Geralyn Spollett1
1Spollett is an adult nurse practitioner at Yale Diabetes Center, New Haven, CT.
Peripheral vascular disease is an inclusive term referring to peripheral arterial disease (PAD), vasculitis, venous thrombosis, venous insufficiency, and disorders of the vessel wall and lymphatic system. PAD is a marker for atherosclerosis in other areas, such as the coronary and cerebrovascular arteries, and in its broad scope PAD can include aneurysms, traumatic or congenital arteriovenous fistulas, or malformations as well as vascular tumors.1Vascular disease in the peripheral arteries is a major cause of myocardial infarction, stroke, and limb morbidity.
This chapter focuses on atherosclerotic arterial occlusive disease that impairs blood flow to the lower extremities. Diabetes is a specific risk factor for PAD, and its prevalence among those with diabetes is double that of the total population. Not only does it occur more often in those with diabetes, PAD is more severe in that population and is a major risk factor for the occurrence of lower-extremity amputations (LEA). The combination of PAD, diabetes, and peripheral neuropathy accounts for >60% of the LEA in the U.S.2 Although amputation rates have reduced significantly over the past 20 years, the loss of a limb has a significant impact on the physical, socioeconomic, and psychosocial aspects of the patient’s life, further underscoring the importance of screening, education, and intervention to reduce the occurrence of LEA. This requires a team approach in the management of PAD in which the nurse can play an essential role.
EPIDEMIOLOGY
Research findings show that PAD affects 9.5% of U.S. adults (approximately 8.5 million) with 78% of cases being nonsymptomatic, including 12–20% of individuals older than age 60. General population awareness of PAD is estimated at 25%, based on prior studies.3
Even in studies that have used the traditional form of the ankle-brachial index (ABI), however, the incidence of PAD may be underreported. ABI misses single-vessel disease and does not differentiate exercise-related changes versus those at rest.1 The occurrence of PAD is unusual in those <55 years of age but rises sharply in the older population. Prevalence rates in individuals older than 60 years of age is estimated to be 12–20%. In those ≥80 years, prevalence rises to ~30%.1,4 A screening study, PAD Awareness, Risk and Treatment (PARTNERS), documented that most of these individuals go undiagnosed and are much less likely to receive appropriate treatment.5 PAD is more prevalent among men, African Americans, and Hispanics.6 Longer duration of disease, poor glucose control as measured by A1C, and neuropathy all are associated with increased risk for PAD. Selvin et al. report that there is a 30% relative increase in PAD with each 1% increase in A1C levels.7 Although the major risk factors for PAD are similar to those for coronary and cerebrovascular disease (e.g., hypertension, hyperlipidemia), the presence or past history of smoking is a strong, major risk factor for PAD. Amputation rates among those with PAD and diabetes is as much as five times greater than among those without diabetes. Mortality rates in those with PAD and diabetes is double that of the population without diabetes, indicating the severity of this complication.
PATHOPHYSIOLOGY
Atherosclerotic disease of the lower extremities, with vascular inflammation, altered cellular contents of the vasculature and blood cells, and abnormal hemostatic factors defines PAD. Furthermore, there are abnormalities of endothelial function and regulation of the vasculature, including loss of normal nitric oxide function; increased atherosclerotic activity in the smooth muscle cells lining the blood vessel walls; and increased oxidative stress, platelet aggregation, and hypercoagulation. Individuals with diabetes have an increase in PAD because of vascular inflammation and derangement in cellular components. Hyperglycemia blocks endothelial nitric oxide synthase (eNOS) and increases reactive oxygen species, causing wall damage. Insulin resistance also can lead to an increase in free fatty acid levels, causing oxidative damage and activating the proinflammatory pathways. Elevated levels of C-reactive protein (CRP) are strongly associated with the development of PAD.8 In diabetes and impaired glucose tolerance, CRP levels are elevated abnormally. Not only is CRP a marker for the disease process, but it is known to promote apoptosis of endothelial cells as well as cause further vascular dysfunction through a variety of mechanisms, such as stimulation of tissue factor and chemotactic substances, leukocyte adhesion, and inhibition of eNOS.9 Therefore, CRP plays a causative role in the impairment of fibrinolysis and the regulation of vascular tone.10
Tobacco exposure, by far the most potent and deleterious risk factor for PAD, has up to a sixfold risk noted with a dose-dependent effect. Scientists have observed that nicotinic acetylcholine receptors are expressed by blood vessels and mediate several vascular processes related to atherosclerosis, including neovascularization of atherosclerotic plaque and proliferation of smooth muscle cells.11 Exposure to secondhand smoke carries a similar dose-dependent risk based on the numbers of cigarettes smoked per day and minutes of exposure.12
In diabetes, PAD frequently is associated with vascular calcifications and plaques in the intimal and in the medial layers.2 When comparing the extent of PAD in those with diabetes to that of the general population, the arteries have a more diffuse disease process with greater involvement in the distal area. PAD can extend to the digital arteries of the toes. The mechanisms underlying these characteristics are not well understood.
Although scientists suspect that genetic factors contribute to the risk of developing PAD, research has not yielded any definitive answers. The Multi-Ethnic Study of Atherosclerosis revealed that PAD affects African Americans twofold more than other groups, even when accounting for ethnic differences in the burden of risk factors.13
ASSESSMENT AND CLINICAL PRESENTATION
PAD symptoms depend on the location and severity of the stenosis. In many patients, PAD will be asymptomatic, but in others, the pain can range from mild to severe. On closer assessment, many patients who do not report symptoms of claudication may have leg fatigue or discomfort that has been bothersome enough that they have reduced their amount of physical activity or slowed their walking speed to make accommodations for the symptoms.14 Some may attribute the leg discomfort to a preexisting condition, such as osteoarthritis or peripheral neuropathy. Other individuals will not have any symptoms at all, but disease is present.
Intermittent claudication, usually occurring in the calf, is the most common manifestation associated with PAD. Because the gastrocnemius muscle uses the highest amount of oxygen during exertion, it correlates to pain in the calf area. Claudication is brought on by walking or other exercise and is relieved by rest. The patient may describe the claudication as aching, numbness, weakness, or heaviness in lower-extremity muscles. Discomfort in the buttocks, thigh, or foot may occur depending on the location of the 1occlusion. The pain usually localizes distal to the occluded artery. For example, occlusions in the iliac arteries will cause pain in the buttock or thigh. Unlike diabetic peripheral neuropathy with its bilateral, symmetric presentation, PAD can be unilateral or have different degrees of severity for each leg.
Patients with diabetes may have diffuse and severe disease more commonly affecting the tibial arteries with a high prevalence of long occlusion manifesting in foot pain. Patients who are symptomatic usually include those who are sedentary or have limited exertion activity. Individuals with diabetes, however, may present with atypical pain largely because of peripheral neuropathy. The symptoms may be altered or more subtle, such as leg fatigue or progressively slowing ambulation, which reduces oxygen consumption by the calf muscle and reduces symptoms. Conversely, collateral circulatory formation is reduced in many patients with diabetes, making them more likely to have severe and acute ischemia, presenting with deep duskiness and pain in the affected extremity. Table 11.1 provides guidance for forming assessment questions for PAD.
Table 11.1—Nursing Assessment and Interventions and Patient Self-Management Education for Diabetes Patients with Peripheral Arterial and Venous Disease
HEALTH HISTORY
During the patient’s health history, any risk factors for or existing cardiovascular or cerebrovascular disease needs to be elucidated and any current treatment should be noted. If claudication is present, the history must include a thorough description of the precipitating factors, particularly the intensity of the exercise (e.g., flat or inclined surface) and duration and distance walked before pain began. Pain present without exertion, while at rest or with change in position, may indicate severe ischemia. Pain also may be aggravated by leg elevation and improved with dependent positioning. Unlike peripheral neuropathy, it usually does not present as nocturnal pain or cramping, but the pain may increase in a recumbent position and patients may feel more comfortable sleeping in a chair with legs dependent.
PHYSICAL EXAMINATION
Each patient presenting with symptoms suggestive of PAD should have a comprehensive physical examination focusing on the circulatory system. The basics of the exam include vital signs, including heart rate, blood pressure, respiratory rate, oxygen saturation, and temperature; and auscultation of the neck, back, and abdomen to assess for carotid, renal, or aortic artery changes, respectively. Auscultation of the vessels while palpating the radial artery can better discriminate subtle bruits from ambient noise.15 In those patient who are asymptomatic and have no leg symptoms of exertion, pathologic changes in muscle and peripheral nerves may exist. Reduced calf muscle mass, increased calf muscle fat content, and reduced lower-extremity nerve function can be present on physical exam.16
Examination of the radial pulses detecting any changes in volume difference or delay and examination of the carotid arteries are necessary. In the lower extremities, bilateral palpation of the pulses femoral and popliteal, posterior tibial, and dorsalis pedis should be done simultaneously for comparison and grading. The popliteal pulse may be difficult to find and should be examined in both a sitting and supine position.16 Evaluation of the skin of both feet and lower legs is a critical part of the exam. Changes in skin color, texture, diminished pulses, and audible bruits all can be indicators of PAD.
Inspection of the skin and connective tissue can indicate poor circulation. Muscle atrophy in the affected extremity as well as changes in color or temperature can be signs of poor perfusion. A classic finding on exam of the patient suspected of PAD is rubor of the lower extremities when dependent and pallor on elevation. Shiny skin with hair loss should be assessed, as well as the condition of the nails, which may be dystrophic in PAD. The areas at the tip of and between the toes (interdigital spaces) should be inspected for cracks, fissures, and infection, as these are common locations for ulceration in PAD.
During the history or exam, any suspicion of total arterial occlusion or complete limb ischemia (CLI) calls for immediate action. Emergency diagnostic testing and a vascular consult with surgical interventions, such as vascular shunting or bypass surgery, may be needed to save the limb. Table 11.1 delineates assessment and intervention strategies for patients with PAD or venous disease.
DIAGNOSTIC TESTING
Noninvasive Studies
The ABI measures PAD noninvasively, recording a ratio of Doppler-recorded systolic pressure in the lower and upper extremities.14 It is the most appropriate test to screen for PAD. Although it is possible to use this method to establish the diagnosis and severity of PAD in an office setting, Medicare and many insurance companies do not reimburse for this test unless arterial waveforms also are measured and interpreted, making this a complicated practice.14
Recommendations on screening vary across current guidelines. Most notably, an evidence review of the U.S. Preventive Services Task Force concluded that the addition of the ABI to predict cardiovascular disease was not well established and therefore was not included in their recommendations.17 The American College of Cardiology Foundation/American Heart Association (ACCF/AHA) Focused Update of the Guideline for the Management of Patients with Peripheral Artery Disease does speak to the utility of screening for PAD and includes ABI testing. They recommend ABI screening in patients with exertion leg symptoms, nonhealing leg wounds, ≥65 years old, and ≥50 years old with a history of diabetes and smoking.18
The International Working Group on the Diabetic Foot discusses the importance of screening for PAD in any patient with diabetes and a foot ulcer and recommends handheld Doppler evaluation of the flow signals from both foot arteries (dorsalis pedis and posterior tibial); measurement of the ABI; and, if there is diagnostic uncertainty, measurement of the toe-brachial index.19 Patients with symptoms of claudication or decreased or absent pedal pulses should be referred for ABI and for further vascular assessment as appropriate.
The ABI involves measuring the systolic blood pressure just above the ankle and over the brachial artery in the arm with a straight cuff in both arms and legs and a handheld Doppler device. The higher of the two ankle systolic pressure measurements for a given limb is divided by the higher of the two brachial systolic blood pressure measurements to give the ABI (see Table 11.2 for interpretation of the ABI).
Table 11.2—Interpretation of ABI
|
Ratio |
Interpretation |
|
0.9–1.3 |
Normal |
|
0.5–0.9 |
PAD; associated with IC |
|
<0.5 |
CLI; associated with ulceration and rest pain |
|
>1.3 |
False elevation, heavy vessel calcification* |
ABI, Ankle-Brachial Index; CLI, critical limb ischemia; IC, intermittent claudication; PAD, peripheral arterial disease. *ABI less reliable.
In patients with longstanding diabetes, ABI may be less reliable because of vessel calcifications and noncompressible blood vessels. An ABI >1.3 seen in stiff vessels is associated with increased cardiovascular event rates.19Conditions associated with media calcification, such as diabetes, chronic kidney disease, or advanced age, can lead to falsely elevated or falsely normal ankle pressure as a result of this stiffness.20 In these patients, the toe-brachial index should be used because the toe vessels are less susceptible to vessel stiffness and usually are spared from atherosclerosis. The toe-brachial index is calculated from the highest toe systolic pressure divided by the highest brachial pressure. A ratio of ≥0.7 usually is considered normal, but this cut point is not strictly evidence based.20 Toe pressures <30 mmHg usually indicate that a wound is unlikely to heal on that extremity.9
If a borderline ABI, either low normal or low abnormal, occurs, it is likely an indicator of functional decline and accelerated panatherosclerosis.21 These borderline cases were shown to have a threefold increased functional decline at 5 years in the Walking and Leg Circulation Study.13 Even moderately reduced ABI values have important prognostic implications, comparable to a reduced left ventricular ejection fraction in patients with cardiac failure.22
If PAD is diagnosed or strongly suspected, patients should have segmental pressures and pulse volume recordings in a vascular laboratory. Patients who have a normal ABI but a high suspicion for PAD may require treadmill testing, during which a >20 mmHg decrease in ankle pressure usually indicates PAD.23 This test is particularly useful in that it also can give important information on exertion versus nonexertion causes of leg pain indicated by pain-free walking time and distance.
Duplex ultrasound (DUS) is a fast, cost-effective way to measure blood flow. Easily performed in an outpatient setting, it requires a skilled technician to obtain accurate results. The procedure has some limitations. The aortic iliac segments may not be as clearly visualized because of obesity and bowel gas.2 In addition, edema, skin ulceration, and vessel calcification can interfere with the ability to obtain accurate results for PAD diagnosis or evaluation. DUS is not as accurate in visualizing the more distal and smallest vessels, but it does allow for direct visualization of the artery. It uses a combination of real-time B-mode imaging and color pulse–waved Doppler ultrasonography to look at layers of the arterial wall, characterize atherosclerotic plaques, and measure blood flow velocity and turbulence. DUS is a valuable test in those cases in which it is essential to precisely locate and characterize the stenosis for revascularization.2 The test also can be used following revascularization surgery to monitor graft and native vessels for continuing patency.
Computed tomography angiography (CTA) is a noninvasive test that can image the smaller and heavier calcified tibial vessels frequently diseased in diabetic individuals with PAD. Reported to be highly specific and sensitive, it can evaluate the vessel wall and atherosclerotic lesions for plaque characteristics, ulceration, calcification, and thrombus.9 It also can define soft tissue abnormalities, such as aneurysms. It has an advantage over other diagnostic tests in that it can be used with metal clips, stents, and prostheses. A drawback of CTA is its use of ionizing radiation and nephrotoxic contrast agents. This may limit its use in people who have diabetes or underlying renal insufficiency.
Although magnetic resonance angiogram (MRA) does not use ionizing radiation and the contrast used is less nephrotoxic, its use is limited in people with diabetes. The tibial-level vessel imaging may be less accurate, especially in those with CLI and diabetic foot ulcers. Additionally, most centers will not use MRA in patients with glomerular filtration rates <30 mL/min because of reports of nephrogenic systemic fibrosis.9 The test can take up to 60 min, and patient with claustrophobia may not be able to tolerate it. Pacemakers, defibrillators, and other metallic devices preclude the use of this testing modality.
Intra-arterial digital subtraction angiography (DSA) with its high spatial resolution is the most accurate among all imaging modalities and is considered the gold standard in vascular imaging.2 It is superior in visualizing distal small-caliber vessels and can be used during catheter-based interventions for the treatment of lower-extremity ischemia. Drawbacks of DSA include the need for intra-arterial access and the related risks of hematoma, infections, bleeding, and atheroembolism as well as the possibility of nephrotoxicity in patients who have diabetes or renal insufficiency.2
Medical Treatment And Surgical Interventions
Medical management addressing the conventional risk factors for cardiovascular disease is the first step in treating PAD. These treatments include medical nutrition therapy and medications for lipid and blood pressure management. Smoking and the use of tobacco products is the single most important modifiable risk factor for the development and exacerbation of PAD.23 Cigarette smoke activates many mechanisms contributing to atherosclerosis, including thrombosis, insulin resistance, dyslipidemia, vascular inflammation, abnormal vascular growth, and angiogenesis. It also triggers loss of endothelial homeostatic and regenerative functions.11 Tobacco use is associated with increased risk of amputation.
In some cases, cardiovascular risk management and smoking cessation is not only the primary but also the only intervention for patients with PAD and diabetes because the patient may not be a suitable surgical candidate. Because PAD becomes more prevalent both with duration of disease as well as aging, some patients will have other disease entities that place them at high surgical risk. Statin therapy, specifically simvastatin in the Scandinavian Simvastatin Survival Study (4S), improved cholesterol levels and reduced the risk of new or progressive claudication by 38%.24 Although no specific clinical trials assessing hypertension in patients with PAD and diabetes exist, hypertension is associated with a two- to threefold increase in claudication and contributes to the development of atherosclerosis. Aggressive blood pressure control, achieving a level of <130/80 mmHg in patients with PAD and diabetes, will help reduce cardiovascular risk. Clinical consensus based on studies examining the effect of hypertension management in cardiovascular risk reduction supports the use of angiotensin-converting enzyme inhibitors.
Two lifestyle changes are core components of PAD treatment: smoking cessation and a therapeutic walking program. Smoking cessation is essential in treating PAD and in the prevention of cardiovascular and cerebrovascular events, but it is difficult for many patients to achieve. The rate of relapse is high, and patients need continuing support and encouragement to make the repeated attempts that often are necessary before achieving success. Hospital-based and community programs as well as online resources educate and support the patient who is trying to quit smoking. A smoking cessation program must include a patient-selected quit date, an assessment of perceived barriers to quitting, discussion concerning helpful coping behaviors, and the possible use of pharmacologic therapies, such as nicotine replacement, bupropion, and varenicline (unless medically contraindicated). Although the goal is complete cessation, many patients will use a gradual reduction plan, setting a goal for the number of cigarettes or amount of tobacco used during a day. Studies indicate, however, that those in a structured, intensive counseling program with education, social support, and monthly counseling sessions were three times more likely to remain free of smoking for 6 months.25 The use of e-cigarettes as a substitute for cigarette smoking is controversial and data regarding this method to facilitate smoking cessation is inconsistent.
Progressive physical activity is an effective treatment to improve walking distance and to reduce mortality and cardiovascular events in patients with PAD.26 It is an important therapeutic modality and can lead to patients’ ability to walk longer distances pain free. Identified as a primary therapeutic treatment for PAD, the benefits of walking programs include increased blood flow, improved collateral circulation, lengthening of walking distance capability, a decrease in the oxygen cost of exercise and reduction in heart rate, and improved functional well-being.26 Walking programs may be part of a structured program through a cardiac rehabilitation or physical therapy department. In patients with claudication, structured programs have been effective, increasing pain-free walking time and maximal walking time by more than 100%. This higher level of physical activity can reduce functional decline. Drawbacks to these programs include lack of accessibility, underutilization by medical providers, and issues of patient adherence to the structured program.27 Although studies indicate that the structured programs have superior outcomes to home-based exercise programs, all of the physical improvements were demonstrated in both program groups. In addition to the improvement in ambulation and functional capacity, the quality-of-life scores were superior in the home-based programs. In the home-based programs, tools such as pedometers help to monitor patient progress. These meters can track activity and also be used as part of an online coaching activity. For those without access to these tools, the recording of time and frequency of walking in a logbook is an effective and inexpensive intervention. Regardless of the tools used, patients need encouragement and support to maintain any walking program. Some of the community-based programs offered may include group participation or follow-up telephone calls by a trainer or buddy. The walking regimen may involve family members in the physical activity, further increasing motivation and support while contributing to a healthier lifestyle.
In general, exercise programs effective in improving “pain distances” recommend a minimum duration of 30–45 min of walking exercise, at least three times per week, and a program length of >12 weeks.28 Programs may use the symptom of near-maximal pain during training as the claudication pain end point. When patients cannot walk any farther because of claudication, they are encouraged to rest briefly until the discomfort abates and then to begin walking again to improve vascular function. Instructions need to be modified in those patients with other muscle or joint problems or with neurologic, cardiac, or pulmonary diseases.
INFECTIONS
Patients with diabetes and PAD are more likely to develop severe foot infections. When both neuropathy and PAD are present, the foot is at much greater risk for traumatic ulceration, infection, and gangrene. Patient education in preventive foot care measures becomes critically important in reducing amputation risk. Ischemic ulcers typically form at the edges of the foot, including the tips of the toes and the backs of the heels. Footwear for the neuroischemic foot must fit well to avoid the creation of pressure points or shearing force (see Chapter 17, Evaluation and Management of the Diabetic Foot).
Education and Behavioral Considerations for Peripheral Vascular Disease
|
Problem |
Considerations |
|
Patients with PAD have pain associated with walking. |
• Encourage and assist to implement a walking program. • Identify barriers to program (external barriers are more easily overcome than internal). • Problem solve ways to overcome these barriers. • Identify or assist patients to identify community resources, such as cardiac rehabilitation, local community centers, senior centers, and shopping mall walking programs, as people are more apt to stay with exercise programs if they have social support. |
|
Many people cannot adequately examine their feet because of obesity, decreased vision, or decreased flexibility. |
• Mirrors on handles may facilitate visual inspection of the plantar surfaces of their feet. • Problem solve methods to raise the feet so patients can reach their feet to wash and dry them appropriately. • Long-handled sponges can enable people to clean their feet and long-handled pointed sponges enable cleaning of the interdigital spaces. |
In individuals with diabetes and foot infection, the presenting signs and symptoms of infection often are diminished. An impairment of the neuroinflammatory response reduces the early warning signs of infection. Differentiating between the erythema of cellulitis and the rubor of ischemia may be difficult. The redness of ischemia will disappear on elevation, but in cellulitis, the redness remains, irrespective of positioning.
In cases of severe infection, broad-spectrum intravenous antibiotics will be necessary because these infections frequently are polymicrobial. Antibiotic treatment alone, however, is not enough to treat most infections. Surgical assessment for debridement and drainage, offloading the ulcer, and applying appropriate dressings each play a vital role in the treatment process (see Chapter 17, Evaluation and Management of the Diabetic Foot).
The Role of Medical Therapy
Medications used in the treatment of PAD are not disease-modifying agents. None of the drugs currently used act to preserve vascular integrity as effectively as exercise. A report of the ACCF/AHA task force on the management of patients with PAD reviews the medications recommended for treatment.28
Antiplatelet therapy with cilostazol (100 mg orally two times per day) is an effective therapy to improve symptoms and increase walking distance, but it cannot be used in patients with a history of congestive heart failure. In patients who have lifestyle-limiting claudication, the ACCF/AHA guidelines recommend a therapeutic trial of the medication.28 Cilostazol causes a cascade of biochemical changes that lead to arterial smooth muscle dilatation, lead to increased nitric oxide signaling, and have some impact in decreasing platelet aggregation. It also has the pleiotropic effect of increasing HDL levels and lowering triglycerides. The side effects, such as headache, palpitations, and diarrhea, can be intolerable to some patients, however, and they will stop therapy.21
As a second-line alternative, pentoxifylline (400 mg three times per day) may be used in patients who cannot take cilostazol. It increases erythrocyte flexibility, increases fibrin levels, and reduces blood viscosity. The clinical efficacy of this drug, however, has not been well established and may provide only marginal benefit.
The benefits of aspirin (ASA) for PAD treatment are controversial. Recent studies failed to show any improvement in low ABI with aspirin use.29 Because the frequent association of PAD with more generalized atherosclerosis is present in many people with diabetes, low-dose aspirin continues to be used, particularly in those with high cardiovascular risk factors.30 When studied, the use of antiplatelet therapy and aspirin together did not yield an additional benefit over the use of low-dose aspirin alone. In general, this dual therapy is not recommended unless there are absolute indications.
Warfarin in conjunction with antiplatelet therapy for PAD is not indicated and can do definite harm, causing bleeding events. Other new anticoagulants used in place of warfarin have not been evaluated for use in PAD.18
Surgical Interventions
Surgical and endovascular interventions are called for when severe claudication limits lifestyle despite pharmacological treatment and supervised exercise, for pain at rest indicating CLI, or for the presence of nonhealing ulcers.9 One of the criteria for surgery is that the limb must be viable postintervention and contribute to the patient’s quality of life. Revascularization surgery is considered the gold standard and the usual intervention is an arterial bypass graft with an autologous saphenous vein graft. The aim of the surgery is to establish a straight-line pulsatile flow to a target ulcer, if present. The most common bypass procedure is the femoropopliteal bypass, which has a limb salvage rate of 89%.9 Because patients with diabetes have more infrapopliteal disease, this surgical procedure is important in reestablishing blood flow. In some cases, a more distal revascularization is needed to increase flow. Even if the graft occludes, the increased blood flow and oxygenation may be sufficient to improve healing of an ulcer.
When bypass surgery has been compared to angioplasty in severe ischemia no significant difference was indicated in amputation-free survival, all-cause mortality, or quality of life between the groups. The angioplasty group had a higher rate of reintervention.31
Endovascular intervention or percutaneous revascularization may be a first-line therapy for some patients. The risks are lower, outcomes are comparable, and the newer techniques now permit complex occlusions to be treated successfully.2 Surgery is more expensive and has a higher morbidity rate. A variety of methods can be used for recanalization, but if possible, most surgeons prefer the transluminal approach. In general, patients with a focal or discrete lesion as the main problem respond well to endovascular surgery.1 If, however, the disease is more diffuse with long areas of total occlusion or concomitant aneurysms, then surgery is preferred. Other factors may play a role in determining whether a surgical or an endovascular procedure is indicated. Unfortunately, diabetes is a predictor of poorer outcomes after any vascular surgery. New devices and techniques, such as drug-eluting balloons, bare metal stents, drug-eluting or bioabsorbable stents, and laser atherectomy, currently are available but have not been evaluated in the diabetic population.9
Whichever intervention is selected for the revascularization, postprocedural care is critically important. Prevention of a reocclusion is paramount, and the patient needs careful and consistent follow-up care. Nurses should assess blood flow and circulation, healing of the surgical sites, and other lesions or ulcerations. Education regarding foot care as well as the signs and symptoms of infection or of material occlusion are important components of self-care for the patient with PAD.
SUMMARY
PAD is significantly underdiagnosed and undertreated. Although careful examination of the lower extremities can identify PAD, a careful nursing assessment, particularly of exercise patterns and barriers, may identify clues, such as leg pain, that indicate PAD. Clues uncovered during a nursing assessment also can generate ideas for strategies to assist patients in implementing and maintaining an exercise program. These clues include, but are not limited to, previous activity or exercise patterns; occasions when walking was pleasurable; support systems, such as family, friends, pets, and seniors groups; and interest in walking groups that might lend support for the initiation and maintenance of a walking program.
PAD is a serious complication associated with diabetes and is often asymptomatic. The clinical presentation varies greatly. Some patients will maintain activity, whereas others will have difficulty performing daily activities. Because patients with diabetes can present with symptoms that can be confused with neuropathy, PAD can be missed. Clinical evaluation that includes diagnostic vascular testing is important to establish the diagnosis. Vascular consultation followed by appropriate treatment is necessary to preserve and protect the affected limb. Foot care education is a main component in the prevention of foot ulcers and infections. Surgery to restore circulation may be necessary to avoid loss of the limb.
REFERENCES
1. Cooke JP, Chen Z. A compendium on peripheral arterial disease. Circ Res 2015;116:1505–1508
2. Cagliero, E. Peripheral arterial disease: Diagnosis and management. In Therapy for Diabetes Mellitus and Related Disorders. 6th ed. Umpierrez GE, Ed. Alexandria, VA, American Diabetes Association, 2014, p. 898–907
3. Roger VL, Go AS, Lloyd-Jones DM, et. al. Heart disease and stroke statistics 2011 update: a report from the American Heart Association.Circulation 2011;123:e18–e209
4. Ostchega Y, Paulose-Ram R, Dillon CF, Gu Q, Hughes JP. Prevalence of peripheral arterial disease and risk factors in persons aged 60 and older: data from the National Health and Nutrition Examination Survey, 1999–2004. J Am Geriatr Soc 2007;55:583–589
5. Criqui MH, Aboyans V. Epidemiology of peripheral artery disease. Circ Res 2015;116:1509–1526
6. Hankey GJ, Norman PE, Eikelboon JW. Medical treatment of peripheral arterial disease. JAMA 2006;295:547–553
7. Selvin E, Marinopoulos S, Berkenblit G, Rami T, Brancati FL, Powe NR, Golden SH. Meta-analysis: glycosylated hemoglobin and cardiovascular disease in diabetes mellitus. Ann Inter Med 2004;141:421–431
8. Shammas ND, Eric J. Evidence-based management of peripheral vascular disease. Current Atheroscler Rep 2005;7:358–363
9. Chin JA, Sumpio BE. Diabetes mellitus and peripheral vascular disease: diagnosis and management. Clin Podiatr Med Surg 2014;31:11–26
10. American Diabetes Association. Peripheral arterial disease in people with diabetes (Consensus Statement). Diabetes Care 2003;26:3333–3341
11. Lee J, Cooke JP. The role of nicotine in the pathogenesis of atherosclerosis. Atherosclerosis 2011;215:281–283
12. He Y, Lam TH, Jiang B, Wang J, Xiaoyong S, Li F, Xiaoying L, Yinhe Q, Hu FB. Passive smoking and risk of peripheral arterial disease and ischemic stroke in Chinese women who never smoked. Circulation2008;118:535–540
13. Allison MA, Criqui MH, McClelland RL, Scott JM, McDermott MM, Kiang L, Folsom AR, Bertoni AG, Sharrett AR, Homma S, Sujata K. The effect of novel cardiovascular risk factors on the ethnic-specific odds for peripheral arterial disease in the Multi-Ethnic Study of Atherosclerosis (MESA). J Am Coll Cardiol 2006;48:1190–1197
14. McDermott, MM. Lower extremity manifestations of peripheral artery disease: the pathophysiologic and functional implications of leg ischemia. Circ Res 2015;116:1540–1550
15. Wennberg PW. Approach to the patient with peripheral arterial disease. Circulation 2013;28:2241–2250
16. McDermott MM, Guralnik JM, Ferrucci L, Tian J, Liu K, Liao Y, Green D, Sufit R, Hoff F, Nishida T, Sharma L, Pearce WH, Schneider JR, Criqui MH. Asymptomatic peripheral arterial disease is associated with more adverse lower extremity characteristics than intermittent claudication. Circulation 2008;117:2484–2491
17. Lin JS, Olson CM, Johnson ES, Whitlock EP. The ankle-brachial index for peripheral artery disease screening and cardiovascular disease prediction among asymptomatic adults: a systematic evidence review for the U.S. Preventive Services Task Force. Ann Int Med 2013;159:333–341
18. Rooke TW, Hirsch AT, Misra S, Sidawy AN, Beckman JA, Findeiss LK, Golzarian J, Gornik HL, Halperin JL, Jaff MR, Moneta GL, Olin JW, Stanley JC, White CJ, White JV, Zierler RE. 2011 ACCF/AHA focused update of the guideline for the management of patients with peripheral artery disease (updating the 2005 guideline): a report of the American College of Cardiology Foundation /American Heart Association Task Force on Practice Guidelines: developed in collaboration with the Society for Cardiovascular Angiography and Interventions, Society for Interventional Radiology, Society for Vascular Medicine , and Society for Vascular Surgery. J Am Coll Cardiol 2011;58:2020–2045
19. Schaper NC, Andros G, Apelqvist J, Bakker K, Lammer J, Lepantolo M, Mills JL, Reekers J, Shearman CP, Sierler RE, Hinschliffe FJ. Diagnosis and treatment of peripheral arterial disease in diabetic patients with a foot ulcer: a progress report of the International Working Group on the Diabetic Foot. Diabetes Metab Rev 2012;28:218–224
20. Hoyer C, Sandermann J, Petersen LJ. The toe-brachial index in the diagnosis of peripheral arterial disease. J Vasc Surg 2013;58:231–238
21. Agrawal K, Eberhardt RT. Contemporary medical management of peripheral arterial disease: a focus on risk reduction and symptom relief for intermittent claudication. Cardiol Clin 2015;33:111–137
22. Halperin J. Evaluation of patients with peripheral vascular disease. Throm Res 2002;106:V303–V311
23. Hirsch AT, Haskal ZJ, Hertzer NR, Bakal CW, Creager MA. ACCF/AHA guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic) (Executive Summary). J Am Coll Cardiol 2006;47:1239–1312
24. Kjekshus J, Pedersen TR. Reducing the risk of coronary events: evidence from the Scandinavian Simvastatin Survival Study (4S). Am J Cardiol 1995;76:64C–68C
25. Hennrikus D, Joseph AM, Lando HA, et al. Effectiveness of a smoking cessation program for peripheral artery disease patients: a randomized controlled study. J Am Coll Cardiol 2010;56:2105–2112
26. Schiattarella G, Perrino C, Magliulo F, Carbone A, Bruno A, DePaulis M, Sorropago A, Corrado R, Bottino R, Menafra G, Abete R, Toscano E, Giugliano G, Trimarco B, Esposito G. Physical activity in the prevention of peripheral artery disease in the elderly. Front Physiol 2014;5:1–6
27. Makris GC, Lattimer CR, Lavida AC, Geroulakos G. Availability of supervised exercise programs and the role of structured home-based exercise in peripheral arterial disease. Eur J Vascul Endovascul Surg 2012;44:569–575
28. Anderson, JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH, DeMets D, Guyton RA, Hochman JS, Kovacs RJ, Ohman EM, Pressler SJ, Sellke FW, Shen W-K. Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guidelines recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force Practice Guidelines. Circulation2013;127:1425–1443.
29. Bonaca MP, Creager MA. Pharmacological treatment and current management of peripheral artery disease. Circ Res 2015;116:1579–1598
30. Beckman JA, Paneni F, Cosentino F, Creager MA. Diabetes and vascular disease pathophysiology, clinical consequences, and medical therapy: part II. Eur Heart J 2013;34:2444–2456
31. Adam DJ, Beard JD, Cleveland T, Bell J, Bradbury AW, Forbes JF, Fowkes FG, Gillepsie I, Ruckley CV, Raab G, Storkey H, BASIL Trial Participants. Bypass versus Angioplasty in Severe Ischaemia of the Leg (BASIL): multicentre, randomized controlled trial. Lancet 2005;366:1925–1934