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Peripheral Arterial Occlusive Disease

Author: Vincent Lopez Rowe, MD, Assistant Professor of Surgery, Department of Surgery, Division of Vascular Surgery, University of Southern California Medical Center
Contributor Information and Disclosures

Updated: Oct 26, 2009

Introduction

Background

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

Pathophysiology

Single or multiple arterial stenoses produce impaired hemodynamics at the tissue level in patients with peripheral arterial occlusive disease (PAOD). Arterial stenoses lead to alterations in the distal pressures available to affected muscle groups and to blood flow.

In patients with PAOD, resting blood flow is similar to that of a healthy person. However, during exercise, blood flow cannot maximally increase in muscle tissue because of proximal arterial stenoses. 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 of 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, in which Q is flow, v is viscosity, L is the length of the stenotic area, r is the radius of the open area within the stenosis, and k is constant:

Resistance = pressure = Q8vL/kr4

Applying this equation, the pressure gradient is directly proportional to the flow and length of stenosis and inversely proportional to the fourth power of the radius.

Therefore, while increasing the rate of flow 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.

As the radius is raised to the fourth power, it has the most dramatic impact on a pressure gradient across a lesion. This impact is additive when 2 or more occlusive lesions are located sequentially within the same artery.

Frequency

United States

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. When claudication is used as an indicator, estimates are that 2% of the population aged 40-60 years and 6% older than 70 years are affected.

Mortality/Morbidity

The most feared consequence is severe limb-threatening ischemia leading to amputation. However, studies of large patient groups with claudication reveal that amputation is uncommon. Boyd prospectively followed 1440 patients with intermittent claudication for as long as 10 years and reported that only 12.2% required amputation.¹ In the Framingham study, only 1.6% of patients with claudication reached the amputation stage after 8.3 years of follow-up.

• Limb amputation largely depends on the number and severity of cardiovascular risk factors (ie, smoking, hypertension, diabetes). Continued smoking has been identified as the most consistent adverse risk factor associated with the progression of peripheral arterial occlusive disease (PAOD). Other factors are the severity of disease at the time of the initial patient encounter and, in some studies, the presence of diabetes.
• 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 mortality rates for patients with claudication at 5, 10, and 15 years of follow-up are approximately 30%, 50%, and 70%, respectively.

Race

• Peripheral arterial occlusive disease (PAOD) has no racial predilection.

Sex

• 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.

Clinical

History

Intermittent claudication typically causes pain that occurs with physical activity. Determining how much physical activity is needed before the onset of pain is crucial.

• Typically, vascular surgeons relate the onset of pain to a particular walking distance in terms of street blocks (eg, 2-block claudication). This helps to quantify patients with some standard measure of walking distance before and after therapy.
• Other important aspects of claudication pain are that the pain is reproducible within the same muscle groups and that it ceases with a resting period of 2-5 minutes.
• Location of the pain is determined by the anatomical location of the arterial lesions. Peripheral arterial occlusive disease (PAOD) is most common with the distal superficial femoral artery (located just above the knee joint), which corresponds to claudication in the calf muscle area (the muscle group just distal to the arterial disease).
• When atherosclerosis is distributed throughout the aortoiliac area, thigh and buttock muscle claudication predominates.
• The perceived significance of claudication is variable. Most patients appear to accept a decrease in walking distance as a normal part of aging. Investigators report that 50-90% of patients with definite intermittent claudication do not report this symptom to their clinician.
• Atherosclerosis is a systemic disease process. Patients who present with claudication due to PAOD can be expected to have atherosclerosis elsewhere. A full assessment of the patient's risk factors for vascular disease should be performed.
• The risk factors for PAOD are the same as those for coronary artery disease or cerebrovascular disease and include diabetes, hypertension, hyperlipidemia, family history, sedentary lifestyle, and tobacco use.
• Smoking is the greatest of all the cardiovascular risk factors. The mechanism by which smoking causes or accentuates atherosclerosis is unknown. What is known is that the degree of damage is directly related to the amount of tobacco used. Counseling patients on the importance of smoking cessation is paramount in PAOD management.

Physical

• Palpation of pulses should be attempted from the abdominal aorta to the foot, with auscultation for bruits in the abdominal and pelvic regions. This can be difficult in a patient who is obese, in whom palpable pulses may be hidden under a deep subcutaneous layer.
• Except in the rare case of a congenital absence of a pulse (eg, persistent sciatic artery), the absence of a pulse signifies arterial obstruction proximal to the area palpated. For example, if no femoral artery pulse is palpated, significant PAOD is present in the aortoiliac distribution. The same can be said if no palpable popliteal artery pulse is present because of existing superficial femoral artery occlusive disease.
• Patients who report intermittent claudication and have palpable pulses can present a clinical dilemma.
  • If the history is consistent with typical claudication symptoms, the clinician can have the patient walk around the office (or perform toe raises) until the symptoms are reproduced and then palpate for pulses.
  • The exercise should cause the atherosclerotic lesion to become significant and should diminish the strength of the pulses distal to the lesion.
• When palpable pulses are not present, further assessment of the circulation can be made with a handheld Doppler device.
  • An audible Doppler signal assures the clinician that some blood flow is perfusing the extremity.
  • If no Doppler signals can be heard, a vascular surgeon should be immediately consulted.
• Pressure measurements can be performed to gain objective data on the circulatory status.
  • To obtain an accurate pressure reading, (1) place the pneumatic cuff around the ankle, (2) position the Doppler probe over the dorsalis pedis or posterior tibial artery, and (3) inflate the cuff to a reading above the systolic pressure and deflate. The systolic tone at the ankle vessel is the pressure recorded.
  • A healthy person has no pressure drop from the heart to the ankle. In fact, the pressure at the ankle may be 10-20 mm Hg higher due to the augmentation of the pressure wave with travel distally.
  • In patients with claudication, the measured pressure is diminished to some extent, depending on the severity of PAOD.
• A useful tool in assessing a patient with claudication is the ankle-brachial index (ABI), which is calculated as the ratio of systolic blood pressure at the ankle to the arm.
  • Determining the ABI provides an assessment of the impact that the PAOD is having on the patient. A normal ABI is 0.9-1.1. However, any patient with an ABI less than 0.9, by definition, has some degree of PAOD. The ABI decreases with worsening PAOD.
  • One area of inaccuracy with the ABI is in patients with diabetes who have PAOD. Peripheral vessels in patients with diabetes may have extensive medial layer calcinosis, rendering the vessel resistant to compression by the pneumatic cuff. These patients should be referred to a vascular laboratory for further evaluation.

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