ACC/AHA PRACTICE GUIDELINE
ACC/AHA 2005 Guidelines for the Management of Patients With Peripheral Arterial Disease (Lower Extremity, Renal, Mesenteric, and Abdominal Aortic): Executive Summary A Collaborative Report From the American Association for Vascular Surgery/Society for Vascular Surgery,* Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease)
Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation
Alan T. Hirsch, MD, FACC, FAHA, Chair, WRITING COMMITTEE MEMBERS,
Ziv J. Haskal, MD, FAHA, FSIR, Co-Chair, WRITING COMMITTEE MEMBERS,
Norman R. Hertzer, MD, FACS, Co-Chair, WRITING COMMITTEE MEMBERS,
Curtis W. Bakal, MD, MPH, FAHA, FSIR, WRITING COMMITTEE MEMBERS,
Mark A. Creager, MD, FACC, FAHA, WRITING COMMITTEE MEMBERS,
Jonathan L. Halperin, MD, FACC, FAHA, WRITING COMMITTEE MEMBERS ,
Loren F. Hiratzka, MD, FACC, FAHA, FACS, WRITING COMMITTEE MEMBERS,
William R.C. Murphy, MD, FACC, FACS, WRITING COMMITTEE MEMBERS,
Jeffrey W. Olin, DO, FACC, WRITING COMMITTEE MEMBERS,
Jules B. Puschett, MD, FAHA, WRITING COMMITTEE MEMBERS,
Kenneth A. Rosenfield, MD, FACC, WRITING COMMITTEE MEMBERS,
David Sacks, MD, FACR, FSIR, WRITING COMMITTEE MEMBERS ,
James C. Stanley, MD, FACS, WRITING COMMITTEE MEMBERS ,
Lloyd M. Taylor, Jr, MD, FACS, WRITING COMMITTEE MEMBERS,
Christopher J. White, MD, FACC, FAHA, FESC, FSCAI, WRITING COMMITTEE MEMBERS¶,
John White, MD, FACS, WRITING COMMITTEE MEMBERS,
Rodney A. White, MD, FACS, WRITING COMMITTEE MEMBERS,
Elliott M. Antman, MD, FACC, FAHA, Chair, TASK FORCE MEMBERS,
Sidney C. Smith, Jr, MD, FACC, FAHA, Vice-Chair, TASK FORCE MEMBERS,
Cynthia D. Adams, MSN, APRN-BC, FAHA, TASK FORCE MEMBERS,
Jeffrey L. Anderson, MD, FACC, FAHA, TASK FORCE MEMBERS,
David P. Faxon, MD, FACC, FAHA, TASK FORCE MEMBERS**,
Valentin Fuster, MD, PhD, FACC, FAHA, FESC, TASK FORCE MEMBERS**,
Raymond J. Gibbons, MD, FACC, FAHA, TASK FORCE MEMBERS,
Jonathan L. Halperin, MD, FACC, FAHA, TASK FORCE MEMBERS,
Loren F. Hiratzka, MD, FACC, FAHA, FACS, TASK FORCE MEMBERS,
Sharon A. Hunt, MD, FACC, FAHA, TASK FORCE MEMBERS,
Alice K. Jacobs, MD, FACC, FAHA, TASK FORCE MEMBERS,
Rick Nishimura, MD, FACC, FAHA, TASK FORCE MEMBERS,
Joseph P. Ornato, MD, FACC, FAHA, TASK FORCE MEMBERS,
Richard L. Page, MD, FACC, FAHA, TASK FORCE MEMBERS and
Barbara Riegel, DNSc, RN, FAHA, TASK FORCE MEMBERS
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I. Introduction
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These guidelines address the diagnosis and management of atherosclerotic, aneurysmal, and thromboembolic peripheral arterial diseases (PADs). The clinical manifestations of PAD are a major cause of acute and chronic illness, are associated with decrements in functional capacity and quality of life, cause limb amputation, and increase the risk of death. Whereas the term "peripheral arterial disease" encompasses a large series of disorders that affect arterial beds exclusive of the coronary arteries, this writing committee chose to limit the scope of the work of this document to include the disorders of the abdominal aorta, renal and mesenteric arteries, and lower extremity arteries. The purposes of the full guidelines are to (a) aid in the recognition, diagnosis, and treatment of PAD of the aorta and lower extremities, addressing its prevalence, impact on quality of life, cardiovascular ischemic risk, and risk of critical limb ischemia (CLI); (b) aid in the recognition, diagnosis, and treatment of renal and visceral arterial diseases; and (c) improve the detection and treatment of abdominal and branch artery aneurysms. Clinical management guidelines for other arterial beds (e.g., the thoracic aorta, carotid and vertebral arteries, and upper-extremity arteries) have been excluded from the current guidelines to focus on the infradiaphragmatic arterial system and in recognition of the robust evidence base that exists for the aortic, visceral, and lower extremity arteries.
The reader should note that the text, recommendations, and tables included in this executive summary represent a succinct summary of the more extensive evidence base, critical evaluation, tables, and references that are included in the full-text document. Readers are strongly encouraged to refer to this source document to gain full access to the 65 tables, more than 1300 references, and supporting text assembled by the writing committee. The full-text document can be accessed at http://www.acc.org/clinical/guidelines/pad/index.pdf.
A classification of recommendation and level of evidence have been assigned to each recommendation. Classifications of recommendations and levels of evidence are expressed in the American College of Cardiology (ACC)/American Heart Association (AHA) format as follows.
Classification of Recommendations
- Class I: Conditions for which there is evidence for and/or general agreement that a given procedure or treatment is beneficial, useful, and effective.
- Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment.
- Class IIa: Weight of evidence/opinion is in favor of usefulness/efficacy.
- Class IIb: Usefulness/efficacy is less well established by evidence/opinion.
- Class III: Conditions for which there is evidence and/or general agreement that a procedure/treatment is not useful/effective and in some cases may be harmful.
Level of Evidence
- Level of Evidence A: Data derived from multiple randomized clinical trials or meta-analyses.
- Level of Evidence B: Data derived from a single randomized trial or nonrandomized studies.
- Level of Evidence C: Only consensus opinion of experts, case studies, or standard of care. (Please refer to Table 1 in the full-text guidelines for more details.)
A. Definitions.
For the purposes of these guidelines, the term "peripheral arterial disease" broadly encompasses the vascular diseases caused primarily by atherosclerosis and thromboembolic pathophysiological processes that alter the normal structure and function of the aorta, its visceral arterial branches, and the arteries of the lower extremity. Peripheral arterial disease is the preferred clinical term that should be used to denote stenotic, occlusive, and aneurysmal diseases of the aorta and its branch arteries, exclusive of the coronary arteries.
B. Vascular History and Physical Examination.
RECOMMENDATIONS
Class I
- 1 Individuals at risk for lower extremity PAD (see Section 2.1.1 of the full-text guidelines) should undergo a vascular review of symptoms to assess walking impairment, claudication, ischemic rest pain, and/or the presence of nonhealing wounds. (Level of Evidence: C)
- 2 Individuals at risk for lower extremity PAD (see Section 2.1.1 of the full-text guidelines) should undergo comprehensive pulse examination and inspection of the feet. (Level of Evidence: C)
- 3 Individuals over 50 years of age should be asked if they have a family history of a first-order relative with an abdominal aortic aneurysm. (Level of Evidence: C)
The full-text guidelines offer suggestions for creation of a vascular review of systems as outlined below.
Key components of the vascular review of systems (not usually included in the review of systems of the extremities) and family history include the following:
- • Any exertional limitation of the lower extremity muscles or any history of walking impairment. The characteristics of this limitation may be described as fatigue, aching, numbness, or pain. The primary site(s) of discomfort in the buttock, thigh, calf, or foot should be recorded, along with the relation of such discomfort to rest or exertion.
- • Any poorly healing or nonhealing wounds of the legs or feet.
- • Any pain at rest localized to the lower leg or foot and its association with the upright or recumbent positions.
- • Postprandial abdominal pain that reproducibly is provoked by eating and is associated with weight loss.
- • Family history of a first-degree relative with an abdominal aortic aneurysm.
The Vascular Physical Examination
Key components of the vascular physical examination are as follows:
- • Measurement of blood pressure in both arms and notation of any interarm asymmetry.
- • Palpation of the carotid pulses and notation of the carotid upstroke and amplitude and presence of bruits.
- • Auscultation of the abdomen and flank for bruits.
- • Palpation of the abdomen and notation of the presence of the aortic pulsation and its maximal diameter.
- • Palpation of pulses at the brachial, radial, ulnar, femoral, popliteal, dorsalis pedis, and posterior tibial sites. Perform Allen’s test when knowledge of hand perfusion is needed.
- • Auscultation of both femoral arteries for the presence of bruits.
- • Pulse intensity should be assessed and should be recorded numerically as follows: 0, absent; 1, diminished; 2, normal; and 3, bounding.
- • The shoes and socks should be removed; the feet inspected; the color, temperature, and integrity of the skin and intertriginous areas evaluated; and the presence of ulcerations recorded.
- • Additional findings suggestive of severe PAD, including distal hair loss, trophic skin changes, and hypertrophic nails, should be sought and recorded.
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II. Lower extremity PAD
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A. Epidemiology.
1. Risk Factors
The major cause of lower extremity PAD is atherosclerosis. Risk factors for atherosclerosis such as cigarette smoking, diabetes, dyslipidemia, hypertension, and hyperhomocysteinemia increase the likelihood of developing lower extremity PAD (Fig. 1).
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Figure 1 Risk of developing lower extremity peripheral arterial disease. The range for each risk factor is estimated from epidemiologic studies (see text). The relative risks take into consideration current smokers vs. former smokers and nonsmokers; the presence vs. the absence of diabetes and hypertension; and the highest vs. the lowest quartile of homocysteine and C-reactive protein. The estimate for hypercholesterolemia is based on a 10% risk for each 10 mg/dl rise in total cholesterol. Adapted from J Vasc Surg, 31, Dormandy JA, Rutherford RB, for the TransAtlantic Inter-Society Consensus (TASC) Working Group, Management of peripheral arterial disease (PAD), S1–S296, Copyright 2000, with permission from Elsevier (16).
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2. Prevalence
Lower extremity PAD is a common syndrome that affects a large proportion of most adult populations worldwide (1,2). Peripheral arterial disease can be present in subclinical forms that can be detected by use of sensitive vascular imaging techniques, which may reveal early manifestations of arterial disease before it is detected by either limb-pressure measurements or clinical symptoms. When so defined, as, for example, by measurement of the intimal-medial thickness (IMT) in the carotid or femoral artery, early forms of PAD are easily detected in populations at risk (3). Claudication, a symptomatic expression of lower extremity PAD, defines a significantly smaller subset of the total population with the disease.
B. Prognosis and Natural History.
1. Coprevalence of Coronary Arterial Disease and Carotid Disease
The prognosis of patients with lower extremity PAD is characterized by an increased risk for cardiovascular ischemic events due to concomitant coronary artery disease and cerebrovascular disease (1,4). These cardiovascular ischemic events are more frequent than ischemic limb events in any lower extremity PAD cohort, whether individuals present without symptoms or with atypical leg pain, classic claudication, or CLI (Fig. 2) (5).
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Figure 2 The natural history of atherosclerotic lower extremity peripheral arterial disease (PAD). Individuals with atherosclerotic lower extremity PAD may be: (a) asymptomatic (without identified ischemic leg symptoms, albeit with a functional impairment); (b) present with leg symptoms (classic claudication or atypical leg symptoms); or (c) present with critical limb ischemia. All individuals with PAD face a risk of progressive limb ischemic symptoms, as well as a high short-term cardiovascular ischemic event rate and increased mortality. These event rates are most clearly defined for individuals with claudication or critical limb ischemia (CLI), and less well defined for individuals with asymptomatic PAD. CV = cardiovascular; MI = myocardial infarction. Adapted with permission from Weitz JL et al. Circulation 1996;94:3026–49 (5).
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C. Other Causes of Lower Extremity PAD.
Peripheral arterial disease has a diversity of causes beyond atherosclerosis. Aneurysms may be associated with atherosclerosis, may be due to underlying hereditary (familial) reasons, or may be of acquired (e.g., due to smoking or trauma) origin. Renal arterial disease may be due to atherosclerosis, fibromuscular dysplasia, or arteritides. Lower extremity PAD may be caused by atherosclerotic, thromboembolic, inflammatory, or aneurysmal disease; by trauma, adventitial cysts, or entrapment syndromes; or by congenital abnormalities. Establishment of an accurate diagnosis is necessary if individual patients are to receive ideal pharmacological, endovascular, surgical, or rehabilitative interventions.
D. Clinical Presentation.
1. Asymptomatic
RECOMMENDATIONS
Class I
- 1 A history of walking impairment, claudication, ischemic rest pain, and/or nonhealing wounds is recommended as a required component of a standard review of systems for adults 50 years and older who have atherosclerosis risk factors and for adults 70 years and older. (Level of Evidence: C)
- 2 Individuals with asymptomatic lower extremity PAD should be identified by examination and/or measurement of the ankle-brachial index (ABI) so that therapeutic interventions known to diminish their increased risk of myocardial infarction (MI), stroke, and death may be offered. (Level of Evidence: B)
- 3 Smoking cessation, lipid lowering, and diabetes and hypertension treatment according to current national treatment guidelines are recommended for individuals with asymptomatic lower extremity PAD. (Level of Evidence: B)
- 4 Antiplatelet therapy is indicated for individuals with asymptomatic lower extremity PAD to reduce the risk of adverse cardiovascular ischemic events. (Level of Evidence: C)
Class IIa
- 1 An exercise ABI measurement can be useful to diagnose lower extremity PAD in individuals who are at risk for lower extremity PAD (Table 1) who have a normal ABI (0.91 to 1.30), are without classic claudication symptoms, and have no other clinical evidence of atherosclerosis. (Level of Evidence: C)
- 2 A toe-brachial index or pulse volume recording measurement can be useful to diagnose lower extremity PAD in individuals who are at risk for lower extremity PAD who have an ABI greater than 1.30 and no other clinical evidence of atherosclerosis. (Level of Evidence: C)
Class IIb
- 1 Angiotensin-converting enzyme (ACE) inhibition may be considered for individuals with asymptomatic lower extremity PAD for cardiovascular risk reduction. (Level of Evidence: C)
Current data document that lower extremity PAD is common, that the traditional term "asymptomatic" may inaccurately imply that limb function is normal, and that lower extremity PAD is invariably and independently associated with impaired lower extremity functioning (6–8). Thus, most individuals with lower extremity PAD do not have classic (typical) claudication but may have more subtle impairments of lower extremity function.
Individuals with asymptomatic lower extremity PAD are characterized by a risk factor profile comparable to that of those with symptomatic lower extremity PAD (9,10). The high prevalence of diabetes, a history of past or current smoking, hypertension, and/or hypercholesterolemia place such individuals at a markedly increased risk of atherosclerotic ischemic events, including MI and stroke (9,11) and higher degrees of internal carotid artery stenosis (12,13). Given these data, current U.S. national hypertension, lipid, and antiplatelet treatment guidelines include all patients with lower extremity PAD, regardless of symptom status, as a "high-risk" category. All patients with lower extremity PAD should achieve risk reduction and specific treatment targets comparable to those of individuals with established coronary artery disease (14,15).
The responsibility for the detection of lower extremity PAD should be with the primary care provider. Programs of lower extremity PAD detection, whether applied in office practice or in community-based detection programs, should ideally utilize the epidemiological database to apply the detection tool to a population "at risk." The most cost-effective tool for lower extremity PAD detection is the ABI, which has been used in numerous field surveys and cross-sectional practice surveys, as cited in the full-text guidelines.
2. Claudication
RECOMMENDATIONS
Class I
- 1 Patients with symptoms of intermittent claudication should undergo a vascular physical examination, including measurement of the ABI. (Level of Evidence: B)
- 2 In patients with symptoms of intermittent claudication, the ABI should be measured after exercise if the resting index is normal. (Level of Evidence: B)
- 3 Patients with intermittent claudication should have significant functional impairment with a reasonable likelihood of symptomatic improvement and absence of other disease that would comparably limit exercise even if the claudication was improved (e.g., angina, heart failure, chronic respiratory disease, or orthopedic limitations) before undergoing an evaluation for revascularization. (Level of Evidence: C)
- 4 Individuals with intermittent claudication who are offered the option of endovascular or surgical therapies should (a) be provided information regarding supervised claudication exercise therapy and pharmacotherapy; (b) receive comprehensive risk factor modification and antiplatelet therapy; (c) have a significant disability, either being unable to perform normal work or having serious impairment of other activities important to the patient; and (d) have lower extremity PAD lesion anatomy such that the revascularization procedure would have low risk and a high probability of initial and long-term success. (Level of Evidence: C)
Class III
- 1 Arterial imaging is not indicated for patients with a normal postexercise ABI. This does not apply if other causes (e.g., entrapment syndromes or isolated internal iliac artery occlusive disease) are suspected. (Level of Evidence: C)
Vascular claudication due to lower extremity PAD is produced consistently by exercise and is relieved with rest and is therefore traditionally referred to as "intermittent" claudication, or simply "claudication." The severity of the symptoms can be classified according to either the Fontaine or Rutherford categories (Table 2).
Vascular claudication must be distinguished from other disorders that cause exertional leg pain, which has been called "pseudoclaudication." Distinguishing features of these various causes of leg pain are summarized in Table 3 (16).
The ABI should be measured in all patients with claudication. For individuals who present with classic claudication and in whom the ABI is borderline or normal (0.91 to 1.30) or supranormal (greater than 1.30), alternative diagnostic strategies should be used (including the toe-brachial index, segmental pressure examination, or duplex ultrasound), to confirm the lower extremity PAD diagnosis (see Section 2.5 of the full-text guidelines).
Most individuals with claudication benefit from a comprehensive medical approach that includes risk factor modification, antiplatelet therapy, exercise rehabilitation, and use of claudication medications (see Sections 2.6.1 and 2.6.2). In these individuals, more complex imaging studies are not required for effective management. Decisions regarding revascularization of individuals with claudication should be based on the severity of symptoms, a significant disability as assessed by the patient, failure of medical therapies, lack of significant comorbid conditions, vascular anatomy suitable for the planned revascularization, and a favorable risk-benefit ratio. These recommendations are summarized in Table 4 (16). Patients selected for possible revascularization may then undergo additional imaging studies as required to determine whether their arterial anatomy is suitable for percutaneous or surgical revascularization.
3. Critical Limb Ischemia
RECOMMENDATIONS
Class I
- 1 Patients with CLI should undergo expedited evaluation and treatment of factors that are known to increase the risk of amputation (see text). (Level of Evidence: C)
- 2 Patients with CLI in whom open surgical repair is anticipated should undergo assessment of cardiovascular risk. (Level of Evidence: B)
- 3 Patients with a prior history of CLI or who have undergone successful treatment for CLI should be evaluated at least twice annually by a vascular specialist owing to the relatively high incidence of recurrence. (Level of Evidence: C)
- 4 Patients at risk of CLI (ABI less than 0.4 in a nondiabetic individual, or any diabetic individual with known lower extremity PAD) should undergo regular inspection of the feet to detect objective signs of CLI. (Level of Evidence: B)
- 5 The feet should be examined directly, with shoes and socks removed, at regular intervals after successful treatment of CLI. (Level of Evidence: C)
- 6 Patients with CLI and features to suggest atheroembolization should be evaluated for aneurysmal disease (e.g., abdominal aortic, popliteal, or common femoral aneurysms). (Level of Evidence: B)
- 7 Systemic antibiotics should be initiated promptly in patients with CLI, skin ulcerations, and evidence of limb infection. (Level of Evidence: B)
- 8 Patients with CLI and skin breakdown should be referred to healthcare providers with specialized expertise in wound care. (Level of Evidence: B)
- 9 Patients at risk for CLI (those with diabetes, neuropathy, chronic renal failure, or infection) who develop acute limb symptoms represent potential vascular emergencies and should be assessed immediately and treated by a specialist competent in treating vascular disease. (Level of Evidence: C)
- 10 Patients at risk for or who have been treated for CLI should receive verbal and written instructions regarding self-surveillance for potential recurrence. (Level of Evidence: C)
Critical limb ischemia is defined by most vascular clinicians in patients who present with lower extremity ischemic rest pain, ulceration, or gangrene. In these individuals, the untreated natural history of severe PAD would lead to major limb amputation within 6 months. The Rutherford clinical categories (described earlier) are used to classify the degree of ischemia and salvageability of the limb. Critical limb ischemia is also a component of the Fontaine clinical classification system (Table 2).
Patients with CLI usually present with limb pain at rest, with or without trophic skin changes or tissue loss. The discomfort is often worse when the patient is supine (e.g., in bed) and may lessen when the limb is maintained in the dependent position. Typically, narcotic medications are required for analgesia. Those factors that are known to increase the risk of limb loss in patients with CLI are delineated in Table 5.
It is fundamentally important for the clinician to determine the time course of development of the ischemia. If the clinical history and physical examination suggest relatively rapid progression, then early or "semiurgent" revascularization may be required to prevent further deterioration and irreversible tissue loss. A vascular history should also be obtained. This should include evaluation for arterial disease in other territories, assessment of global risk factors for atherosclerosis, and clarification of any specific precipitating factors or events (e.g., trauma or infection) that may have caused initial skin ulceration. The objectives for the diagnostic evaluation of patients with CLI are summarized in Table 6. Specific investigations that are helpful in evaluating patients with CLI are summarized in Table 7.
Distinctions should be made between ulcers that are arterial and those that are venous or neurotrophic (Tables 8, 9, and 10).
The evaluation of patients presenting with CLI should include a complete blood count, chemistries (including blood glucose and renal function tests), electrocardiogram, and ABI. In the absence of "noncompressible vessels," measurement of an absolute systolic blood pressure 50 mm Hg or lower at the ankle and 30 mm Hg at the toe will often imply that amputation may be required in the absence of successful revascularization (16,17). Individuals with CLI who present with clinical features to suggest atheroembolization should be evaluated for more proximal aneurysmal disease (e.g., abdominal aortic, popliteal, or common femoral aneurysms). Atheroembolism is suggested by the onset of signs and symptoms of CLI after recent endovascular catheter manipulation, the onset of associated systemic fatigue or muscle discomfort, symmetrical bilateral limb symptoms, livido reticularis, or rising creatinine values.
Treatment of CLI is dependent on increasing blood flow to the affected extremity to relieve pain, heal ischemic ulcerations, and avoid limb loss. Individuals with minimal or no skin breakdown or in whom comorbid conditions prevent consideration of revascularization can occasionally be treated by medical therapies in the absence of revascularization. Medical care strategies have included the use of antiplatelet agents, anticoagulant medications, intravenous prostanoids, rheologic agents, and maintenance of the limb in a dependent position. However, none of these clinical interventions has been adequately evaluated or proven in prospective clinical trials to offer predictable improvements in limb outcomes. Recent investigation of angiogenic therapies, via administration of gene or protein, to enhance collateral blood flow has offered promise as a potential strategy to treat CLI; however, these are not yet proven interventions and are not available as established therapies.
In the absence of revascularization, most patients with CLI are expected to require amputation within 6 months. Therefore, timely referral to a vascular specialist is indicated. Detailed arterial mapping requires vascular expertise to (a) identify the cause of the ischemia and (b) define the options available for revascularization.
4. Acute Limb Ischemia
RECOMMENDATIONS
Class I
- 1 Patients with acute limb ischemia and a salvageable extremity should undergo an emergent evaluation that defines the anatomic level of occlusion and that leads to prompt endovascular or surgical revascularization. (Level of Evidence: B)
Class III
- 1 Patients with acute limb ischemia and a nonviable extremity should not undergo an evaluation to define vascular anatomy or efforts to attempt revascularization. (Level of Evidence: B)
Acute limb ischemia arises when a rapid or sudden decrease in limb perfusion threatens tissue viability. This form of CLI may be the first manifestation of arterial disease in a previously asymptomatic patient or may occur as an acute event that causes symptomatic deterioration in a patient with antecedent lower extremity PAD and intermittent claudication. Although attempts have been made to define various levels of ischemia (18), it is frequently not possible to precisely delineate the status of the patient with an acutely ischemic limb, because many of the classification schemes are based on subjective clinical criteria and not discrete end points. Table 11 displays the Society for Vascular Surgery/International Society for Cardiovascular Surgery classification scheme and provides the most useful clinical method to describe this entity.
The hallmark clinical symptoms and physical examination signs of acute limb ischemia include the 5 "Ps" that suggest limb jeopardy: pain, paralysis, paresthesias, pulseless, and pallor. Some clinicians would also include a sixth "P," polar, to indicate a cold extremity. However, arterial embolism can occur without symptoms, whereas thrombosis can produce sudden, severe limb ischemia. The clinical diagnosis of arterial embolism is suggested by (a) the sudden onset or sudden worsening of symptoms, (b) a known embolic source, (c) the absence of antecedent claudication or other manifestations of obstructive arterial disease, or (d) the presence of normal arterial pulses and Doppler systolic blood pressures in the contralateral limb. Acute limb ischemia is a situation that requires prompt diagnosis and treatment to preserve the limb and prevent the systemic illness or death that might result from the metabolic abnormalities associated with tissue necrosis. Although the technical ability to recanalize or revascularize occluded arteries that perfuse ischemic tissues has improved significantly, the pathophysiology of the local and systemic clinical sequelae associated with reperfusion of an ischemic limb is only partially understood. Revascularization of an ischemic extremity may be complicated by reperfusion injury to the damaged tissues and precipitate systemic responses, including cardiac, renal, and pulmonary dysfunction.
5. Prior Limb Arterial Revascularization
RECOMMENDATIONS
Class I
- 1 Long-term patency of infrainguinal bypass grafts should be evaluated in a surveillance program, which should include an interval vascular history, resting ABIs, physical examination, and a duplex ultrasound at regular intervals if a venous conduit has been used. (Level of Evidence: B)
Class IIa
- 1 Long-term patency of infrainguinal bypass grafts may be considered for evaluation in a surveillance program, which may include conducting exercise ABIs and other arterial imaging studies at regular intervals (see duplex ultrasound recommendations, Section 2.5.5 of the full-text guidelines). (Level of Evidence: B)
- 2 Long-term patency of endovascular sites may be evaluated in a surveillance program, which may include conducting exercise ABIs and other arterial imaging studies at regular intervals (see duplex ultrasound recommendations, Section 2.5.5 of the full-text guidelines). (Level of Evidence: B)
Despite increasing short-term success rates for both endovascular and surgical revascularization procedures, the possibility of recurrence remains throughout the lifetime of the patient. Early revascularization interventions for recurrent hemodynamic compromise are preferred, because delay in detection or treatment can lead to higher morbidity and poorer outcome (19–24). Participation in a follow-up surveillance program is imperative for patients undergoing both percutaneous and surgical revascularization. There are inadequate data to permit creation of consensus-based standards to define exact time intervals for surveillance visits after each type of revascularization procedure. In the absence of evidence-based standards, the clinical timeframe has customarily been based on the judgment of the vascular specialist, by evaluating the specific level and type of revascularization procedure and taking into account specific patient characteristics (Tables 12, 13, and 14).
Recommendations have been made that follow-up of autogenous vein bypass grafts be performed with duplex ultrasonography at intervals of 1, 3, 6, 12, 18, and 24 months after surgery and then yearly thereafter (16). Prompt evaluation with invasive techniques (angiography) is then indicated when noninvasive methods suggest hemodynamically significant lesions (e.g., greater than 50% stenosis) (25,26). Some patients with failing lower extremity grafts due to stenosis documented by duplex ultrasound may proceed to have operative repair without angiography. The benefit of surveillance with duplex ultrasound is less well established for prosthetic grafts.
Postprocedure surveillance after percutaneous or endovascular procedures is less well studied, and standards are less well established. Regular visits, with assessment of interval change in symptoms, vascular examination, and ABI measurement, is considered the standard of care. Postexercise ABI determinations may be useful in some individuals. These modalities are clearly useful for patients in whom there is evidence of recurrent narrowing at the interventional site. Similarly, distal or small-caliber endovascular sites (with or without stenting) at high risk of restenosis may merit more careful noninvasive evaluation. Whereas the role of surveillance duplex imaging of autogenous and prosthetic grafts has been evaluated (see full-text guidelines), the utility and role of duplex ultrasound and other noninvasive diagnostic modalities (magnetic resonance angiography [MRA] and computed tomographic angiography [CTA]) for such routine surveillance of endovascular sites have yet to be determined.
There is no uniformly accepted threshold for repeat angiography and intervention in the patient with evidence of recurrent stenosis. Patients who have recurrent symptoms in association with evidence of hemodynamic compromise require restudy and repeat intervention. Likewise, evidence of rapidly progressive restenosis, even in the absence of symptoms, should provide a clue that may identify individuals who might benefit from future invasive management. For grafts as well as native vessels, a stenosis of less than 50% appears to be associated with favorable prognosis and patency, whereas a stenosis greater than 70% is a harbinger of poor long-term patency, and thus, reintervention may be warranted (27,28).
E. Diagnostic Methods.
Patients with vascular disorders can usually be assured that an accurate anatomic diagnosis will be established with modern noninvasive vascular diagnostic techniques (e.g., ankle- and toe-brachial indices, segmental pressure measurements, pulse volume recordings, duplex ultrasound imaging, Doppler waveform analysis, and exercise testing). These tests will usually provide adequate information for creation of a therapeutic plan. When required, these physiological and anatomic data can be supplemented by use of MRA or CTA and selective use of invasive aortic and lower extremity angiographic techniques. Table 15 summarizes the evidence base that defines the benefits and limitations of each of these vascular diagnostic techniques. Table 16 summarizes typical use of noninvasive tests based on clinical presentation. For a detailed discussion of each of these techniques, see the full text of the guidelines.
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Table 16. Typical Noninvasive Vascular Laboratory Tests for Lower Extremity PAD Patients by Clinical Presentation
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1. Ankle-Brachial and Toe-Brachial Indices, Segmental Pressure Examination
RECOMMENDATIONS
Class I
- 1 The resting ABI should be used to establish the lower extremity PAD diagnosis in patients with suspected lower extremity PAD, defined as individuals with exertional leg symptoms, with nonhealing wounds, who are 70 years and older or who are 50 years and older with a history of smoking or diabetes. (Level of Evidence: C)
- 2 The ABI should be measured in both legs in all new patients with PAD of any severity to confirm the diagnosis of lower extremity PAD and establish a baseline. (Level of Evidence: B)
- 3 The toe-brachial index should be used to establish the lower extremity PAD diagnosis in patients in whom lower extremity PAD is clinically suspected but in whom the ABI test is not reliable due to noncompressible vessels (usually patients with long-standing diabetes or advanced age). (Level of Evidence: B)
- 4 Leg segmental pressure measurements are useful to establish the lower extremity PAD diagnosis when anatomic localization of lower extremity PAD is required to create a therapeutic plan. (Level of Evidence: B)
2. Pulse Volume Recording
RECOMMENDATION
Class IIa
- 1 Pulse volume recordings are reasonable to establish the initial lower extremity PAD diagnosis, assess localization and severity, and follow the status of lower extremity revascularization procedures. (Level of Evidence: B)
3. Continuous-Wave Doppler Ultrasound
RECOMMENDATION
Class I
- 1 Continuous-wave Doppler ultrasound blood flow measurements are useful to provide an accurate assessment of lower extremity PAD location and severity, to follow lower extremity PAD progression, and to provide quantitative follow-up after revascularization procedures. (Level of Evidence: B)
4. Treadmill Exercise Testing With and Without ABI Assessments and 6-Minute Walk Test
RECOMMENDATIONS
Class I
- 1 Exercise treadmill tests are recommended to provide the most objective evidence of the magnitude of the functional limitation of claudication and to measure the response to therapy. (Level of Evidence: B)
- 2 A standardized exercise protocol (either fixed or graded) with a motorized treadmill should be used to ensure reproducibility of measurements of pain-free walking distance and maximal walking distance. (Level of Evidence: B)
- 3 Exercise treadmill tests with measurement of pre-exercise and postexercise ABI values are recommended to provide diagnostic data useful in differentiating arterial claudication from nonarterial claudication ("pseudoclaudication"). (Level of Evidence: B)
- 4 Exercise treadmill tests should be performed in individuals with claudication who are to undergo exercise training (lower extremity PAD rehabilitation) so as to determine functional capacity, assess nonvascular exercise limitations, and demonstrate the safety of exercise. (Level of Evidence: B)
Class IIb
- 1 A 6-minute walk test may be reasonable to provide an objective assessment of the functional limitation of claudication and response to therapy in elderly individuals or others not amenable to treadmill testing. (Level of Evidence: B)
5. Duplex Ultrasound
RECOMMENDATIONS
Class I
- 1 Duplex ultrasound of the extremities is useful to diagnose anatomic location and degree of stenosis of PAD. (Level of Evidence: A)
- 2 Duplex ultrasound is recommended for routine surveillance after femoral-popliteal or femoral-tibial-pedal bypass with a venous conduit. Minimum surveillance intervals are approximately 3, 6, and 12 months, and then yearly after graft placement. (Level of Evidence: A)
Class IIa
- 1 Duplex ultrasound of the extremities can be useful to select patients as candidates for endovascular intervention. (Level of Evidence: B)
- 2 Duplex ultrasound can be useful to select patients as candidates for surgical bypass and to select the sites of surgical anastomosis. (Level of Evidence: B)
Class IIb
- 1 The use of duplex ultrasound is not well established to assess long-term patency of percutaneous transluminal angioplasty. (Level of Evidence: B)
- 2 Duplex ultrasound may be considered for routine surveillance after femoral-popliteal bypass with a synthetic conduit. (Level of Evidence: B)
6. Computed Tomographic Angiography
RECOMMENDATIONS
Class IIb
- 1 Computed tomographic angiography of the extremities may be considered to diagnose anatomic location and presence of significant stenosis in patients with lower extremity PAD. (Level of Evidence: B)
- 2 Computed tomographic angiography of the extremities may be considered as a substitute for MRA for those patients with contraindications to MRA. (Level of Evidence: B)
7. Magnetic Resonance Angiography
RECOMMENDATIONS
Class I
- 1 Magnetic resonance angiography of the extremities is useful to diagnose anatomic location and degree of stenosis of PAD. (Level of Evidence: A)
- 2 Magnetic resonance angiography of the extremities should be performed with gadolinium enhancement. (Level of Evidence: B)
- 3 Magnetic resonance angiography of the extremities is useful in selecting patients with lower extremity PAD as candidates for endovascular intervention. (Level of Evidence: A)
Class IIb
- 1 Magnetic resonance angiography of the extremities may be considered to select patients with lower extremity PAD as candidates for surgical bypass and to select the sites of surgical anastomosis. (Level of Evidence: B)
- 2 Magnetic resonance angiography of the extremities may be considered for postrevascularization (endovascular and surgical bypass) surveillance in patients with lower extremity PAD. (Level of Evidence: B)
8. Contrast Angiography
RECOMMENDATIONS
Class I
- 1 Contrast angiography provides detailed information about arterial anatomy and is recommended for evaluation of patients with lower extremity PAD when revascularization is contemplated. (Level of Evidence: B)
- 2 A history of contrast reaction should be documented before the performance of contrast angiography and appropriate pretreatment administered before contrast is given. (Level of Evidence: B)
- 3 Decisions regarding the potential utility of invasive therapeutic interventions (percutaneous or surgical) in patients with lower extremity PAD should be made with a complete anatomic assessment of the affected arterial territory, including imaging of the occlusive lesion, as well as arterial inflow and outflow with angiography or a combination of angiography and noninvasive vascular techniques. (Level of Evidence: B)
- 4 Digital subtraction angiography is recommended for contrast angiographic studies because this technique allows for enhanced imaging capabilities compared with conventional unsubtracted contrast angiography. (Level of Evidence: A)
- 5 Before performance of contrast angiography, a full history and complete vascular examination should be performed to optimize decisions regarding the access site, as well as to minimize contrast dose and catheter manipulation. (Level of Evidence: C)
- 6 Selective or superselective catheter placement during lower extremity angiography is indicated because this can enhance imaging, reduce contrast dose, and improve sensitivity and specificity of the procedure. (Level of Evidence: C)
- 7 The diagnostic lower extremity arteriogram should image the iliac, femoral, and tibial bifurcations in profile without vessel overlap. (Level of Evidence: B)
- 8 When conducting a diagnostic lower extremity arteriogram in which the significance of an obstructive lesion is ambiguous, transstenotic pressure gradients and supplementary angulated views should be obtained. (Level of Evidence: B)
- 9 Patients with baseline renal insufficiency should receive hydration before undergoing contrast angiography. (Level of Evidence: B)
- 10 Follow-up clinical evaluation, including a physical examination and measurement of renal function, is recommended within 2 weeks after contrast angiography to detect the presence of delayed adverse effects such as atheroembolism, deterioration in renal function, or access site injury (e.g., pseudoaneurysm or arteriovenous fistula). (Level of Evidence: C)
Class IIa
- 1 Noninvasive imaging modalities, including MRA, CTA, and color flow duplex imaging, may be used in advance of invasive imaging to develop an individualized diagnostic strategic plan, including assistance in selection of access sites, identification of significant lesions, and determination of the need for invasive evaluation. (Level of Evidence: B)
- 2 Treatment with n-acetylcysteine in advance of contrast angiography is suggested for patients with baseline renal insufficiency (creatinine greater than 2.0 mg per dl). (Level of Evidence: B)
F. Treatment.
1. Cardiovascular Risk Reduction
A. Lipid-lowering drugs
RECOMMENDATIONS
Class I
- 1 Treatment with a hydroxymethyl glutaryl coenzyme-A reductase inhibitor (statin) medication is indicated for all patients with PAD to achieve a target low-density lipoprotein (LDL) cholesterol level of less than 100 mg per dl. (Level of Evidence: B)
Class IIa
- 1 Treatment with a hydroxymethyl glutaryl coenzyme-A reductase inhibitor (statin) medication to achieve a target LDL cholesterol level of less than 70 mg per dl is reasonable for patients with lower extremity PAD at very high risk of ischemic events. (Level of Evidence: B)
- 2 Treatment with a fibric acid derivative can be useful for patients with PAD and low high-density lipoprotein (HDL) cholesterol, normal LDL cholesterol, and elevated triglycerides. (Level of Evidence: C)
It is recommended that patients with PAD and LDL cholesterol of 100 mg per dl or greater be treated with a statin, but when risk is very high, an LDL cholesterol goal of less than 70 mg per dl is a therapeutic option (29,30). Among the factors that define very high risk in individuals with established PAD are (a) multiple major risk factors (especially diabetes), (b) severe and poorly controlled risk factors (especially continued cigarette smoking), (c) multiple risk factors of the metabolic syndrome (especially high triglycerides; i.e., greater than or equal to 200 mg per dl plus non-HDL cholesterol greater than or equal to 130 mg per dl with low HDL cholesterol [less than or equal to 40 mg per dl]), and (d) individuals with acute coronary syndromes. The efficacy of this treatment with fibric acid derivatives in patients with PAD is not known. In patients with coronary artery disease and low HDL cholesterol levels, one study found that gemfibrozil reduced the risk of nonfatal myocardial infarction or cardiovascular death by 22% (31).
B. Antihypertensive drugs
RECOMMENDATIONS
Class I
- 1 Antihypertensive therapy should be administered to hypertensive patients with lower extremity PAD to achieve a goal of less than 140 mm Hg systolic over 90 mm Hg diastolic (nondiabetics) or less than 130 mm Hg systolic over 80 mm Hg diastolic (diabetics and individuals with chronic renal disease) to reduce the risk of MI, stroke, congestive heart failure, and cardiovascular death. (Level of Evidence: A)
- 2 Beta-adrenergic blocking drugs are effective antihypertensive agents and are not contraindicated in patients with PAD. (Level of Evidence: A)
Class IIa
- 1 The use of ACE inhibitors is reasonable for symptomatic patients with lower extremity PAD to reduce the risk of adverse cardiovascular events. (Level of Evidence: B)
Class IIb
- 1 Angiotensin-converting enzyme inhibitors may be considered for patients with asymptomatic lower extremity PAD to reduce the risk of adverse cardiovascular events. (Level of Evidence: C)
Treatment of high blood pressure is indicated to reduce the risk of cardiovascular events (32). Beta-blockers, which have been shown to reduce the risk of MI and death in patients with coronary atherosclerosis (33), do not adversely affect walking capacity (34). Angiotensin-converting enzyme inhibitors reduce the risk of death and nonfatal cardiovascular events in patients with coronary artery disease and left ventricular dysfunction (35,36). The Heart Outcomes Prevention Evaluation (HOPE) trial found that in patients with symptomatic PAD, ramipril reduced the risk of MI, stroke, or vascular death by approximately 25%, a level of efficacy comparable to that achieved in the entire study population (37). There is currently no evidence base for the efficacy of ACE inhibitors in patients with asymptomatic PAD, and thus, the use of ACE-inhibitor medications to lower cardiovascular ischemic event rates in this population must be extrapolated from the data on symptomatic patients.
C. Diabetes therapies
RECOMMENDATIONS
Class I
- 1 Proper foot care, including use of appropriate footwear, chiropody/podiatric medicine, daily foot inspection, skin cleansing, and use of topical moisturizing creams should be encouraged, and skin lesions and ulcerations should be addressed urgently in all diabetic patients with lower extremity PAD. (Level of Evidence: B)
Class IIa
- 1 Treatment of diabetes in individuals with lower extremity PAD by administration of glucose control therapies to reduce the hemoglobin A1C to less than 7% can be effective to reduce microvascular complications and potentially improve cardiovascular outcomes. (Level of Evidence: C)
Aggressive treatment of diabetes is known to decrease the risk for microvascular events such as nephropathy and retinopathy (38,39). Patients with lower extremity PAD and diabetes should be treated to reduce their glycosylated hemoglobin to less than 7%, per the American Diabetes Association recommendation (40). Frequent foot inspection by patients and physicians will enable early identification of foot lesions and ulcerations and facilitate prompt referral for treatment (41).
D. Smoking cessation
RECOMMENDATION
Class I
- 1 Individuals with lower extremity PAD who smoke cigarettes or use other forms of tobacco should be advised by each of their clinicians to stop smoking and should be offered comprehensive smoking cessation interventions, including behavior modification therapy, nicotine replacement therapy, or bupropion. (Level of Evidence: B)
Physician advice coupled with frequent follow-up achieves 1-year smoking cessation rates of approximately 5% compared with only 0.1% in those attempting to quit smoking without a physician’s intervention (42). Pharmacological interventions such as nicotine replacement therapy and bupropion achieve 1-year smoking cessation rates of approximately 16% and 30%, respectively (43). Tobacco cessation interventions are particularly critical in individuals with thromboangiitis obliterans, because continued use is associated with a particularly adverse outcome (44).
E. Homocysteine-lowering drugs
RECOMMENDATION
Class IIb
- 1 The effectiveness of the therapeutic use of folic acid and B12 vitamin supplements in individuals with lower extremity PAD and homocysteine levels greater than 14 micromoles per liter is not well established. (Level of Evidence: C)
F. Antiplatelet and antithrombotic drugs
RECOMMENDATIONS
Class I
- 1 Antiplatelet therapy is indicated to reduce the risk of MI, stroke, or vascular death in individuals with atherosclerotic lower extremity PAD. (Level of Evidence: A)
- 2 Aspirin, in daily doses of 75 to 325 mg, is recommended as safe and effective antiplatelet therapy to reduce the risk of MI, stroke, or vascular death in individuals with atherosclerotic lower extremity PAD. (Level of Evidence: A)
- 3 Clopidogrel (75 mg per day) is recommended as an effective alternative antiplatelet therapy to aspirin to reduce the risk of MI, stroke, or vascular death in individuals with atherosclerotic lower extremity PAD. (Level of Evidence: B)
Class III
- 1 Oral anticoagulation therapy with warfarin is not indicated to reduce the risk of adverse cardiovascular ischemic events in individuals with atherosclerotic lower extremity PAD. (Level of Evidence: C)
In the Antithrombotic Trialists’ Collaboration (ATC) (45), patients treated with antiplatelet therapy had a 32% proportional reduction of cardiovascular events with 75 to 150 mg daily, 26% with 160 to 325 mg daily, and 19% with 500 to 1500 mg daily. There was a significantly smaller (13%) reduction in cardiovascular events in patients being treated with less than 75 mg of aspirin per day. In the CAPRIE trial (Clopidogrel Versus Aspirin in Patients at Risk of Ischemic Events), clopidogrel reduced the risk of MI, stroke, or vascular death by 23.8% compared with aspirin in patients with PAD (46). To date, there is no evidence to support the efficacy of combined aspirin and clopidogrel treatment versus a single antiplatelet agent in patients with lower extremity PAD. Information regarding the efficacy of oral anticoagulants (i.e., coumarin derivatives such as warfarin) in reducing adverse cardiovascular events in patients with atherosclerosis is derived primarily from studies of patients with coronary |
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I. Introduction
II. Lower extremity PAD