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Ulnar Artery Reconstruction With LCFA Graft for Hypothenar Hammer Syndrome

Zachary S. Gala, BSE; Haripriya Ayyala, MD; Stephen L. Viviano, MD; Ashley Ignatiuk, MD, MSc, FRCSC

Disclosures

ePlasty. 2020;20(e10) 

In This Article

Discussion

Hypothenar hammer syndrome refers to thrombosis/aneurysm of ulnar artery at Guyon's canal in wrist, with resultant arterial insufficiency in the ulnar artery distribution. This condition was first described by Van Rosen in 1934. Overall, the disease is quite rare, with about a 1.6% incidence rate, and a male predominance of M:F = 9:1. The term "hypothenar hammer" syndrome was coined by Conn et al in 1970,[2–6] in which the hook of the hamate bone acts as an anvil for the ulnar artery, which is subject to repetitive forces (the hammer). The cause, for all intents and purposes, is effectively trauma. Risk factors include repeated vibration and occupations such as carpenters and mechanics. Ferris and Stone's[7] landmark study suggested that underlying vascular anomalies, such as intimal hyperplasia, can predispose individuals to developing this disease. Patients typically describe unilateral symptoms in the fourth and/or fifth fingers of the hand. Symptoms can range from asymptomatic to pain, pallor, paresthesia, weakness, cold intolerance, and eventually ulceration, necrosis, and gangrene of the distal digits. If an aneurysm is present, some patients may present with a pulsatile mass. Workup usually contains a positive Tinel's test, in which tapping over the ulnar artery distribution elicits pain. However, some studies have shown that up to 17% of patients with this condition have normal Allen's tests.[8] Workup is confirmed with contrast imaging (magnetic resonance angiography [MRA]) that shows segmental occlusion or aneurysm in the ulnar artery and a resultant incomplete superficial arch.

Treatment options range from conservative lifestyle management to medication and, ultimately, to surgical intervention. Regimens typically begin with nonoperative lifestyle management: smoking cessation, avoidance of recurrent trauma and exacerbating factors, or the use of padded/protective gloves. Medical treatments are the second step and traditionally target the Raynaud's-like phenomenon with the use of calcium channel blockers (CCBs) and antiplatelet (anti-PLT) medications.[1,5,6] If these interventions are unsuccessful, medical professionals proceed to surgical treatment. Endovascular fibrinolysis is indicated for thrombotic lesions without aneurysm that have been present for less than 2 weeks. The most common operative treatment is arterial ligation and reconstruction. This procedure is indicated for patients with a digital-brachial index less than 0.7 and if conservative treatment measures have failed.[1] The last-resort effort is typically the Leriche procedure, which is resection of the diseased arterial segment without reconstruction, indicated if the digital-brachial index is greater than 0.7. Surgical treatments typically consist of dissection and resection of the diseased arterial segment with arterial reconstruction. The repair was first done by end-to-end anastomosis of the ulnar artery. Lifchez and Higgins's 2009 study showed that venous graft reconstruction showed better long-term outcomes compared with end-to end anastomosis of the ulnar artery.[9] Dethmers[10] and Endress[11] showed that most venous grafts used in ulnar artery reconstruction were occluded at various long-term study endpoints. Temming first described the use of a lateral circumflex femoral artery (LCFA) arterial graft for ulnar artery reconstruction of the ulnar artery in the setting of hypothenar hammer syndrome.[12,13] Ultimately, in 2017, De Niet showed that arterial grafts had better outcomes when compared with venous grafts in terms of long-term patency.[14] At a 63-month follow-up, 11 of 11 grafts were patent, and 9 of 11 patients showed clinical improvement for LCFA reconstruction of the ulnar artery.

To our knowledge, the use of intraoperative ICG imaging has not been previously described. There are no true indications for the use of intraoperative ICG, but its postoperative use and efficacy have been well described. The authors decided to use ICG imaging before arterial ligation and sympathetctomy. This revealed an additional area of stenosis in the ulnar artery previously unseen on the preoperative MRA scan. Because the pathologic segment was larger than originally thought, a more radical dissection, ligation, sympathectomy, and LCFA graft ensued. Although the procedure was more drastic, it was also more appropriate, as it successfully identified all pathologic segments of the artery. If the authors solely used MRA, there would have been an incomplete resection of the ulnar artery, and it is likely that the patient's symptoms would not have completely resolved.

The authors would strongly consider using intraoperative ICG imaging in future cases to ensure that all pathologic segments were correctly identified and that an adequate surgical intervention was planned. More research needs to be done, however, as to the success and efficacy of intraoperative ICG compared with preoperative MRA alone.

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