Exploring Limb Salvage Options In Patients With Chronic Limb Ischemia

By John E. Aruny, MD, Peter Blume, DPM, Bauer Sumpio, MD, PhD, and Benjamin Buren, DPM

   Chronic critical limb ischemia has been defined as a non-healing ulceration or gangrene of the foot or toes, and/or rest pain that requires regular use of analgesics.1 These patients will require some type of intervention to resolve their condition. It can be particularly challenging to salvage the limb of a patient who has failed a bypass. The objective of revascularization is to augment blood flow to allow for wound healing and avoid major amputation resulting in the need for a prosthesis.    Amputation of one or more digits or even transmetatarsal amputation preserves enough of the foot to allow for ambulation. However, after excision of the gangrenous segment, the surgical wound will not heal if there is inadequate blood flow to the area. Diabetic patients and others with limb-threatening ischemia often have few choices. Bypass surgery may not be possible due to poor vein quality or previous harvesting of saphenous veins for coronary artery bypass.    Angioplasty for infrapopliteal vascular occlusive disease is not new. Dotter and Judkins described three patients with peroneal-tibial trunk angioplasty in their initial report in 1964.2 At first, coronary balloons were utilized and then specialized angioplasty balloons designed for tibial vessels became available.3 Limb salvage rates were similar to surgery. However, only 20 to 30 percent of patients with isolated tibial disease were candidates for endovascular therapy due to the number and length of lesions. Recently, Bolia, Brennan and Bell described subintimal angioplasty.4 Others have supported the role of this technique for limb salvage and have successfully treated longer lesions with close to 90 percent technical success.1,5    The development of cryoplasty therapy has advanced the mechanical properties of the angioplasty balloon, potentially transforming it into an instrument that alters the physiology of the plaque and smooth muscle cells. One uses liquid nitrous oxide to inflate the balloon for 20 seconds at 8 ATM. This cools the balloon to –10º C. The thinking is that this freezing action alters the plaque response to angioplasty, causing it to fracture more uniformly and reduce the incidence of flow-limiting dissections. There is a reduction in vessel wall recoil. Finally, the freezing action has been shown in vitro to activate markers of apoptosis. TUNEL assay and Annexin V assay revealed an apoptotic peak at –10º C and no apoptosis above 15º C. In theory, this suspends the ability of smooth muscle cells to secrete matrix, the basis of the restenotic lesion.    With this in mind, let us consider a case study in which cyroplasty therapy was utilized in a combination approach to salvage the limb of a patient with chronic limb ischemia.

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