Journal of Vascular Nursing
Volume 21, Issue 1 , Pages 5-16, March 2003

Treating patients with peripheral arterial disease and claudication☆☆

University of Minnesota School of Nursing, Minneapolis, Minnesota; and Jobst Vascular Center, Toledo, Ohio

Article Outline

Abstract 

The vascular nurse plays an important role in the treatment of patients with peripheral arterial disease (PAD), a prevalent atherosclerotic occlusive disease that affects approximately 8 to 12 million people in the United States. Approximately 4 to 5 million individuals with PAD experience claudication, the exercise-induced ischemic pain in the lower extremities that is relieved upon rest. Both PAD and claudication are associated with increased morbidity and mortality, limitations in functional capacity, and a decreased quality of life. Despite its prevalence, PAD is often undiagnosed and, therefore, increases the risk for cardiovascular ischemic events, disease progression, functional disability, amputation, and death. Risk factors for PAD and claudication are similar to those for other atherosclerotic diseases, including age, cigarette smoking, diabetes mellitus, hypertension, dyslipidemia, and hyperhomocysteinemia. Effective treatment to normalize these risk factors can reduce disease progression and the incidence of cardiovascular ischemic events. Claudication symptoms can be improved most effectively through exercise training, which may be used in conjunction with medications specifically indicated to improve these symptoms. Vascular nurses, practicing in a multitude of inpatient and outpatient settings, can assist patients with risk-factor modifications and behavioral changes to help them stop smoking, maintain glycemic control, normalize high blood pressure and lipid levels, and ensure initiation of lifelong antiplatelet therapy and participation in exercise rehabilitation programs, thus, promoting positive outcomes for patients with claudication. (J Vasc Nurs 2003;21:5-14)

 

Peripheral arterial disease (PAD) is a prevalent atherosclerotic occlusive disease associated with increased morbidity and mortality, limitations in functional capacity, and a decreased quality of life. Individuals with PAD often experience exercise-induced ischemic pain in the lower extremities, known as claudication. This condition is characterized by cramping, aching, or fatigue, typically occurring in the calf muscles, but also in the thighs or buttocks. Because this pain is caused by an inadequate blood supply to the muscles during exercise, it is relieved when activity ceases.

Despite the high prevalence and associated functional impairment, PAD often goes undiagnosed; consequently, little or no treatment is provided. Treatment of atherosclerotic risk factors by both behavioral modification and pharmacologic intervention tends to be less intensive in patients with PAD than in those with coronary artery disease.1, 2 There are several possible reasons for this, including lack of awareness of the importance of PAD among primary care clinicians, a limited understanding of the disease among the public, an assumption that exertional leg pain is a normal part of aging, inadequate understanding of appropriate office-based disease detection methods, and limited knowledge of treatment options. As a result, patients with PAD are at increased risk of ischemic cardiovascular events, disease progression, functional disability, and amputation or even death. The purpose of this article is to review the epidemiology of PAD and claudication, review risk factors associated with development of PAD, describe how to accurately diagnose this disease, and examine treatment options, while emphasizing the role of the vascular nurse in caring for these patients.

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Epidemiology 

Morbidity and mortality 

PAD affects an estimated 8 to 10 million people in the United States, however, only 4 to 5 million have claudication manifest.3 Thus, approximately 40% to 50% of individuals with detectable PAD are asymptomatic. An additional 10% of patients have more severe disease, involving ischemic pain at rest, tissue ischemia, and limb necrosis. Some 3% to 8% of patients with PAD require amputation each year.4 Development of PAD strongly correlates with advancing age. Epidemiologic studies show a PAD prevalence of 2.5% in people < 60 years of age, 8.3% in those aged 60 to 69 years, and 18.8% in those > 70 years old.5

PAD is associated with a significant increase in cardiovascular morbidity and mortality. Patients with PAD are approximately 5 times more likely to have a myocardial infarction (MI) and 2 to 3 times more likely to have a stroke. The mortality in patients with claudication is 30% at 5 years, 50% at 10 years, and 70% at 15 years,6 and the mortality increases with disease severity.7 This increased risk of death is almost entirely a result of an increase in cardiovascular ischemic events.8

Many patients with PAD also have significant ambulatory disabilities. This walking impairment is often of a magnitude that leads to further limitations in physical, social, leisure, and occupational functioning.9, 10 Some patients with PAD are so severely compromised in their ability to perform daily activities that their self-perception is affected, often leading to a sense of inadequacy. The disease is experienced as a burden on them and their families.11

Risk factors 

In addition to age, there are several risk factors related to the development of PAD and claudication that are similar to those associated with other atherosclerotic diseases. These include cigarette smoking, diabetes mellitus (DM), hypertension, dyslipidemia, and hyperhomocysteinemia.

Cigarette smoking 

Cigarette smoking is one of the most potent contributing factors for PAD,12 raising the risk of claudication as much as 8- to 10-fold and contributing significantly to mortality.13, 14 Approximately 80% of patients with stable claudication have a history of smoking,15 30% to 40% of claudicants are current smokers, and their 5-year mortality is 40% to 50%.4 There are a variety of interrelated mechanisms responsible for the adverse effects of smoking.

Smoking affects the cardiovascular and hematologic systems and the vessel wall, causes deleterious changes in metabolic and biochemic markers, and negatively impacts serum lipids. Specific effects include acute increases in systolic blood pressure, heart rate, and myocardial oxygen demand; increased platelet aggregation and activation; endothelial cell damage; increased free fatty acids; and increased low-density lipoprotein (LDL) and very LDL cholesterol.16 Continued smoking by patients with PAD is associated with progressive worsening of claudication, decreased graft patency after revascularization,17 and increased rates of amputation, MI, stroke, and death.18

DM 

DM is another independent atherosclerotic risk factor. Framingham data indicate that individuals with DM are almost 3 times more likely to have claudication develop than are those who do not have this condition.19 In addition, DM is strongly related to development of critical limb ischemia and the subsequent need for amputation.15 These risks are greater in women than in men.

Hypertension 

Hypertension is a major risk factor for development of PAD20, 21 incurring a 2-fold risk of development of claudication.22 This increased risk is magnified as blood pressure increases, and has been shown to be greater in women than in men.12, 14 Hypertension has also been shown to be independently related to increased mortality in patients who have existing claudication.23

Dyslipidemia 

Abnormal serum lipids are also related to development of PAD.12, 23, 24 Presence or development of PAD has been shown to be related to increased total cholesterol, LDL cholesterol, and triglycerides, and low high-density lipoprotein cholesterol.14, 25, 26 Unlike coronary disease, where increased LDL confers the biggest risk for development and progression of disease, some studies have indicated that high triglycerides and low high-density lipoprotein seem to be more closely related to presence or development of PAD.5, 27

Hyperhomocysteinemia 

Hyperhomocysteinemia has been increasingly recognized as an important risk factor in the development of PAD.28, 29, 30 Homocysteine is derived solely from the intracellular metabolism of methionine, an essential dietary amino acid. Patients with high levels of homocysteine have increased morbidity and mortality from atherosclerotic disease and venous thromboembolism.31 Thus, a mild to moderate level of homocysteine (15-25 mmol/L) has been found to be an independent risk factor for atherosclerotic disease in the coronary, cerebral, and peripheral circulation, and in venous thrombosis.31, 32, 33 Dietary supplementation with folic acid and vitamins B6 and B12 can normalize serum homocysteine. However, it is not yet known if this normalization changes atherosclerotic risk associated with hyperhomocysteinemia.28

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Patient assessment and treatment 

Role of the vascular nurse 

The role and responsibilities of the vascular nurse in the care of the patient with PAD and claudication can vary depending on the clinical setting, the nurse's position, and scope of practice. Vascular nurses are well suited to care for patients with PAD. They contribute to the assessment and treatment of patients with PAD through a variety of activities in both inpatient and outpatient settings. Through communication and collaboration with the patient, family, and health care team, the vascular nurses help ensure continuity and consistency of care across all settings. Vascular nurses use sound clinical judgment, established standards of care, and clinical pathways to guide care delivery.

Patient assessment 

History 

Assessment of the patient with PAD begins with taking a detailed history, including identifying risk factors as mentioned above, and obtaining a history of other cardiovascular diseases such as angina, MI, and transient ischemic attack or stroke.34 A careful assessment of walking ability should be made, as many patients may not voluntarily mention walking pain or discomfort, assuming it to be a normal part of aging. As a result, many patients with PAD are not aware that this condition is treatable. During the interview process, patients should be asked to describe the character of the pain, its location and duration, and the time or distance walked before onset. Typically, the pain is described as an aching, cramping, or fatigue in the leg muscles as opposed to the joints. It is usually reproducible, occurring at approximately the same distance, pace, and grade from day to day, and resolves within 2 to 5 minutes with rest. The location of the pain often corresponds to the level of stenosis. For example, patients with an iliac lesion often experience claudication in the thigh or buttock, whereas popliteal lesions are more often associated with calf claudication.

The clinician (physician or nurse) should evaluate walking or exercise behavior to accurately determine the level of activity actually being performed. In addition, informal assessment of PAD-specific limitations may help the clinician ascertain if there is a discrepancy between actual and desired functional levels. This information can help guide treatment recommendations. For example, asking the patient, “What do you want or need to do that you are unable to do now?” can help the clinician understand the level of improvement required to meet the functional needs of the patient.

Physical examination 

All patients ≥ 70 years of age and those ≥ 50 years of age with one or more risk factor should be further evaluated for PAD whether or not there is a suspicion of claudication. A vascular physical examination should be performed. This examination includes inspection of all extremities for skin color; capillary refill; hair loss; thin, smooth, shiny skin; brittle, thickened nails; and any sign of skin breakdown such as ulceration or gangrene. The clinician should also palpate the abdominal aorta to detect an aneurysm. Palpation of the peripheral pulses, ie, femoral, popliteal, posterior tibial, and dorsalis pedis, is also essential. The clinician may choose to mark the skin at the point where the pulses are palpated. Pulses are quantified using a rating scale that denotes differences and serves as a reference point for subsequent pulse assessments. It is also important to note that, on average, approximately 8% of the population will have a congenitally absent dorsalis pedis pulse.35

Noninvasive vascular testing 

In patients at risk for PAD, the clinician should obtain an ankle-brachial index (ABI) measurement, a simple noninvasive test that can be used to confirm the diagnosis of PAD. The ABI has been shown to correlate with disease severity and is predictive of mortality.36 The ABI is a ratio of the systolic blood pressure at the ankle to the systolic blood pressure in the arm. The measurement is obtained by determining the dorsalis pedis and posterior tibial pressures in both ankles and the brachial pressures in both arms using a 5- to 7-MHz Doppler. To calculate the ABI, the highest ankle pressure in each leg is divided by the higher brachial pressure. An ABI ≤ 0.9 is diagnostic of PAD with 95% sensitivity and almost 100% specificity.37 A normal ABI ranges from 0.9 to 1.3. The method for obtaining an ABI and the interpretation of values are is illustrated in Figure 1.

  • View full-size image.
  • Fig. 1. 

    Sample ankle-brachial index work sheet. Reprinted with permission from Hiatt WR, Hirsch AT, Regensteiner J. Peripheral arterial disease handbook. 2001. p. 106. Copyright CRC Press, Boca Raton, Florida.

It is important to note that the ABI can be abnormally increased in individuals with calcified vessels, such as patients with DM. In cases where pedal arteries are noncompressible, pressure measurements may be taken in the toes. Patients with diabetes and an ABI of 1.3 to 1.5 or greater should be referred to a vascular laboratory for further studies to confirm the diagnosis of PAD. Arterial waveforms may be obtained using the Doppler system. Segmental pressure measurements at different levels in the leg can be performed to help identify the location of obstruction. A decrease in pressure > 20 mm Hg between 2 levels indicates the presence of an obstruction.38

Occasionally patients present with typical claudication symptoms but have a normal ABI at rest. This finding can occur with mild occlusive disease or high-grade iliac stenoses. In these patients, an ABI is obtained before and after a treadmill exercise test to establish the diagnosis of PAD. Patients with PAD experience a decrease in ABI after exercising to maximal claudication.39 Table I summarizes the noninvasive vascular testing available to assist in the diagnosis of PAD.40

Table I. NON-INVASIVE VASCULAR TESTING FOR PERIPHERAL ARTERIAL DISEASE
TestIndicationInformation ObtainedLimitations
Segmental Limb Pressures○Moderate to severe claudication or ischemia.○Helps to localize disease to specific arterial segments○Multiple cuffs required
○Revascularization under consideration○May predict likelihood of wound healing○Inaccurate in patients with noncompressible vessels
Pulse Volume Recordings○Moderate to severe claudication or ischemia.○Helps to localize disease to specific arterial segments○Requires expert technician
○Revascularization under consideration○May predict likelihood of wound healing○Provides limited information
○Useful if arteries are calcified
Exercise ABI○Atypical leg symptoms○Confirms PAD diagnosis with normal resting ABI○Requires calibrated treadmill
○Pre-post intervention
○Provides functional information○Skilled technician
○Patients may not be able to complete study
Arterial Duplex Ultrasonography○Advanced PAD requiring revascularization○Identification of specific sites of arterial stenosis or occlusion○Expensive equipment
Skilled technician
○Postcatheterization site complications○Can clarify revascularization options○Time-consuming
○Gives anatomic but not functional information

Adapted from Jaff, M.R. and Hiatt, W.R. Clinical and Vascular Laboratory Evaluation of Peripheral Arterial Disease, 2002, p. 88-90.40

Questionnaires 

In addition to the ABI and vascular laboratory testing, formal subjective measurements are also useful. The Walking Impairment Questionnaire was developed to assess the degree of walking impairment in patients with PAD. It has 3 subscales: walking distance, speed, and stair climbing. Individual scores within each category are aggregated and scored on a 0-to-100 scale with “100” being no impairment and “0” being complete impairment. This questionnaire has been shown to be reliable and valid, correlates well with treadmill walking distance, and is sensitive to change during time.41

The Medical Outcomes Study Short Form-3642 assesses 8 health concepts: physical functioning, role limitations as a result of physical problems, bodily pain, social functioning, general mental health, role limitations as a result of emotional problems, vitality, and general health perceptions. There are also 2 composite scores, physical and mental component scores. Each of the subscales is scored separately on a 0% to 100% scale. This instrument has been shown to be reliable and valid in numerous chronic disease populations and has been used to assess functional changes in several PAD clinical trials.

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Treatment of PAD 

Treatment of PAD is on the basis of 2 major therapeutic goals. The first goal is to prevent progression of atherosclerosis, thus, decreasing the risk of cardiovascular ischemic events (MI and stroke), decreasing progression of PAD, and preventing limb loss. The second goal is to provide symptomatic relief and improve functional disability and quality of life. An algorithm for treating patients with PAD and claudication is presented in Figure 2.34

Risk-factor modification 

Modification of atherosclerotic risk factors can significantly affect PAD progression and cardiovascular ischemic events and should be vigorously pursued in all patients with PAD, regardless of symptom or disease severity. Vascular nurses play a critical role in educating patients about PAD and claudication. This includes an explanation of the systemic nature of the disease, the contribution of risk factors to both disease progression and cardiovascular ischemic events, therapeutic options for symptom relief, and the importance of an exercise rehabilitation program. Furthermore, the vascular nurse is essential in translating education into behavioral changes, thus, actually modifying the course of the disease through better, more consistent patient care.

Smoking cessation 

As previously stated, cigarette smoking is the single most important risk factor for PAD. Conversely, smoking cessation can stabilize or improve claudication symptoms,43 reduce the rate of progression from claudication to rest pain, reduce the rates of cardiovascular ischemic events, decrease amputation rates, and improve survival.18, 44, 45

The most successful approaches to smoking cessation involve a combination of behavioral strategies and pharmacologic intervention. Nicotine replacement, available in several forms, has been shown to improve long-term cessation rates46 and is safe even in patients with cardiovascular diseases.47 Bupropion, a nonnicotine product, has also been shown to improve smoking-cessation rates.48

Clinical practice guidelines for smoking cessation have been outlined by Fiore and colleagues46 and are on the basis of the “5 A's”: ask, advise, assess, assist, and arrange. Specifically, clinicians should identify tobacco users at each visit, and provide them with a clear, strong message to stop smoking. In addition, clinicians should assess the patient's current readiness to quit smoking within 30 days, provide educational material and counseling to those who are not ready, and help those who are ready to quit to make a stop-smoking plan. Such a plan should include behavioral counseling and medications as indicated. If possible, patients should be referred to a tobacco-health educator for additional assistance. Finally, the clinician should help arrange follow up contacts by telephone or, for individuals who would benefit most from face-to-face contact, follow-up in the clinic may be indicated.49

Diabetes management 

Tight control of diabetes, defined by a level of glycosylated hemoglobin ≤ 7%, is thought to slow the rate of progression of lower-extremity disease and to reduce the incidence of myocardial ischemic events.4 In the United Kingdom Prospective Diabetes Study, intensive treatment for diabetes was shown to reduce microvascular events, MI, stroke, and mortality. However, the ability of this intensive treatment to modify PAD outcomes was not clearly demonstrated.50, 51 Conversely, the Diabetes Control and Complications Trial found a reduced incidence of all major cardiovascular and peripheral vascular events in patients receiving intensive treatment for diabetes.52 These investigators found that patients who had diabetes, with intensive therapy, could average an additional 5.6 years free from lower-extremity amputation.53

Individuals with DM may experience decreased sensation in their feet, putting them at risk for foot injury, infection, and nonhealing wounds. Therefore, it is paramount that these patients receive detailed instruction about meticulous foot care, including the importance of daily inspection of the feet, routine washing with mild soap and warm water, and careful application of small amounts of lubricant. Patients with DM also need to be instructed on appropriate foot wear, the importance of wearing socks or stockings with shoes, and the need to inspect shoes regularly.

Vascular nurses in both inpatient and outpatient settings have the skills to educate patients with PAD about diabetes, nutrition, and exercise, and to strongly emphasize the importance of the tightest possible control of blood glucose. Clearly delineating the relationship between increased blood glucose and progression of PAD may help motivate patients to effect lifestyle changes necessary to control DM.

Antihypertensive therapy 

The effective treatment of hypertension has been shown to reduce the incidence of coronary artery disease, stroke, and mortality, although there are few data specifically examining the effect of hypertension control on PAD. All patients with PAD should have blood pressure control consistent with the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure guidelines (systolic blood pressure < 130 mm Hg; diastolic blood pressure < 90 mm Hg).20 There are numerous options available to achieve ideal blood pressure control using both pharmacologic and lifestyle interventions, such as weight loss, dietary modification, and stress management.

The vascular nurse plays an important role in treating patients with hypertension. Blood pressure should be measured at each visit, with medication adjusted appropriately to enable consistent maintenance of target levels. Patients must be made aware of their blood pressure goals and instructed to report any adverse events associated with their medication. Educating patients about the importance of taking medication for this asymptomatic but serious condition, and the importance of regular monitoring by health care professionals, should increase patient adherence to necessary lifestyle changes.

Antiplatelet therapy 

All patients with PAD should be considered candidates for lifelong antiplatelet therapy, the benefits in patients with PAD being unequivocal. By inhibiting platelet aggregation, antiplatelet agents help prevent the formation of thrombi, which can lead to MI and stroke. Antiplatelet medications have also been shown to reduce the incidence of graft occlusion in patients with PAD.54

Aspirin has been shown to reduce the risk of MI, stroke, and vascular death in patients with vascular disease. A meta-analysis completed by the Antiplatelet Trialists' Collaboration concluded that aspirin reduces vascular events by 25%.54 Adverse events associated with aspirin use primarily include gastrointestinal upset or bleeding.

Another class of antiplatelet agents, adenosine diphosphate receptor antagonists, is also effective in reducing cardiovascular ischemic events in patients with vascular disease. Ticlopidine, while effective, has also been associated with significant hematologic side effects and is not well tolerated by patients,55 and, thus, not routinely prescribed for patients with PAD. Clopidogrel, indicated for prevention of cardiovascular ischemic events in patients with PAD, was shown in the Clopidogrel Versus Aspirin in Patients at Risk of Ischaemic Events (CAPRIE) trial to have an 8.7% overall reduction in such events in patients with a history of MI, stroke, or PAD.56 This effect was especially large in the PAD subgroup, which had a 23.8% reduction in cardiovascular ischemic events. Clopidogrel is well tolerated by patients and has few side effects. The side effects most frequently reported include gastrointestinal upset, diarrhea, and rash.

It is important to emphasize that antiplatelet medications are indicated for prevention of cardiovascular ischemic events, not for treatment of the symptoms of claudication associated with PAD. Also, none of these medications has demonstrated a positive effect on walking distance.

Chronic anticoagulation with heparin or warfarin may be indicated for patients at high risk of thromboembolism. However, these medications are not indicated for the majority of patients with PAD because of the high risk of hemorrhage.

Normalization of dyslipidemia 

Nearly 20 years ago, normalization of lipid levels was proven to lower the incidence of coronary disease.57 More recent clinical trials have demonstrated that reducing serum lipid levels also decreases morbidity and mortality. The Scandinavian Simvastatin Survival Study found that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (“statins”) were associated with a 38% reduction in the risk of new or worsening claudication developing.58 Coronary intervention trials suggest that reducing LDL cholesterol levels to ≤ 100 mg/dL can prolong the lives of people with PAD.59 The National Cholesterol Education Program (NCEP) ATPIII guidelines recommend that patients with objective evidence of atherosclerotic disease receive dietary and drug therapy to reduce LDL cholesterol levels to < 100 mg/dL.60 These NCEP guidelines apply to patients with both asymptomatic and symptomatic PAD, as PAD is now considered a coronary heart disease risk equivalent.4

Reversing obesity 

Although obesity is an independent risk factor for development of coronary artery disease, it is not known whether there is an independent relation between obesity and the development of PAD. Promotion of weight loss in patients with PAD who are obese is recommended, however, because obesity contributes to the development of atherosclerosis through an association with other risk factors such as insulin resistance, dyslipidemia, and hypertension. Weight loss seems to correlate with improvement in these risk factors; however, no studies have been done to examine the specific effects on individuals with PAD.

Treatment of claudication 

Exercise 

Exercise training is one of the most effective interventions available for the treatment of claudication as a result of PAD. The efficacy of exercise for treating claudication has been established by numerous investigations during the past decade.61, 62, 63 Exercise training has been shown to significantly improve both the onset of leg discomfort, or initial claudication distance, and the point at which the pain becomes unbearable, forcing the patient to stop walking, or absolute claudication distance.64, 65 The scientific database61, 62, 63, 64, 65 demonstrating the efficacy of supervised exercise is stronger than that for many other claudication interventions (eg, surgical or percutaneous revascularization), and has been proposed as the mainstay of care for treatment of symptomatic PAD (intermittent claudication). The body of evidence supporting the efficacy of exercise training in patients with PAD contributed to the establishment of a new current procedural terminology code for exercise rehabilitation for PAD.66 The establishment of this new code should accelerate development and growth of therapeutic exercise programs as an intervention for those with PAD.

A meta-analysis by Gardner and Poehlman62 identified characteristics of training programs associated with greatest clinical improvement. Walking was found to be more effective than other modes of exercise. Training sessions > 30 minutes, for ≥ 3 sessions/wk, lasting ≥ 6 months in duration, and encouraging patients to exercise to moderately severe claudication levels were associated with the greatest efficacy.

The mechanism of improvement in claudication symptoms with exercise is not well understood, but several processes appear to be involved in the training response. Training results in skeletal muscle metabolic adaptation, including an increase in the number of mitochondria; an increased level of oxidative enzymes; a greater reliance on fatty acid oxidation; and, thus, a decrease in anaerobic metabolism and lactic acid accumulation at a given workload.67, 68, 69

Before initiating an exercise program, the patient should undergo a treadmill exercise test to establish baseline initial and absolute claudication distances. Training should then begin at 50% to 85% of the patient's functional capacity.70 Patients are given an exercise prescription on the basis of the severity of disease and their individual goals. Usually treadmill walking is the preferred training modality. Other types of exercise, such as bicycle ergometry, stair stepping, and even upper-extremity exercise, can also be useful in augmenting the benefits of treadmill training. During a typical session, patients should exercise at a moderate intensity until they experience moderately severe claudication. This is determined by the patient's evaluation of claudication pain intensity and rating of perceived exertion. At that point they rest until the pain subsides. This exercise/rest pattern is repeated throughout the session.61

Vascular nurses working in vascular rehabilitation are afforded a unique opportunity to help patients with PAD initiate and sustain significant behavioral changes. The frequency of the exercise sessions allows ample opportunity to educate patients about claudication, exercise, nutrition, lipids, blood pressure management, antiplatelet therapy, and smoking cessation. Furthermore, this information can be provided one-to-one or through interactive group classes, and reinforced during the exercise sessions. In the program, patients also learn specific exercises that can be readily translated into a home program, so that the benefits of the supervised setting can be continued even after the formal exercise program is completed.

Pharmacotherapy 

Although some patients remain stable or improve with lifestyle modification alone, many others may require pharmacologic therapy. Pentoxifylline and cilostazol are the only medications specifically indicated for the treatment of claudication.

Medication prescribed for the treatment of claudication should be evaluated after a 90-day trial and continued in patients who show symptomatic improvement. The dose may need to be decreased to lessen adverse effects or increased (within prescribed guidelines) to achieve a better therapeutic outcome. Repeated assessment is necessary whenever a patient is on long-term medication.

Pentoxifylline, a methylxanthine derivative, increases the flexibility of red blood cells, reduces blood viscosity, and retards platelet aggregation. The recommended dosage is 400 mg 3 times a day, and side effects include gastrointestinal disturbance, headache, and dizziness. Although some patients have experienced improvements in walking distances when treated with pentoxifylline, 2 meta-analyses have questioned the efficacy and cost-effectiveness of this medication.71, 72

Cilostazol, a phosphodiesterase III inhibitor, is a vasodilator with mild antiplatelet effects. Clinical trials have demonstrated that treatment with cilostazol increases walking distances in patients with claudication.73, 74, 75 The recommended dosage of cilostazol is 100 or 50 mg twice a day, and side effects include headache, diarrhea, and palpitations.

In addition to improving functional ability in study patients, cilostazol has demonstrated a favorable effect on plasma lipid profiles. Triglyceride levels are lowered and high-density lipoprotein levels are raised in patients taking this medication.75, 76 However, there is no current evidence that cilostazol decreases risk of cardiovascular events.

Because other medications that inhibit phosphodiesterase III have been linked to decreased survival in patients with severe heart failure, cilostazol is contraindicated in patients with heart failure of any severity. In patients with claudication for whom heart failure is suspected but not definitively established, cardiac echocardiography can confirm normal left-ventricular function before initiation of drug therapy.

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Conclusion 

In summary, PAD is a prevalent atherosclerotic disease associated with significant cardiovascular morbidity and mortality. Patients with PAD experience life-limiting claudication, functional disability, and diminished quality of life. Many health care professionals are unaware of the magnitude of disability associated with PAD and the treatment options available to ameliorate claudication symptoms. Treatment goals include prevention of cardiovascular ischemic events, decrease in disease progression and the need for revascularization, and relief of symptoms. Atherosclerotic risk factors should be normalized, and exercise and pharmacologic interventions should be initiated when indicated. Vascular nurses can play a significant role in all aspects of PAD management: detection, assessment, treatment, and therapeutic intervention.

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Treating patients with peripheral arterial disease and claudication 

Contact Hours: 1.0 Minimum Passing Score: 70% Test ID: JVN03031 Test Processing Fee: $10.00

OBJECTIVES:

1.Identify risk factors associated with PAD.

2.Describe effects of claudication on patient's health.

3.Discuss nursing considerations in caring for patients with PAD and claudication.


1. Claudication exhibits with the following localized symptoms EXCEPT:

1.itching.

2.cramping.

3.aching.

4.fatigue.


2. What percentage of patients with PAD also experience claudication?

1.10%

2.25% to 30%

3.40% to 50%

4.75% to 80%


3. What percentage of PAD patients each year require amputation?

1.3% to 8%

2.9% to 12%

3.18% to 20%

4.35% to 38%


4. The prevalence of PAD is greatest in which age group?

1.20 to 40 years of age

2.40 to 60 years of age

3.60 to 70 years of age

4.over 70 years of age


5. Which is the most potent contributing factor for PAD?

1.Diabetes

2.Hypertension

3.Cigarette smoking

4.Dyslipidemia


6. What is the risk of developing claudication in patients with diabetes?

1.Twice as likely

2.Three times as likely

3.Five times as likely

4.Ten times as likely


7. What is the risk of developing claudication in patients with hypertension?

1.Twice as likely

2.Three times as likely

3.Five times as likely

4.Ten times as likely


8. Which of the following was NOT mentioned as helping to normalize serum homocysteine?

1.Vitamin B-6

2.Vitamin B-12

3.Folic acid

4.Vitamin A


9. The paint described by patients with PAD does NOT involve:

1.aching.

2.cramping.

3.joint pain.

4.fatigue.


10. Normal ABI is:

1.less than 0.5.

2.less than 0.9.

3.0.9 to 1.3.

4.greater than 1.3.


11. Smoking cessation by Fiore and colleagues defines the “5 A's” as:

1.ask, advise, assess, assist, arrange.

2.advise, attempt, adhere, adjust, assist.

3.admonish, assist, associated, adjunct, add.

4.alter administer, adjust, assess, abstain.


12. Blood pressure guidelines are to help the BP to be:

1.120/80.

2.less than 130/90.

3.100 to 140/95.

4.130 to 150/90 to 95.


13. Aspirin can reduce vascular events by:

1.10%.

2.25%.

3.35%.

4.80%.

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References 

  1. McDermott MM, Mehta S, Ahn H, Greenland P. Atherosclerotic risk factors are less intensively treated in patients with peripheral arterial disease than in patients with coronary artery disease. J Gen Intern Med. 1997;12:209–215
  2. Hirsch AT, Criqui MH, Treat-Jacobson D, Regensteiner JG, Creager MA, Olin JW, et al.  Peripheral arterial disease detection, awareness, and treatment in primary care. JAMA. 2001;286:1317–1324
  3. Hiatt WR. Morbidity of PAD: medical approaches to claudication. Introduction and overview. In:  Hirsch AT editors. An office-based approach to the diagnosis and treatment of PAD, part IV: management of peripheral arterial disease: moderate claudication. Hillsborough (NJ): Excerpta Medica; 2000;p. 76–87
  4. Hirsch AT, Treat-Jacobson D, Lando HA, Hatsukami DK. The role of tobacco cessation, antiplatelet and lipid-lowering therapies in the treatment of peripheral arterial disease. Vasc Med. 1997;2:243–251
  5. Criqui MH, Denenberg JO, Langer RD, Fronek A. The epidemiology of peripheral arterial disease: importance of identifying the population at risk. Vasc Med. 1997;2:221–226
  6. TransAtlantic Inter-Society Consensus TASC Working Group . Management of peripheral arterial disease (PAD). J Vasc Surg. 2000;31(suppl 1):S1–S296
  7. Leng GC, Lee AJ, Fowkes FGR, Whiteman M, Dunbar J, Housley E, et al.  Incidence, natural history and cardiovascular events in symptomatic and asymptomatic peripheral arterial disease in the general population. Int J Epidemiol. 1996;25:1172–1181
  8. Criqui MH, Langer RD, Fronek A, Feigelson HS, Klauber MR, McCann TJ, et al.  Mortality over a period of 10 years in patients with peripheral arterial disease. N Engl J Med. 1992;326:381–386
  9. Khaira HS, Hanger R, Shearman CP. Quality of life in patients with intermittent claudication. Eur J Vasc Endovasc Surg. 1996;11:65–69
  10. Ponte E, Cattinelli S. Quality of life in a group of patients with intermittent claudication. Angiology. 1996;47:247–251
  11. Treat-Jacobson D, Halverson SL, Ratchford A, Regensteiner JG, Lindquist R, Hirsch AT. A patient-derived perspective of health-related quality of life in peripheral arterial disease. J Nurs Scholarsh. 2002;34:55–60
  12. Kannel WB. The demographics of claudication and the aging of the American population. Vasc Med. 1996;1:60–64
  13. Ingolfsson IO, Sigurdsson G, Sigvaldason H, Thorgeirsson G, Sigfusson N. A marked decline in the prevalence and incidence of intermittent claudication in Icelandic men 1968-1986: a strong relationship to smoking and serum cholesterol—the Reykjavik study. J Clin Epidemiol. 1994;47:1237–1243
  14. Reunanen A, Takkunen H, Aromaa A. Prevalence of intermittent claudication and its effect on mortality. Acta Med Scand. 1982;211:249–256
  15. Hilleman DE. Management of peripheral arterial disease. Am J Health Syst Pharm. 1998;55(suppl 1):S21–S27
  16. Krupski WC. The peripheral vascular consequences of smoking. Ann Vasc Surg. 1991;5:291–304
  17. Powell JT, Greenhalgh RM. Changing the smoking habit and its influence on the management of vascular disease. Acta Chir Scand. 1990;555(suppl):99–103
  18. Lassila R, Seyberth HW, Haapanen A, Schweer H, Koskenvuo M, Laustiola KE. Vasoactive and atherogenic effects of cigarette smoking: a study of monozygotic twins discordant for smoking. BMJ. 1988;297:955–957
  19. Beach KW, Brunzell JD, Strandness DE. Prevalence of severe atherosclerosis obliterans in patients with diabetes mellitus. Atherosclerosis. 1982;2:275–280
  20. Joint National Committee . The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure. Arch Intern Med. 1997;157:2413–2446
  21. Fowkes FGR, Dunbar JT, Lee AJ. Risk factor profile of nonsmokers with peripheral arterial disease. Angiology. 1995;46:657–662
  22. Kannel WB, McGee DL. Update on some epidemiological features of intermittent claudication: The Framingham Study. J Am Geriatric Soc. 1985;33:13–18
  23. Murabito JM, D'Agostino RB, Silbershatz H, Wilson WF. Intermittent claudication: risk profile from the Framingham Study. Circulation. 1997;96:44–49
  24. Johansson J, Egberg N, Johnsson H, Carlson LA. Serum lipoproteins and hemostatic function in intermittent claudication. Arterioscler Thromb Vasc Biol. 1993;13:1441–1448
  25. Drexel H, Steurer J, Muntwyler J, Meienberg S, Schmid HR, Schneider E, et al.  Predictors of the presence and extent of peripheral arterial occlusive disease. Circulation. 1996;94(Suppl):II199–II205
  26. Hiatt WR, Hoag S, Hamman RF. Effect of diagnostic criteria on the prevalence of peripheral arterial disease. The San Luis Valley Diabetes Study. Circulation. 1995;91:1472–1479
  27. Mowat BF, Skinner ER, Wilson HM, Leng GC, Fowkes FG, Horrobin D. Alterations in plasma lipids, lipoproteins and high density lipoprotein subfractions in peripheral arterial disease. Atherosclerosis. 1997;131:161–166
  28. Robinson K. Newer risk factors and peripheral arterial disease. In:  Hirsch AT editors. An office-based approach to the diagnosis and treatment of PAD, part VIII: PAD and risk-factor management. Hillsborough (NJ): Excerpta Medica; 2000;p. 20–25
  29. Malinow MR, Kang SS, Taylor LM, Wong PW, Coull B, Inahara T, et al.  Prevalence of hyperhomocysteinemia in patients with peripheral arterial disease. Circulation. 1989;79:1180–1188
  30. Creager MA. Medical management of peripheral arterial disease. Cardiol Rev. 2002;9:238–245
  31. Ridker PM, Hennekins CH, Selhub J, Miletich JP, Malinow MR, Stmpfer MJ. Interrelation of hyperhomocysteinemia, factor V Leiden, and risk of future venous thromboembolism. Circulation. 1997;95:1777–1782
  32. Taylor LM, Moneta GL, Sexton GJ, Schuff RA, Porter JM. Prospective blinded study of the relationship between plasma homocysteine and progression of symptomatic peripheral arterial disease. J Vasc Surg. 1999;29:8–19
  33. Towend J, O'Sullivan J, Wilde JT. Hyperhomocysteinemia and vascular disease. Blood Rev. 1998;12:23–24
  34. Regensteiner JG, Hirsch AT. Claudication: the primary symptom of peripheral arterial disease. In:  Hiatt WR,  Hirsch AT,  Regensteiner JG editor. Peripheral arterial disease handbook. Boca Raton (FL): CRC; 2001;p. 95–117
  35. McGee SR, Boyko EJ. Physical examination and chronic lower-extremity ischemia: a critical review. Arch Intern Med. 1998;158:1357–1364
  36. Dormandy JA, Murray GD. The fate of the claudicant—a prospective study of 1969 claudicants. Eur J Vasc Surg. 1991;5:131–133
  37. Yao ST, Hobbs JT, Irvine WT. Ankle systolic pressure measurements in arterial disease affecting the lower extremities. Br J Surg. 1969;56:676–679
  38. Carter SA. The role of pressure measurements in vascular disease. In:  Bernstein EF editors. Non-invasive diagnostic techniques in vascular disease. St Louis (MO): Mosby; 1985;p. 513–544
  39. Olin JW. Clinical evaluation and office-based detection of peripheral arterial disease. In:  Hirsch AT editors. An office-based approach to the diagnosis and treatment of PAD, part I: the epidemiology and practical detection of PAD. Hillsborough (NJ): Excerpta Medica; 2001;p. 12–19
  40. Jaff MR, Hiatt WR. Clinical and vascular laboratory evaluation of peripheral arterial disease. In:  Hiatt WR,  Hirsch AT,  Regensteiner JG editor. Peripheral arterial disease handbook. Boca Raton (FL): CRC; 2001;p. 81–94
  41. Regensteiner JG, Steiner JF, Panzer RJ, Hiatt WR. Evaluation of walking impairment by questionnaire in patients with peripheral arterial disease. J Vasc Med Biol. 1990;2:142–152
  42. McHorney CA, Ware JE, Raczek AE, The MOS. 36-Item Short-Form Health Survey (SF-36): II. Psychometric and clinical tests of validity in measuring physical and mental health constructs. Med Care. 1993;31:247–263
  43. Gardner AW. The effect of cigarette smoking on exercise capacity in patients with intermittent claudication. Vasc Med. 1996;1:181–186
  44. Jonason T, Bergstrom R. Cessation of smoking in patients with intermittent claudication. Effects on the risk of peripheral vascular complications, myocardial infarction and mortality. Acta Med Scand. 1987;221:253–260
  45. Faulkner KW, House AK, Castleden WM. The effect of cessation of smoking on the accumulative survival rates of patients with symptomatic peripheral vascular disease. Med J Aust. 1983;1:217–219
  46. Fiore MC, Bailey WC, Cohen SJ, Dorfman SF, Goldstein MG, Gritz ER. Treating tobacco use and dependence.. A clinical practice guideline. Rockville, MD: US Dept of Health and Human Services, Agency for Healthcare Research and Quality;; 2000; AHRQ Publication No. 00-0032
  47. Joseph AM, Norman S, Ferry L, Prochazka AV, Westman EC, Steele BG, et al.  The safety of transdermal nicotine as an aid to smoking cessation in patients with cardiac disease. N Engl J Med. 1996;335:1792–1798
  48. Hurt RD, Sachs DP, Glover ED, Offord KP, Johnston JA, Dale LC, et al.  A comparison of sustained-release buproprion and placebo for smoking cessation. N Engl J Med. 1997;337:1195–1202
  49. Halverson SL, Hirsch AT. Tobacco and peripheral arterial disease: pathogenesis of PAD and the management of tobacco addiction. In:  Hirsch AT editors. An office-based approach to the diagnosis and treatment of peripheral arterial disease, part VIII: PAD and risk-factor management. Hillsborough (NJ): Excerpta Medica; 2001;p. 181–187
  50. UK Prospective Diabetes Study UKPDS Group . Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet. 1998;352:837–853
  51. UK Prospective Diabetes Study UKPDS Group . Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). Lancet. 1998;352:854–865
  52. The Diabetes Control , Complications Trial Research Group . The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med. 1993;329:977–986
  53. The Diabetes Control , Complications Trial Research Group . Lifetime benefits and costs of intensive therapy as practiced in the Diabetes Control and Complications Trial. JAMA. 1996;276:1409–1415
  54. Antiplatelet Trialists' Collaboration . Secondary prevention of vascular disease by prolonged antiplatelet treatment. BMJ. 1988;296:320–331
  55. Fagher B. Long-term effects of ticlopidine on lower limb blood flow, ankle/brachial index and symptoms in peripheral arteriosclerosis: a double-blind study. Angiology. 1994;45:777–788
  56. CAPRIE Steering Committee . A randomized, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). Lancet. 1996;348:1329–1339
  57. Lipid Research Clinics Program . The Lipid Research Clinics Coronary Primary Prevention Trial Results. I. Reduction in incidence of coronary heart disease. JAMA. 1984;251:351–364
  58. Scandinavian Simvastatin Survival Study Group . Randomized trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994;344:1383–1389
  59. Leng GC, Price JF, Jepson RG. Lipid lowering for lower limb atherosclerosis (Cochrane Review). In: The Cochrane library. Oxford, England: Update Software; 2001;p. CD000123
  60. Expert Panel on Detection , Evaluation , Treatment of High Blood Cholesterol in Adults . Executive summary of the third report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults. JAMA. 2001;285:2486–2497
  61. Hiatt WR, Regensteiner JG, Hargarten ME, Wolfel EE, Brass EP. Benefit of exercise conditioning for patients with peripheral arterial disease. Circulation. 1990;81:602–609
  62. Gardner AW, Poehlman ET. Exercise rehabilitation programs for the treatment of claudication pain. A meta-analysis. JAMA. 1995;274:975–980
  63. Regensteiner JG, Steiner JF, Hiatt WR. Exercise training improves functional status in patients with peripheral arterial disease. J Vasc Surg. 1996;23:104–115
  64. Regensteiner JG. Exercise in the treatment of claudication: assessment and treatment of functional impairment. Vasc Med. 1997;2:238–242
  65. Regensteiner JG, Hiatt WR. Exercise rehabilitation for patients with peripheral arterial disease. Exerc Sport Sci Rev. 1995;23:1–24
  66. Current procedural terminology codebook. Chicago (IL): American Medical Association; 2001;
  67. Holloszy JO, Coyle EF. Adaptations of skeletal muscle to endurance exercise and their metabolic consequences. J Appl Physiol. 1984;56:831–838
  68. Hiatt WR, Nawaz D, Brass EP. Carnitine metabolism during exercise in patients with peripheral vascular disease. J Appl Physiol. 1987;62:2383–2387
  69. Holm J, Dahloff AG, Bjorntorp B, Schersten T. Enzyme studies in muscles of patients with intermittent claudication, effect of training. Scand J Clin Lab Invest. 1973;31(suppl 128):201–205
  70. Hirsch AT, Ekers MA. A comprehensive vascular medical therapeutic approach to peripheral arterial disease: the foundation of effective vascular rehabilitation. In:  Fahey VA editors. Vascular nursing. Philadelphia (PA): WB Saunders; 1999;
  71. Hood SC, Moher D, Barber GG. Management of intermittent claudication with pentoxifylline: meta-analysis of randomized controlled trials. Can Med Assoc J. 1996;155:1053–1059
  72. Radack K, Wyderski RJ. Conservative management of intermittent claudication. Ann Intern Med. 1990;113:135–146
  73. Dawson DL, Cutler BS, Meissner MH, Strandness DE. Cilostazol has beneficial effects in treatment of intermittent claudication: results from a multicenter, randomized, prospective, double-blind trial. Circulation. 1998;98:678–686
  74. Sorkin EM, Markham A. Cilostazol. Drugs Aging. 1999;14:63–71
  75. Money SR, Herd JA, Isaacsohn JL, Davidson M, Cutler B, Heckman J, et al.  Effect of cilostazol on walking distances in patients with intermittent claudication caused by peripheral vascular disease. J Vasc Surg. 1998;27:267–275
  76. Elam MB, Heckman J, Crouse JR, Hunninghake DB, Herd JA, Davidson M, et al.  Effect of the novel antiplatelet agent cilostazol on plasma lipoproteins in patients with intermittent claudication. Arterioscler Thromb Vasc Biol. 1998;18:1942–1947

 Supported by an unrestricted educational grant from Otsuka America Pharmaceuticals Inc, Rockville, MD, and Pharmacia Corp, Peapack, NJ.

☆☆ Address reprint requests to Diane Treat-Jacobson, PhD, RN, University of Minnesota School of Nursing, 6-101 Weaver-Densford Hall, 308 Harvard St SE, Minneapolis, MN 55455.

 1062-0303/2003/$30.00 + 0

PII: S1062-0303(03)00003-7

doi:10.1067/mvn.2003.2

Journal of Vascular Nursing
Volume 21, Issue 1 , Pages 5-16, March 2003