lateral digital sheet (lateral), retrovascular fascia (medial), Cleland’s ligament (dorsal), and Grayson’s ligament (volar).
Dupuytren’s disease is progressive over time and can involve any of the longitudinally oriented ligaments, as well as the transversely oriented natatory. Predictable patterns of pathologic nodules and cord formations can be based off this anatomy. Pathology typically starts with nodule formation in the pretendinous band and causes pitting of the skin due to dermal attachments. With deposition of type III collagen, this progresses to pretendinous cord formation, which is the most common. Spiral cords can also form with involvement of spiral bands, lateral digital sheet, and Grayson’s ligaments. Spiral cords are responsible for MCP joint flexion and displacement of the neurovascular bundles into an abnormal superficial and medial position. The natatory ligament and lateral digital sheet may also be involved. Finally, a central cord can form over the proximal phalanx without any normal fascia precursors and contributes to PIP flexion deformity. Cleland’s ligament and the transverse ligament of the palmar aponeurosis are not involved in Dupuytren’s disease.
6.3 Recommended Solution to the Problem
Multiple treatment options exist for disruption of these cords including the following: physical therapy, clostridium histolyticum collagenase, needle aponeurotomy, and surgical intervention with partial or total fasciectomy. Surgery is typically reserved for more severe cases and traditional indications included MCP flexion contracture less than 30 degrees or any PIP flexion contracture. Treatment complications include skin necrosis, infection, hematoma, edema, flare pain syndromes, neurovascular injury, and recurrence. The rate of acute vascular injury is quoted at 2% in the literature with a range of 0.8 to 9%. This rate increases significantly in patients being treated for recurrence. Although the rate of vascular injury is quite low, the surgeon must be prepared to deal with this complication.
Multiple intraoperative techniques can be utilized to prevent vascular injury. Increased visualization of the vessels can be achieved by avoiding total exsanguination of the hand prior to tourniquet insufflation, along with the use of loupe magnification, and access to operating microscope. Incision should be started proximal to the area of the diseased palm. Dissection should proceed from known to unknown, proximal to distal palm, with the understanding that the nerve and artery are not always intimately associated. Damage to the neurovascular structures can occur on initial incision if starting distally at the palm–digit junction. Neurovascular bundles should be handled delicately and protected at all times during fascial excision. Avoiding aggressive passive extension of the MCP and PIP joints can prevent digital artery spasm. Additionally, during closure, care should be taken to avoid tension on vessels from skin flap inset.
If the digit remains pale and cool after release of the tourniquet, then vascular injury should be suspected. The next step is to determine the etiology of injury: vasospasm, intimal hemorrhage, traction rupture, or sharp transection. Initially, the fingers should be placed back into a slightly flexed position and warm saline-soaked gauze should be applied to the operative site and digit. Topical smooth-muscle relaxants, such as 20% lidocaine, calcium channel blockers, and papaverine, should bath the vessel directly and allow this to sit for 10 to 15 minutes prior to manipulation of the digit. Systemic anticoagulation, with heparin 5,000 U, may also be attempted if there are no contraindications. If these interventions fail to restore perfusion to the digit, then further exploration of the neurovascular bundles is warranted.
If brisk pulsatile bleeding from the proximal artery is encountered, then sharp transection likely occurred. Primary anastomosis of the vessel under operative microscope is used to restore flow. If no bleeding is encountered, then further exploration of the bundles is performed to identify rupture with intravascular thrombosis due to intimal trauma. This will require excision of the rupture site and the thrombosed portion of the vessel. Interposition vein graft will need to be harvested and anastomosed to restore flow. Postoperative revascularization monitoring and protocols should ensue.
6.4 Technique
In the above-listed case, neurovascular injury was suspected to both digital arteries. No improvement was noted in the ring finger perfusion with conservative measures, and decision was made to further explore the neurovascular bundles under microscopic assistance. Inspection of the ulnar-sided bundle showed a sharp transection to the artery, which was medially displaced near the palmar–digital junction. Inspection of the radial-sided bundle revealed a large arterial gap spanning from the palm and entirety of the proximal phalanx. The surgical plan included primary repair of ulnar-sided artery and an interposition vein graft for repair of the radial-sided artery.
Attention was first turned to the ulnar-sided digital artery. Yasargil clamps were applied, and the vessel ends were flushed and prepared by removal of adventitia. The vessel was then coapted with 9–0 nylon suture in an interrupted fashion without tension. The Yasargil clips were removed, no leak was identified, and the finger regained perfusion.
Attention was then turned to the radial digital artery. The vessel ends were trimmed, flushed with heparin, and pulsatile bleeding was restored. Yasargil clamps were applied and vessels ends prepared. The defect size was measured. Next, a vein graft was harvested through a longitudinal incision over the volar forearm. The vein was clipped proximally and distally, and then sharply transected for removal. The vein was flushed and placed in a reverse direction between the arterial ends. Again using microscopic assistance, a 9–0 nylon was used to coapt the proximal end in a simple, interrupted, tension-free manner. The added vein length was removed from the distal segment to avoid kinking. This was then anastomosed in a similar fashion. The vascular clamps were removed and good flow was observed (▶Fig. 6.2). The skin flaps were then closed in a loose fashion to avoid compression of the bypass graft. A bulky, noncompressive dressing was placed with fingers in slight flexion. The patient was admitted to the hospital and started on a daily aspirin and heparin 5,000 U thrice a day for the next 3 days.
