Continuing Education Activity

Peripheral arterial disease (PAD) represents a progressive manifestation of systemic atherosclerosis, affecting more than 200 million individuals worldwide and primarily occurring in older adults and those with diabetes, smoking history, or chronic kidney disease. PAD develops from arterial narrowing and occlusion, most often in the aortoiliac, femoropopliteal, or infrapopliteal vessels, resulting in impaired blood flow to the lower extremities. This course reviews the clinical presentation of PAD, which ranges from asymptomatic disease to intermittent claudication and chronic limb-threatening ischemia (CLTI), the latter carrying a high risk of limb loss and mortality. 

This course explores the pathophysiology, underlying etiologies, and clinical presentation of PAD across its clinical spectrum, in addition to identifying at-risk patients, distinguishing vascular from nonvascular leg pain, and applying guideline-directed therapy. Participants will also gain an in-depth understanding of the evaluation of PAD, which involves a detailed clinical assessment, physiologic testing such as the ankle-brachial index, and imaging, as well as its management, integrating risk factor modification, supervised exercise therapy, pharmacologic therapy, and, when necessary, revascularization or surgery. This activity for healthcare professionals is designed to enhance the learner's competence in identifying PAD, performing the recommended evaluation, optimizing risk-factor control, and implementing an appropriate interprofessional approach to managing this condition, ultimately improving outcomes, preventing complications, and reducing adverse cardiovascular and limb events.

Objectives:

• Identify clinical factors that increase the risk of developing peripheral arterial disease.
• Apply the ankle-brachial index (ABI) test interpretation to guide management of peripheral arterial disease. 
• Differentiate patients with peripheral arterial disease that has progressed to chronic limb-threatening ischemia requiring operative intervention from those for whom conservative management is appropriate.
• Implement effective collaboration among interprofessional team members to improve outcomes and treatment efficacy for patients with peripheral arterial disease.

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Introduction

Peripheral arterial disease (PAD) is a common manifestation of systemic atherosclerosis that affects over 200 million people worldwide, particularly older adults and those with diabetes, smoking history, or chronic kidney disease. This condition results from progressive arterial narrowing, most often in the aortoiliac, femoropopliteal, and infrapopliteal segments, leading to reduced or impaired blood flow to the lower extremities.[1][2]

PAD presents along a spectrum, from asymptomatic disease to intermittent claudication and chronic limb-threatening ischemia (CLTI). While many patients remain stable, a subset progresses to CLTI, which carries high risks of limb loss and mortality if not promptly treated. Interprofessional management enhances outcomes by preventing complications and addressing systemic cardiovascular risk factors.

Etiology

PAD is caused by atherosclerosis, a chronic, progressive disease of the arteries characterized by the accumulation of lipid-rich plaque within the arterial walls. This leads to narrowing (stenosis) or complete blockage (occlusion) of the peripheral arteries, most commonly in the lower extremities (see Image. High Grade Stenosis). Less common causes are related to inflammation of the blood vessels (vasculitis), injury, or radiation exposure.[3]

Risk factors for PAD include:

• Smoking (the strongest modifiable risk factor)
• Diabetes
• Age (≥ 65 years)
• Hypertension
• Hyperlipidemia (especially elevated LDL)
• Chronic kidney disease
• Obesity
• Sedentary lifestyle
• Family history of PAD, heart disease, or stroke

Epidemiology

PAD affects over 200 million adults worldwide, with an incidence as high as 20% in individuals older than 70. Although historically thought to be more prevalent in men, the prevalence of PAD is nearly equal among men and women older than 40. Smoking is a major modifiable risk factor, increasing the risk of PAD 4-fold and significantly contributing to disease severity. Compared to nonsmokers, individuals with PAD who smoke have reduced life expectancy and are more likely to progress to chronic limb-threatening ischemia and require amputation. Further research is needed to clarify the impact of race and ethnicity on the prevalence and outcomes associated with PAD.[4]

Pathophysiology

The pathophysiology of PAD primarily involves atherosclerosis, a progressive disease characterized by the accumulation of lipids and inflammatory cells in the walls of arteries, most commonly in the lower extremities. Recent research has investigated the role of complex immune-inflammatory pathways and microvascular dysfunction in PAD, details of which are beyond the scope of this article.[5]

In patients with PAD, atherosclerotic plaque builds up over time on the inside of arteries. In the early stages of PAD, the arteries compensate for the plaque buildup by dilating to preserve flow through the vessel (positive remodeling). Eventually, the artery cannot dilate any further, and the atherosclerotic plaque starts to narrow the arterial flow lumen. As the narrowing progresses, blood flow shifts to smaller arteries that parallel the diseased artery. Although this collateral flow preserves distal perfusion, the network of smaller vessels never carries as much blood flow as the main artery. This blood flow restriction leads to the hallmark symptom of PAD called “intermittent claudication.”

Intermittent claudication is characterized by muscle pain or cramping that occurs during physical activity (eg, walking) and is relieved with rest. This typically occurs in the calves, thighs, or buttocks and is related to the level of atherosclerosis. The muscles of the lower extremity require increased blood flow during ambulation to meet the increased energy demand. When walking or exercising, patients with PAD reach a point at which collateral blood flow is maximized and cannot provide any additional perfusion to the lower extremity muscles. This supply-demand mismatch causes temporary muscle ischemia, which manifests as pain or cramping. Lowering the energy demands of the muscle (by slowing down or resting) allows the blood supply to “catch up,” and the ischemic symptoms resolve.

In advanced cases, atherosclerotic narrowing becomes so severe that the blood flow cannot meet the resting metabolic demands of the lower extremity. This results in ischemic rest pain, which is pain in the forefoot or toes when the legs are elevated or the patient is lying flat. In this position, gravity no longer aids perfusion, further reducing blood flow to distal tissues and precipitating pain. Rest pain is alleviated by placing the foot in a dependent position (dangling the foot or standing), which improves perfusion. At this stage, patients may also develop nonhealing wounds or ulcers representing tissue loss due to critically reduced blood flow to the skin and subcutaneous tissue. These wounds are most commonly located on the toes or foot, and can present as wet or dry gangrene. The presence of rest pain or tissue loss signifies chronic limb-threatening ischemia (CLTI), the most severe form of PAD. 

Patients with underlying PAD can present with acute limb ischemia due to in-situ thrombosis from plaque rupture or from an embolus. Embolic events are often cardiac in origin, particularly in patients with atrial fibrillation, and tend to lodge in areas of arterial bifurcation or branching, where flow is turbulent. In the lower extremities, the most common site of embolic occlusion is the common femoral artery bifurcation.

History and Physical

Clinical History

The hallmark symptom of PAD is intermittent claudication–cramping pain in the lower extremities that occurs with walking or exertion and resolves with rest. Pain typically occurs in the muscles distal to the site of arterial narrowing. Patients with aortoiliac disease often experience pain in the buttocks or thighs, while those with femoropopliteal disease most commonly report calf pain. The distance walked or level of exertion required to provoke symptoms is clinically significant, as a progressive reduction in pain-free walking distance may indicate a worsening of the disease. Evaluation can be complicated by comorbid conditions, eg, osteoarthritis, deconditioning, or cardiac disease. These conditions can also impair mobility or cause discomfort in the lower extremities. Careful history-taking is essential to distinguish claudication from nonvascular causes of leg pain, including joint pain, neuropathy, or generalized fatigue. 

Asking patients about the presence of ischemic rest pain, which typically manifests as pain in the toes, dorsum of the foot, or ankle, is essential. This pain usually resolves when the limb is placed in a dependent position, eg, dangling the leg off the side of the bed or standing, which improves perfusion through gravity. A thorough history should also include any chronic lower extremity wounds, as these may indicate CLTI. Wounds from arterial insufficiency usually develop on the toes or distal forefoot, where perfusion is most compromised. 

Some patients with mild or moderate PAD may remain asymptomatic due to the development of collateral circulation that compensates for reduced arterial flow. Additional clinical features of PAD can include erectile dysfunction, which may serve as an early manifestation of systemic atherosclerosis. Furthermore, a comprehensive history should include assessment of diabetes, hyperlipidemia, atrial fibrillation, prior deep vein thrombosis or pulmonary embolism, history of stroke or transient ischemic attack, inherited or acquired clotting disorders, and a detailed smoking history. Inquiring about any previous vascular interventions or surgeries, as well as the patient’s medication history, with particular attention to the use of anticoagulants or antiplatelet agents, is also vital. 

Physical Examination

The physical exam may reveal the following:

• Loss of palpable pulses or Doppler signals
• Distal paresthesias or numbness
• Slow capillary refill
• Mottling of the skin
• Cool or cyanotic skin
• Pallor
• Pain with palpation
• Muscle atrophy and loss of hair
• Chronic foot or lower extremity wounds
• Wounds with wet or dry gangrene 
• Black or necrotic toes

Peripheral Arterial Disease Clinical Classification 

Several classification systems have been established to help stratify PAD and guide management decisions (see Tables 1 and 2).

Table

Table 1. Fontaine Stages of Peripheral Arterial Disease.

Table

Table 2. Rutherford Categories.

Morphological stratification

The TASC (Trans-Atlantic Inter-Society Consensus) morphological consensus is used to guide the choice between endovascular and surgical revascularization in the management of patients with PAD (see Tables 3 and 4).[6]

Table

Table 3. Morphological Stratification of Iliac Lesions.

Table

Table 4. Morphological Stratification of Femoropopliteal Lesions.

Evaluation

The evaluation of a patient with PAD focuses on confirming the diagnosis, localizing the disease, and assessing its severity, achieved through a combination of noninvasive tests, physiologic measurements, and imaging studies. 

Ankle-Brachial Index

The ankle-brachial index (ABI) is the primary noninvasive bedside tool for diagnosing and classifying the severity of PAD. To measure the ABI, a manual blood pressure cuff is placed just above the ankle, and either the posterior tibial or dorsalis pedis artery is located using a handheld Doppler probe. The cuff is inflated while auscultating with the Doppler until the arterial signal disappears, indicating complete occlusion of flow. The cuff is then slowly deflated, and the pressure at which the Doppler signal reappears is recorded as the systolic ankle pressure. This process is repeated for the other pedal artery and on the contralateral leg.

Brachial systolic pressure is obtained in a similar fashion, using a blood pressure cuff on the upper arm and a Doppler probe over the radial or ulnar artery at the wrist. The ABI is calculated by dividing the highest ankle systolic pressure by the higher of the 2 brachial systolic pressures. A common mistake when taking an ABI involves failure to measure the brachial pressure in both arms. Using the higher brachial pressure as the denominator for both ankle pressures ensures that the ABI will not be underestimated in patients with a discrepancy between upper extremity blood pressures due to subclavian artery stenosis.

A normal ABI ranges from 0.90 to 1.40. PAD is defined as an ABI of 0.90 or less. Patients with ABI 0.70 to 0.90 are categorized as mild PAD and typically are asymptomatic or present with intermittent claudication. Those with ABI 0.50 to 0.70 have moderate PAD and typically present with more frequent claudication and reduced walking distance. An ABI of less than 0.50 indicates severe PAD or CLTI and often presents with ischemic rest pain, nonhealing wounds, or tissue loss. Values greater than 1.40 may indicate noncompressible, calcified arteries, often seen in patients with diabetes or chronic kidney disease. In such cases, the ABI value is unreliable, and alternative testing, eg, the toe-brachial index (TBI) or duplex ultrasound, is required to evaluate for PAD. The TBI, which is less affected by arterial calcification, provides a more accurate assessment; a TBI of less than 0.70 suggests the presence of PAD. If the resting ABI is normal but symptoms persist, an exercise ABI can be performed to unmask exertional ischemia, defined as a 20% or greater drop in postexercise ABI.[7][8]

Diagnostic Imaging 

Once PAD is suspected or confirmed, anatomic imaging helps characterize the extent of the disease and plan for possible intervention. Duplex ultrasonography is typically the first-line imaging modality due to its accessibility, safety, and ability to visualize blood flow and quantify stenosis noninvasively. Duplex ultrasonography combines B-mode imaging, which visualizes arterial wall morphology and the presence of stenosis or occlusion, with Doppler analysis to assess blood flow velocities. A key parameter is the peak systolic velocity (PSV). A PSV ratio (the velocity at the site of stenosis divided by the velocity in a proximal normal segment) greater than 2.0 is consistent with a 50% or more stenosis, while a ratio of greater than 4.0 typically indicates a stenosis of 75% or more. 

Another valuable aspect of duplex ultrasonography is the assessment of waveform morphology, with a triphasic waveform typically observed in normal peripheral arteries. This pattern reflects normal arterial compliance and peripheral resistance. A triphasic waveform consists of a sharp systolic upstroke with a high peak systolic velocity, representing strong forward flow during systole, followed by a brief reversal of flow in early diastole due to elastic recoil of the arterial wall. Finally, a small forward flow component occurs during late diastole. This triphasic pattern suggests unobstructed blood flow and normal vessel wall elasticity.

In contrast, a biphasic waveform may be seen with early atherosclerotic changes, while a monophasic waveform—characterized by a broad systolic peak and continuous forward flow without reversal—indicates hemodynamically significant stenosis. Dampened waveforms can be seen distal to high-grade stenoses. Duplex ultrasonography is especially valuable for surveillance following revascularization. Though operator-dependent, when performed by experienced technologists, duplex ultrasonography is highly sensitive and specific for detecting and grading PAD.[9]

For more detailed evaluation, particularly in patients being considered for revascularization, computed tomography angiography (CTA) and, sometimes, magnetic resonance angiography (MRA) are used. CTA offers high-resolution vascular imaging, which is especially useful for detecting calcified lesions, but requires the use of iodinated contrast and exposes the patient to radiation. MRA, which employs gadolinium contrast, eliminates the need for radiation.

Digital subtraction angiography (DSA) remains the gold standard for vascular imaging. DSA is typically reserved for patients in whom endovascular therapy is anticipated, as it allows for both diagnosis and immediate intervention. Overall, starting with physiologic tests like ABI and TBI, followed by selective imaging with duplex ultrasonography, CTA, MRA, or DSA, enables clinicians to objectively evaluate PAD, localize disease, and guide evidence-based management.

Treatment / Management

The treatment and management of PAD focus on alleviating symptoms, preventing disease progression, and reducing major adverse limb events like amputation, cardiovascular morbidity, and mortality.

Lifestyle Modifications

First-line therapy consists of lifestyle modifications, with smoking cessation recognized as the most critical modifiable risk factor. Supervised exercise therapy has demonstrated significant improvements in pain-free walking distance and overall functional capacity in patients with intermittent claudication. Effective programs typically involve walking to the point of moderate claudication, resting until symptoms subside, and then resuming walking. Sessions last 30 to 45 minutes, 3 to 4 times per week, for a minimum of 12 weeks. Despite its proven efficacy, access to supervised exercise therapy is often limited by a lack of insurance coverage. In addition, nutritional counseling and adherence to a heart-healthy diet are essential components of PAD management, targeting atherosclerotic risk reduction and promoting overall cardiovascular health.[10][11][12]

Pharmacologic Management

Pharmacologic therapy is also used in the management of PAD. Antiplatelet agents, eg, aspirin or clopidogrel, are recommended to lower the risk of myocardial infarction, stroke, and vascular death. Statin therapy is indicated for all patients with PAD, regardless of LDL level, with a goal of achieving LDL-C of less than 70 mg/dL to reduce cardiovascular events. Blood pressure control using angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) has been associated with improved outcomes. Tight glycemic control is also important for diabetic patients to minimize microvascular and macrovascular complications.

For symptom relief, cilostazol, a phosphodiesterase III inhibitor, may be prescribed in patients without heart failure. Cilostazol enhances walking distance and reduces claudication symptoms by promoting arterial vasodilation and inhibiting the proliferation of vascular smooth muscle cells and platelet aggregation. Clinical benefits are typically observed within 8 to 12 weeks of therapy.[13]

Invasive Therapies

Surgical decision-making is highly individualized, taking into account anatomic considerations, comorbid conditions, functional status, life expectancy, and patient preferences. The overarching goal of surgical intervention is to restore perfusion, relieve symptoms, facilitate wound healing, and ultimately preserve limb function and quality of life.[14][15]

Endovascular procedures

Patients with lifestyle-limiting claudication refractory to medical therapy, or those presenting with CLTI, may require revascularization. Endovascular procedures, eg, percutaneous transluminal angioplasty and stenting, are preferred for focal lesions, especially in the iliac and superficial femoral arteries. The technical success and durability of endovascular therapy decrease in patients with long-segment total occlusions (TASC C and D lesions) and infrapopliteal arterial occlusive disease. 

Surgical interventions

Surgical treatment options for PAD are primarily considered for patients with lifestyle-limiting claudication that is refractory to medical and exercise therapy or for those presenting with CLTI. One of the most common surgical interventions is bypass surgery, which reroutes blood flow around a blocked artery using either an autologous vein graft (typically the great saphenous vein) or a synthetic conduit. This approach is favored in patients with long-segment disease, failed endovascular therapy, or anatomy not amenable to percutaneous intervention.

Another option is endarterectomy, which involves the surgical removal of atherosclerotic plaque from within the artery. This procedure is most commonly performed on the common femoral artery, where stenting is less desirable due to high mechanical stress (see Image. Peripheral Arterial Disease Following Arterectomy). In cases where revascularization is not possible or has failed, amputation may be necessary. This can range from minor amputations, eg, toe or transmetatarsal procedures, to major limb loss, including below-knee or above-knee amputations. Additionally, hybrid procedures, which combine open surgical and endovascular techniques, may be used for patients with complex, multilevel disease.[14][15]

Differential Diagnosis

Differential diagnoses that should also be considered when evaluating suspected PAD include:

• Neuropathic pain
• Musculoskeletal pain
• Deep vein thrombosis
• Chronic venous disease
• Superficial thrombophlebitis
• Raynaud phenomenon
• Thromboangiitis obliterans
• Sciatica

Prognosis

The prognosis of someone with PAD is related to the severity of the disease, presence of symptoms, comorbidities, and adherence to treatment. PAD is a chronic condition that typically progresses and needs to be followed over time. Patients with PAD have an increased risk of heart attack, stroke, and cardiovascular death. In patients with claudication, only about 1% to 3% per year progress to critical limb ischemia. In patients with chronic limb-threatening ischemia, the risk of amputation is about 25% to 40% at 1 year. Early diagnosis, modification of risk factors, and appropriate intervention are key to improving long-term prognosis.

Complications

Complications of PAD include:

• Ischemia and gangrene
• Infection
• Osteomyelitis
• Acute limb ischemia
• Compartment syndrome
• Amputation
• Erectile dysfunction

Postoperative and Rehabilitation Care

Postoperative rehabilitation and care following vascular interventions or surgery are critical to optimizing outcomes, promoting limb function, and preventing complications or disease recurrence. Early mobilization is encouraged to reduce the risk of deep vein thrombosis, pulmonary complications, and deconditioning. Wound care must be closely monitored, particularly in patients with groin incisions, with a focus on maintaining clean and dry incisions. Antiplatelet therapy is continued to maintain graft or stent patency, and statin therapy is reinforced to reduce cardiovascular risk.

In bypass patients, graft surveillance, which includes clinical examination and noninvasive imaging, is typically initiated within the first month and continued at regular intervals to detect early graft stenosis or failure. Smoking cessation, ongoing exercise therapy, and management of comorbidities, eg, hypertension, diabetes, and hyperlipidemia, remain essential components of long-term care. For patients recovering from major amputations, prosthetic planning and physical therapy are crucial to maximize mobility and independence. An interprofessional approach involving vascular surgery, primary care, physical therapy, and, in some cases, wound care or infectious disease specialists ensures comprehensive postoperative care and improves long-term outcomes.

Consultations

Interprofessional collaboration optimizes the management of PAD. The following clinicians may be consulted:

• Vascular surgery
• Vascular medicine
• Cardiology
• Podiatry
• Endocrinology
• Infectious disease
• Interventional radiology
• Wound care specialist

Deterrence and Patient Education

Prevention of Peripheral Artery Disease

Smoking cessation remains strongly advised, as it represents the most effective modifiable risk factor for peripheral arterial disease. Glycemic control plays a crucial role in managing diabetes, reducing both microvascular and macrovascular complications. Blood pressure and lipid management through the use of antihypertensives and statins lowers overall cardiovascular risk. Regular physical activity, particularly structured walking programs, enhances limb perfusion and delays symptom progression. Weight management, combined with a heart-healthy diet, further supports vascular health and reduces the burden of comorbid conditions.

Patient Education

Patient education focuses on understanding the chronic nature of PAD and the necessity of long-term management. Clinicians should emphasize symptom recognition, including claudication, ischemic rest pain, and changes in wound healing. Medication adherence, particularly with antiplatelet agents and statins, needs to be reinforced to minimize adverse cardiovascular and limb events. Patients should be encouraged to participate in supervised exercise therapy whenever available. Additional guidance on foot care and wound monitoring, particularly for diabetic individuals, helps prevent ulcer formation, infection, and progression to chronic limb-threatening ischemia.

Enhancing Healthcare Team Outcomes

Managing PAD requires a coordinated, interprofessional healthcare team to deliver patient-centered care, improve outcomes, ensure safety, and enhance team performance. Physicians, advanced practitioners, nurses, pharmacists, dietitians, physical therapists, and wound care specialists all play critical roles in this collaborative approach. Each contributes to risk factor modification, timely intervention, and long-term disease management. For example, early identification of critical limb-threatening ischemia and prompt coordination of care can prevent limb loss and reduce morbidity.

Effective interprofessional communication is essential. Physicians and advanced practitioners guide diagnostic evaluation and procedural decisions, while nurses oversee perioperative and bedside care, and allied health professionals implement exercise, dietary, and wound care regimens. Physical therapists help patients improve mobility and function after vascular interventions. Pharmacists ensure the safe and effective use of antiplatelet agents, statins, and symptom-relieving medications like cilostazol. Regular communication among team members, through structured handoffs, care planning meetings, or case discussions, ensures timely adjustments to therapy and promotes consistent messaging to patients.

Ethical principles, eg, informed consent, patient autonomy, and equitable care, guide all treatment decisions. Shared decision-making ensures that interventions align with patient goals and values. Education and training across disciplines promote best practices and continued professional development. A patient-centered approach, built on collaboration, accountability, and respect, ensures comprehensive PAD care that improves functional outcomes, reduces complications, and preserves quality of life.

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Disclosure: Michael Zemaitis declares no relevant financial relationships with ineligible companies.

Disclosure: Julia Boll declares no relevant financial relationships with ineligible companies.

Disclosure: Morgan Kato declares no relevant financial relationships with ineligible companies.

Disclosure: Maheswara Satya Golla declares no relevant financial relationships with ineligible companies.