Historical Background
Vascular reconstruction of peripheral arterial disease (PAD) using venous autografts dates back to the early twentieth century. Carrel and Guthrie described the technique of vascular anastomosis after developing the model in canines. In 1906 they published their experience of early bypass grafting using “venous transplantation.” Carrel was subsequently awarded the Nobel Prize in Physiology and Medicine in 1912. While Bernheim reported the use of a saphenoues vein interposition graft for treatment of a popliteal aneurysm in 1916 and Elkin and DeBakey noted the treatment of a small number of arterial injuries with interposition vein grafts in World War II, little progress was achieved in the first half of the 20th century prior to widespread availability of heparin, antibiotics, and appropriate vascular needles and suture material. In 1948 Kunlin’s successful femoral-popliteal bypass using reversed saphenous vein graft in a patient with arterial occlusive disease began the modern era of arterial lower extremity bypass.
In the current endovascular era, the femoral-popliteal bypass remains one of the most common open vascular operations. Endovascular interventions are increasingly successful as stand-alone procedures in many patients. However, a significant number of patients continue to require open bypass rather than percutaneous therapy because of extent of disease or after failure of endovascular therapy.
Preoperative Preparation
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History and physical examination. A complete history and a physical examination usually establish PAD as the source of symptoms. Patients with intermittent claudication typically describe exertional, muscular pain in the calves, thighs, or buttocks that is burning or cramping, resolves with rest, and is reproducible at a specific distance. Nocturnal pain, commonly in the forefoot, that occurs with the leg flat or elevated and resolves after placing the limb in a dependent position is typical of ischemic rest pain. Patients with CLI have symptoms including rest pain, tissue loss, or gangrene or develop nonhealing ulcers that arise spontaneously or after minor trauma. Gangrene is a late sign of CLI. PAD patients also often have a personal and family history of cardiovascular, cerebrovascular, or both diseases. Pertinent physical findings include absent pulses, trophic changes, and often, dependent rubor and pallor on elevation. Gangrene and nonhealing ulcers typically appear on the toes, forefoot, or areas of foot trauma.
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Noninvasive vascular laboratory testing. Vascular laboratory studies are required to confirm the degree of limb ischemia, determine the anatomic site or sites of involvement, and differentiate stenotic lesions from total occlusions. An ankle-brachial index (ABI) of less than 0.9 is diagnostic for hemodynamically significant occlusive disease and has been found to be 95% sensitive in identifying angiographically confirmed PAD. Claudicants with proximal PAD may only show a reduction in ABI after exercise. A 20% or greater reduction in ABI after exercise is abnormal. Arterial waveform patterns, toe waveforms and Doppler-derived pressures, and transcutaneous oxygen saturations are useful when the ABI cannot be measured because of incompressibility of calcified vessels (suprasystolic ABI), a frequent finding in individuals with diabetes mellitus or renal failure. Arterial duplex demonstrates sites of arterial occlusion or stenosis with color flow changes (mosaic color pattern) and elevated peak systolic velocities.
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Imaging studies. In patients who have diminished or absent femoral pulses, computed tomography or magnetic resonance imaging defines the length and extent of aortoiliac disease, factors with important implications in selecting the optimal intervention. Percutaneous angiography is the final step in assessing the anatomy of the arterial supply to the lower extremities, either serving as the immediate prelude to endovascular therapy or providing a road map for open bypass.
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Cardiovascular risk factor modification. PAD is a manifestation of a systemic disease process that affects the arterial circulation throughout the body. The incidence of nonfatal myocardial infarction, stroke, and vascular death is reported to be 5% to 7% per year for PAD patients. Mortality in patients with PAD averages 2% per year. PAD should be considered a coronary artery disease equivalent. Optimizing medical therapy is mandatory in all PAD patients, regardless of whether intervention is planned, and consists of risk factor modification to halt the progression of arterial disease not only in the lower extremities but in the body as a whole. Trans-Atlantic Inter-Society Consensus document II regarding the treatment of PAD outlines evidence-based recommendations for the medical management of PAD risk factors. Smoking is an independent risk factor for PAD development and progression. Smokers are three to five times more likely to have an amputation than are nonsmokers. Tobacco cessation rates can be improved with physician advice, group counseling, nicotine replacement, and a variety of pharmacologic adjuncts. Hyperlipidemia, a common independent risk factor for PAD, is preferentially controlled with a statin drug and dietary modification. Goals to achieve are a low-density lipoprotein level of less than 70 mg/dL in patients with coronary disease and a level of less than 100 mg/dL in those without. Fibrates, niacin, or both are useful in raising high-density lipoprotein levels and lowering triglyceride levels. Elevated serum homocysteine levels can be lowered with dietary supplementation of vitamin B 12 , vitamin B 6 , and folate, although beneficial effects of such therapy on PAD are not well substantiated. Hypertension is an additional strong risk factor for PAD. Blood pressure control can reduce PAD events by 22% to 26%, as well as significantly reduce the subsequent occurrence of cardiovascular and cerebrovascular events.
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Diabetes management. Large-scale studies have shown that intensive diabetes management reduces diabetes-related myocardial infarcts and other diabetes-related endpoints. The target hemoglobin A1c is less than 7.0%.
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Antiplatelet therapy. Antiplatelet therapy is a mainstay in the reduction of future cardiovascular and cerebrovascular events. Patients with cardiovascular disease experience a 25% odds reduction in further cardiovascular events by taking daily aspirin.
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Cardiopulmonary status. A chest radiograph and electrocardiogram should be performed as part of the preoperative evaluation. Further cardiopulmonary evaluation or optimization is recommended if the patient has unstable angina, significant arrhythmias, or symptoms of congestive heart failure or shortness of breath.
Pitfalls and Danger Points
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Inadequate vein conduit. Most vein conduit problems can be anticipated preoperatively if proper duplex vein mapping is performed. When vein problems are encountered unexpectedly during the intraoperative preparation of the vein, options are available to preserve the vein graft conduit. If a focal vein abnormality is found, it may be resected and a venovenostomy may be performed. Care is taken to spatulate the ends to create a wide anastomosis. If long segments of the vein are unusable, consideration should be given to harvesting from an alternate site: the contralateral great saphenous vein, the small saphenous vein, or spliced arm veins. Creating the proximal anastomosis to the profunda femoris artery or superficial femoral artery can allow utilization of shorter segments of vein.
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Small-caliber vein. At times, there is a size mismatch between the small-caliber reversed vein and a larger, thick-walled artery at the proximal anastomosis. If possible, a large branch at the distal end of the great saphenous vein should be preserved during harvest ( Fig. 44-1 , A ). The venotomy can incorporate this branch to create a heel that sits away from the artery. Anastomosis of the vein graft to a Linton vein patch can also remedy a size mismatch, particularly if an endarterectomy has been performed.
Figure 44-1
A, A vein tributary is incorporated into the venotomy to create a wider and slightly elevated anastomosis. This help prevents stenosis at heel of the graft. B, The first suture typically begins at the heel. The sutures are sewn continuously to a point halfway along the anastomosis, and then the second suture is started at the toe and sewn to the first suture. C, The two sutures are sewn continuously toward each other. The use of two separate sutures ensures symmetry and prevents “purse stringing,” as noted in the circular schematic.
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Unexpected inflow disease. Perioperative angiography helps the surgeon anticipate the presence of inflow disease. Atherosclerotic disease of the common femoral artery and profunda femoris artery can be addressed with an endarterectomy. This may entail partial division of the inguinal ligament to allow clamp placement on the nondiseased external iliac artery. A long venotomy can be used for the anastomosis if the conduit is of adequate caliber. Otherwise, the arteriotomy may require a vein patch with subsequent anastomosis of the bypass conduit to the patch. Alternatively, a segment of occluded superficial femoral artery can be endarterectomized and used to patch the arteriotomy.
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Unexpected outflow disease. The distal target for a femoral-popliteal bypass graft is an area free of disease with at least one continuous runoff artery to the foot. Unexpected hemodynamically significant popliteal disease may require direct bypass to more distal tibial or pedal target vessels. Intraoperative angiography is used to locate the most proximal segment of tibial or peroneal artery that is continuous with the foot. The distal bypass is performed to this site. Sequential bypass is useful for situations in which an isolated patent popliteal artery exists between severely diseased superficial femoral artery and proximal tibial arteries. A bypass graft from the thigh is connected to the proximal portion of the popliteal island. A separate bypass graft uses the distal popliteal segment as inflow and connects to a tibial or pedal vessel that has continuity with the foot. The advantage of this technique is that it allows shorter bypass segments and avoids creation of long, spliced vein conduits.
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Tunneling problems. It is recommended that an experienced member of the operative team perform the tunneling of the conduit. Passing the conduit through a large-bore tunneler protects it from tearing or shearing as it is pulled into place. Tunneling should always be undertaken along muscles and not through dense fascia or the belly of a muscle. The vein conduit should always be fully distended as it is passed through the tunnel to avoid twisting and kinking. After tunneling, if the proximal anastomosis has not yet been constructed, irrigation through the proximal end of the graft should produce vigorous flow through the distal anastomosis. Upon completion of the proximal anastomosis, the graft should have pulsatile flow. If not observed, the graft should be retunneled.
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Anastomotic stenosis. Prevention is the key to avoiding anastomotic stenoses. Diligence in tailoring the graft during the anastomosis often precludes this problem. When a size mismatch exists between the vein conduit and the artery, branches of the vein graft should be incorporated into the venotomy or a modified Linton patch should be used. Adequate vein length should always be measured with the knee extended before tailoring the vein for the distal anastomosis, because tension on the vein either proximally or distally results in vein stenosis just distal or proximal to the anastomosis. Clamp injury of the artery may also result in an anastomotic stenosis by plaque disruption. Completion angiography, intraoperative Doppler, or duplex ultrasound identifies anastomotic stenoses that occur despite careful operative technique. If a stenosis occurs, the anastomosis is examined and the trapped adventitia is freed or disrupted plaque is excised or tacked down. If this does not help, the heel of the graft requires a vein patch to widen the anastomosis.
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Reoperative bypass. The reoperative bypass is a taxing, time-consuming operation, even for the most experienced surgeon. In general, all efforts are taken to use autogenous vein to provide optimal long-term patency. Meticulous preparation of the conduit is paramount, especially if the primary bypass failed because of technical error. If possible, the surgeon should avoid previously operated fields and consider alternative inflow and outflow sources; these approaches may require exposure of the distal profunda femoris artery, the superficial femoral artery, and tibial or pedal vessels.
Operative Strategy
Surgical Anatomy of the Femoral and Popliteal Arteries
The femoral triangle is the anatomic space bordered by the inguinal ligament superiorly, the sartorius muscle laterally, and the adductor magnus muscle medially ( Fig. 44-2 , A ). The floor of the femoral triangle contains four muscles: the iliacus, psoas major, pectineus, and adductor magnus. A fascial covering called the femoral sheath contains the major vascular structures in the femoral triangle. The common femoral artery is the continuation of the external iliac artery below the inguinal ligament. In the femoral triangle, the common femoral artery divides into two major branches ( Fig. 44-2 , B ). The profunda femoris artery is most commonly a posterolateral branch, not only providing blood to the thigh but also serving as the major collateral to the lower extremity in patients with occlusion of the superficial femoral artery. The superficial femoral artery is the continuation of the common femoral artery and carries blood to the lower leg. Exiting the femoral triangle, the superficial femoral artery proceeds distally on its course into the adductor canal.### The common femoral vein is located just medially to the common femoral artery in the triangle ( Fig. 44-2 , B ). The great saphenous vein enters the common femoral vein at the fossa ovalis. Other important structures in the femoral triangle include the femoral nerve. The nerve is lateral to the artery and provides motor and sensory function primarily to the thigh. Medial to the common femoral vein are the lymphatic structures draining interstitial fluid from the leg.
The popliteal fossa is another anatomic area of significance in lower extremity revascularization. It is a diamond-shaped space defined anteriorly by the femur, upper tibia, and popliteus muscle; posteriorly by the skin, subcutaneous tissue, and fascia; laterally by biceps femoris and gastrocnemius muscles; and medially by semitendinosus and semimembranosus muscles. Figures 44-3 and 44-4 illustrate the common surgical exposures for the above- and below-knee portions of the popliteal artery, respectively. The superficial femoral artery exits the adductor canal at the apex of the popliteal fossa, where it becomes the popliteal artery. Paired popliteal veins are closely adjacent. Below the knee, at variable areas in the distal popliteal fossa, the popliteal artery divides into the anterior tibial artery and the tibioperoneal trunk. The anterior tibial artery exits laterally above the interosseous membrane and enters the anterior compartment of the lower leg. The tibioperoneal trunk continues and divides into the posterior tibial artery and the peroneal artery. These two vessels enter the deep posterior compartment of the lower leg.
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