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Intermittent claudication consists of reproducible lower extremity muscular pain induced by exercise and relieved by short periods of rest. It is caused by arterial obstruction, which restricts the normal exercise-induced increase in blood flow, producing transient muscle ischemia. Studies have shown that more than half of patients with intermittent claudication have never complained of this symptom to their physicians, assuming that difficulty with walking is a normal consequence of aging. Finally, only one-third or less of patients with peripheral arterial disease (PAD) have typical claudication; others have atypical leg pain or are asymptomatic because medical comorbidities limit ambulation. Claudication is a marker of systemic atherosclerotic disease, with associated cardiovascular mortality rates at 5 and 10 years of roughly 42% and 65%, respectively.
Risk factor modification, exercise, and pharmacologic therapies. Smoking cessation reliably doubles walking distances and reduces the need for eventual amputation in patients with PAD. Exercise (defined as walking until onset of leg pain, resting, and then resuming walking) for 30–60 minutes, 3 days per week for 6 months has also been demonstrated in multiple randomized trials to increase walking distance by more than 100%. Currently, the only Food and Drug Administration–approved drugs for the treatment of claudication are Pentoxifylline (minimally effective) and Cilostazol (more effective). Pharmacologic therapy should also target dyslipidemia, hypertension, and glycemic control. In addition, lifelong antiplatelet therapy is essential. Of note, the benefits of lifestyle modification, especially smoking cessation, are also imperative following operative intervention on PAD. Graft failure rates in patients who continue to smoke after peripheral arterial bypass are threefold higher than their nonsmoking equivalents. Nicotine inhalation promotes PAD and graft failure by increasing platelet aggregation, decreasing prostacyclin, and increasing thromboxane, promoting vasoconstriction and thrombosis.
CLI potentially threatens the viability of the limb. Symptoms include rest pain, typically occurring at night when the patient is supine and gravity contribution to foot arterial pressure is no longer present. This pain is relieved with foot dependency. Peripheral circulation in CLI is not sufficient to heal minor skin breakdown caused by incidental trauma. These patients develop ischemic ulcers that are frequently painful and can progress to gangrene. CLI implies chronicity and should be distinguished from acute limb ischemia, which is due to sudden (defined as 2 weeks or less) reduction in limb perfusion.
ABI is the highest ankle pressure (anterior tibial or posterior tibial artery) divided by the higher of the two brachial pressures. The normal ABI is slightly >1 (1.10). An ABI of 0.5–0.8 is typical of patients with claudication. Even in the absence of symptoms, an ABI of <0.9 is 95% sensitive for PAD confirmed by angiography. Patients with rest pain have an ABI <0.5, and patients with tissue necrosis often have an ABI much lower.
Multiple natural history studies have documented the benign nature of claudication. The cumulative 10-year amputation rate is 10%. One-third of patients experience symptom deterioration, and half of these patients require some sort of revascularization. Continued smoking and diabetes are major risk factors for progression. Of note, however, is that PAD is a marker of overall cardiovascular disease status. Patients with PAD have a 20% risk of myocardial infarction (MI) or stroke and a 10% risk of death in 5 years. Given the relatively low 10-year amputation rate, higher cardiovascular mortality rate, and poor compliance with smoking cessation in these patients, many vascular surgeons are increasingly reluctant to perform a major open revascularization for claudication alone.
CLI often requires revascularization or primary amputation. Percutaneous interventions are increasingly used as the primary therapy with surgical procedures or amputation used if they fail. A subgroup of patients with CLI cannot be effectively treated with surgical or endovascular revascularization. Meticulous wound management and intermittent pneumatic compression therapy can help patients with uncomplicated chronic nonhealing ulcers. Again, the presence of CLI is a harbinger of grave overall health status. About 40% of patients with CLI will have an amputation, and 20% will die within 6 months of diagnosis.
Just as the ABI is recorded at the ankle, cuffs at the high thigh, above knee, below knee, and toe level can record pressures. Noting the location of decreases in arterial pressure can determine the level of the vascular obstruction. Typically, a reduction in pressure of 20 mm Hg or greater between segments is considered significant and will help determine the level of obstruction.
Although bypass grafts can dramatically improve lower extremity circulation, they have a limited life expectancy and may require maintenance for longevity. In the first 1–2 years, lesions intrinsic to the graft are often the primary threat to graft patency. After 2 years, inflow and outflow disease are common sources of reduced flow through the graft, which can lead to occlusion. When these grafts fail, the limb involved frequently has poorer perfusion than before the bypass. This is because of division of major arterial collateral pathways during the operation and thrombus propagation or embolization to occlude distal arteries at the time of graft occlusion.
Significant atherosclerosis in young patients (age <40 years) is infrequent. These patients are often heavy smokers with a high incidence of diabetes, renal failure, and/or hypercoagulable states (defective fibrinolysis, anticardiolipin antibodies, homocysteinemia, or deficiencies in natural anticoagulants). Those with limb-threatening conditions frequently progress to limb loss despite attempts at revascularization. Reconstructive procedures have limited success and require frequent revision in this population.
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