Management of Acute Limb Ischemia Complicating Aortic Reconstruction

Scope of the Problem

Historical reports documented acute limb ischemia in up to 25% of patients undergoing abdominal aortic surgery. With refinement of operative technique and the use of local and systemic anticoagulation, the incidence of this complication has decreased significantly, but it has not been eliminated. Data from the randomized aneurysm trials and large retrospective database analyses report perioperative thromboembolic complication rates between 1% and 2% and amputation rates significantly less than 1% for both open and endovascular reconstruction techniques. Though patients with combined aneurysmal and occlusive disease patterns seem to have the highest risk, most reports demonstrate no major differences in occurrence between patients operated on for aneurysmal disease compared to occlusive disease.

Etiology

There are a number of causes of acute limb ischemia associated with aortic surgery and they can be broadly classified as embolic or thrombotic ( Figure 1 ).

Embolic subcategories include macroemboli and microemboli (see Figure 1 B and C). Macroembolic sources found in diseased aortas, such as laminated or friable thrombus (see Figure 1 A), can be dislodged during dissection, clamping, or endovascular manipulations and can result in obstruction of the major named arteries supplying the lower extremity. In the absence of adequate anticoagulation, thrombus can quickly develop in the obstructed artery. In cases of microembolism, the major arteries of the leg remain patent while small fragments of thrombus or debris lodge in the smaller vessels and microcirculation of the lower limb. Atheroembolism, the disruption and release of atherosclerotic plaque contents, is one type of microembolic syndrome that can produce the classic trash foot, but these microparticles can also lodge in the muscles of the legs and buttocks.

Thrombotic etiologies relate primarily to inflow, conduit, and outflow problems. Poor inflow can cause thrombosis of the native artery or graft and is commonly caused by clamp injury, unappreciated proximal stenotic disease, and the use of large occlusive sheaths. Defects in the conduit, such as twisted, kinked, or compressed graft or stent graft limbs can also result in thrombotic complications. Disadvantaged outflow, such as anastomotic defects, arterial wall dissections, and flaps (see Figure 1 D and E) or heavily diseased distal vasculature, can give rise to abnormal flow, leading to thrombus formation and acute limb ischemia. Lastly, systemic conditions, such as profound hypotension and hypercoagulability, can also cause thrombosis of the reconstruction or downstream arteries.