Peripheral Arterial Occlusive Disease

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Claudication, which is defined as reproducible ischemic muscle pain, is one of the most common manifestations of peripheral arterial occlusive disease (PAOD) caused by atherosclerosis. Claudication occurs during physical activity and is relieved after a short rest. Pain develops because of inadequate blood flow.

Angiography is the criterion standard arterial imaging study for the diagnosis of PAOD. The image below depicts a superficial femoral artery occlusion.

Intermittent claudication typically causes pain that occurs with physical activity. Other signs and symptoms associated with peripheral arterial occlusive disease (PAOD) include the following:

See Presentation for more detail.

Examination of a patient with claudication should include a complete lower-extremity evaluation and pulse examination, including measuring segmental pressures. Attempt to palpate pulses from the abdominal aorta to the foot, with auscultation for bruits in the abdominal and pelvic regions. When palpable pulses are not present, a handheld Doppler device may be used to assess circulation.

A useful tool in assessing a patient with claudication is the ankle-brachial index (ABI), which is a noninvasive way of establishing the presence of PAOD and is calculated as the ratio of systolic blood pressure at the ankle to that in the arm (normal range, 0.9-1.1; PAOD, < 0.9).

Laboratory testing

A laboratory workup is helpful only for identifying accompanying silent alterations in renal function and elevated lipid profiles.

Imaging studies

The following radiologic studies may be used to evaluate suspected PAOD:

See Workup for more detail.

Treatment of claudication is medical, with surgery reserved for severe cases. Medical management includes the following:

Pharmacotherapy

The following medications are used in the management of PAOD:

Surgery

For patients in whom medical and exercise therapy fail or those who have claudication symptoms that are lifestyle-limiting, surgical treatment includes either open bypass surgery or endovascular therapy (eg, stents, balloons, or atherectomy devices).

See Treatment and Medication for more detail.

Claudication, which is defined as reproducible ischemic muscle pain, is one of the most common manifestations of peripheral vascular disease caused by atherosclerosis (peripheral arterial occlusive disease [PAOD]). Claudication occurs during physical activity and is relieved after a short rest. Pain develops because of inadequate blood flow.

For patient education resources, see the Circulatory Problems Center and Cholesterol Center, as well as Peripheral Vascular Disease, High Cholesterol, and Cholesterol FAQs.

Single or multiple arterial stenoses produce impaired hemodynamics at the tissue level in patients with PAOD. Arterial stenoses lead to alterations in the distal perfusion pressures available to affected muscle groups.

Under resting conditions, normal blood flow to extremity muscle groups averages 300-400 mL/min. Once exercise begins, blood flow increases as much as 10-fold as a consequence of the increase in cardiac output and compensatory vasodilation at the tissue level. This allows the increase in oxygen demand to be met. When exercise ceases, blood flow returns to normal within minutes.

Resting blood flow in a person with PAOD is similar to that in a healthy person. In PAOD, however, blood flow cannot maximally increase in muscle tissue during exercise, because proximal arterial stenoses prevent compensatory vasodilation. When the metabolic demands of the muscle exceed blood flow, claudication symptoms ensue. At the same time, a longer recovery period is required for blood flow to return to baseline once exercise is terminated.

Similar abnormal alterations occur in distal perfusion pressure in affected extremities. In normal extremities, the mean blood pressure drop from the heart to the ankles is no more than a few millimeters of mercury. In fact, as pressure travels distally, the measured systolic pressure actually increases because of the higher resistance encountered in smaller-diameter vessels.

At baseline, a healthy person may have a higher measured ankle pressure than arm pressure. When exercise begins, no change in measured blood pressure occurs in the healthy extremity.

In the atherosclerotic limb, each stenotic segment acts to reduce the pressure head experienced by distal muscle groups. Correspondingly, at rest, the measured blood pressure at the ankle is less than that measured in a healthy person. Once physical activity starts, the reduction in pressure produced by the atherosclerotic lesion becomes more significant, and the distal pressure is greatly diminished.

The phenomenon of increased blood flow causing decreased pressure distally to an area of stenosis is a matter of physics. Poiseuille calculated energy losses across areas of resistance with varying flow rates by using the following equation:

Pressure difference = 8QvL/πr4

where Q is flow, v is viscosity, L is the length of the stenotic area, and r is the radius of the open area within the stenosis. In this equation, the pressure gradient is directly proportional to the flow and the length of the stenosis and inversely proportional to the fourth power of the radius. Thus, although increasing the flow rate directly increases the pressure gradient at any given radius, these effects are much less marked than those due to changes in the radius of the stenosis.

Because the radius is raised to the fourth power, it is the factor that has the most dramatic impact on a pressure gradient across a lesion. This impact is additive when two or more occlusive lesions are located sequentially within the same artery.

Atherosclerosis affects up to 10% of the Western population older than 65 years. With the elderly population expected to increase 22% by the year 2040, atherosclerosis is expected to have a huge financial impact on medicine.

Estimated PAOD prevalence in the general US population, based on National Health and Nutrition Examination Survey (NHANES) data, was 4.3%. [1] Thus in 2000, about 5 million people in the US were affected by PAOD. That number increases with age; therefore, as the population ages the number of people affected by PAOD increases.

When claudication is used as an indicator, it is estimated that 2% of the population aged 40-60 years and 6% of the population older than 70 years are affected. Intermittent claudication most commonly manifests in men older than 50 years. Although younger patients may present with symptoms consistent with intermittent claudication, other etiologies of leg pain and claudication (eg, popliteal entrapment syndrome) must be strongly considered. There seems to be a higher prevalence of PAOD in non-Hispanic blacks.

Whether a patient progresses to limb amputation largely depends on the number and severity of cardiovascular risk factors (ie, smoking, hypertension, or diabetes). Continued smoking has been identified as the adverse risk factor most consistently associated with the progression of PAOD. Other factors are the severity of disease at the time of the initial patient encounter and, in some studies, the presence of diabetes.

In an effort to identify patients at highest risk for progression to critical limb ischemia (CLI), a simple risk score for PAOD was developed: the Graz CLI score. [2] Age and diabetes were among the most aggressive risk factors (respective odds ratios, 2.0 and 3.1).

As with most patients with vascular disease, survival is less than that of age-matched control groups. Coronary artery disease, with a subsequent myocardial event, is the major contributor to outcome. Predicted all-cause mortality for PAOD patients with claudication is approximately 30% at 5 years of follow-up, 50% at 10 years, and 70% at 15 years. [3]

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Josefina A Dominguez, MD Resident Physician, Department of Surgery, Division of Vascular Surgery, Keck School of Medicine of the University of Southern California, LAC+USC Hospital

Josefina A Dominguez, MD is a member of the following medical societies: Society for Clinical Vascular Surgery

Disclosure: Nothing to disclose.

Vincent Lopez Rowe, MD Professor of Surgery, Program Director, Vascular Surgery Residency, Department of Surgery, Division of Vascular Surgery, Keck School of Medicine of the University of Southern California

Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Surgical Association, Pacific Coast Surgical Association, Society for Clinical Vascular Surgery, Society for Vascular Surgery, Western Vascular Society

Disclosure: Nothing to disclose.

Vincent Lopez Rowe, MD Professor of Surgery, Program Director, Vascular Surgery Residency, Department of Surgery, Division of Vascular Surgery, Keck School of Medicine of the University of Southern California

Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Surgical Association, Pacific Coast Surgical Association, Society for Clinical Vascular Surgery, Society for Vascular Surgery, Western Vascular Society

Disclosure: Nothing to disclose.

William H Pearce, MD Chief, Division of Vascular Surgery, Violet and Charles Baldwin Professor of Vascular Surgery, Department of Surgery, Northwestern University, The Feinberg School of Medicine

William H Pearce, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, American Surgical Association, Association for Academic Surgery, Association of VA Surgeons, Central Surgical Association, New York Academy of Sciences, Society for Vascular Surgery, Society of Critical Care Medicine, Society of University Surgeons, andWestern Surgical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Peripheral Arterial Occlusive Disease

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