The most characteristic symptom of PAD is claudication which is a pain in the lower extremity muscles brought on by walking and relieved with rest. Although claudication has traditionally been described as cramping pain, some patients report leg fatigue, weakness, pressure, or aching. Symptoms during walking occur in the muscle group one level distal to the artery narrowed or blocked by PAD. Patients with aortoiliac artery occlusive disease, therefore, have symptoms in the thigh and buttock muscles while patients with femoropopliteal PAD have symptoms in their calf muscles. The walking distance at which symptoms occur depends on multiple factors including disease severity, walking pace, terrain, and incline.

Surprisingly, many patients with PAD have few if any symptoms. The reason for this absence of symptoms usually falls into 1 of 2 broad categories. Some patients with mild or moderate PAD rarely sustain a walking pace that increases the blood flow requirement of the lower extremity muscles. By being physically inactive, these patients avoid the supply-demand mismatch that triggers claudication symptoms. Other patients with PAD have muscle discomfort when they walk but fail to report these symptoms because they attribute them to the natural consequences of aging.

Patients with severe PAD can develop ischemic rest pain. These patients do not walk enough to claudicate because of their severe disease. Instead, they complain of burning pain in the soles of their feet that is worse at night. They cannot sleep due to the pain and often dangle their lower leg over the side of the bed in an attempt to relieve their discomfort. The slight increase in blood flow due to gravity temporarily diminishes the otherwise intractable pain. In some cases, edema from keeping the leg in a dependent position may be mistakenly attributed to venous thrombosis.

Other features of PAD include erectile dysfunction, which is often an early indicator of the disease.

The physical exam may reveal the following:

• Loss of pulses
• Pain on palpation
• Pallor
• Muscle atrophy and loss of hair
• Cool and cyanotic skin
• Presence of bruit

Making the diagnosis of PAD should factor in the patient’s history, physical exam, and objective test results. Key points in the history include an accurate assessment of the patient’s walking ability. Many patients do not explicitly report the classic claudication symptoms of cramping calf pain after walking 2 blocks that resolves with rest. Some patients may walk very little because of other physical ailments or limitations. Other patients may not volunteer any information about walking unless specifically asked. Important aspects of the history also include cardiovascular risk factors such as smoking, hypertension, high cholesterol, and diabetes.[7][8][9]

On physical exam, patients with PAD may have diminished or absent lower extremity pulses. This finding can be confirmed with the ankle-brachial index (ABI), an objective, bedside measure of lower extremity arterial perfusion. As its name implies, the ABI compares the systolic blood pressure at the ankle to the systolic pressure in the arm. A manual blood pressure cuff should be placed just above the ankle while locating the posterior tibial artery or dorsalis pedis artery with a handheld Doppler probe. While listening to the Doppler signal, the blood pressure cuff is inflated until it obliterates the Doppler signal. As the cuff slowly deflates, the pressure at which the Doppler signal returns is recorded as the systolic ankle pressure. The same steps are repeated for the other pedal artery and the other leg. Likewise, the brachial pressure can be measured with a blood pressure cuff on the upper arm and a Doppler probe positioned over the radial or ulnar artery at the wrist. The ABI is the highest systolic pressure measured at each ankle divided by the higher of the two systolic brachial pressures. A normal ABI ranges from 0.9 to 1.3. PAD is defined as an ABI less than 0.9 and most patients with claudication have an ABI between 0.5 and 0.9. Patients with extremely low ABI’s (less than 0.5) usually have ischemic rest pain or tissue loss. An ABI greater than 1.3 indicates arterial wall stiffening which can occur in patients with diabetes or renal failure. If a cuff pressure of 250mmHg does not obliterate the Doppler signal, the ABI is classified as “non-compressible.” Patients with falsely elevated (greater than 1.3) or non-compressible ABI’s require alternative imaging or physiologic studies to confirm the diagnosis of PAD.[10]

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 upper extremity blood pressure discrepancy due to subclavian artery stenosis. Other measures to increase the accuracy of the ABI include having the patient rest supine for at least 5 minutes to allow their blood pressure to stabilize and choosing an appropriately sized blood pressure cuff. The bladder length of the cuff should be 80%, and the width of 40% of the circumference of the extremity.

Blood work may reveal altered renal function and abnormal electrolyte levels. Elevation in CRP, D-dimer and interleukin 6 have been associated with diminished exercise tolerance.

Doppler studies are done to determine the site of blood flow occlusion and flow velocities. In addition, CT angiography and MRA can help determine the sites of occlusion and assess if the patient is a candidate for angioplasty or bypass surgery.

In patients with ulcers, transcutaneous oximetry is a rapid method of assessing perfusion. Finally, an ECG may reveal the presence of an arrhythmia which may be the cause of an embolic event.

Management strategies for PAD attempt to achieve two distinct goals: lower cardiovascular risk and improve walking ability. All patients with PAD, regardless of the presence or absence of symptoms, have an increased risk of stroke, myocardial infarction, and thrombosis compared to patients without arterial disease. These cardiovascular events probably account for the shorter life expectancy of patients with PAD. Therefore, all patients diagnosed with PAD should undertake lifestyle changes aimed at lowering their cardiovascular risk profile. Key targets for lifestyle changes include quitting smoking, lowering cholesterol, and controlling hypertension and diabetes.[11][12][13]

Treatment options to improve walking ability vary depending on the patient’s symptoms and disease severity. Exercise therapy involves walking until reaching pain tolerance, stopping for a brief rest, and walking again as soon as the pain resolves. These walking sessions should last 30 to 45 minutes, 3 to 4 times per week for at least 12 weeks. Despite being more effective, supervised exercise programs for PAD are not usually covered by insurance companies. Pharmacotherapy for claudication involves the use of cilostazol, a medication that promotes vasodilation and suppresses the proliferation of vascular smooth muscle cells. Patients who respond to cilostazol usually notice a positive effect within 12 weeks. Since cilostazol is a phosphodiesterase type-3 inhibitor, a history of congestive heart failure precludes patients from receiving this type of therapy. Pentoxifylline, a medication that improves oxygen delivery by its rheolytic effect has been approved for the treatment of claudication. However, it has inconsistent results compared to placebo in walking distance studies. Balloon angioplasty or stent placement provides a minimally invasive, percutaneous treatment option for patients with PAD symptoms that do not respond to exercise or medical therapy. These endovascular treatments achieve the best results when applied to focal occlusive lesions in the iliac and superficial femoral arteries. The technical success and durability of endovascular therapy decrease in patients with long-segment total occlusions and infrapopliteal arterial occlusive disease. Since PAD does not usually represent life or limb-threatening condition, surgery should be reserved for highly selected patients who have significant symptoms despite treatment with non-invasive and endovascular therapy. Surgical options for PAD include bypass grafts to divert flow around the blockage or endarterectomy to segmentally remove the obstructive plaque.[14][15]

There is ample evidence supporting the use of statins to improve the atherosclerotic disease. However, the patient must change lifestyle and reduce the risk factors for atherosclerotic disease.

• Deep vein thrombosis
• Low back pain
• Superficial thrombophlebitis
• Raynaud phenomenon
• Thromboangiitis obliterans
• Sciatica

Even with treatment, the prognosis of PAD is generally guarded. If the patient does not change his/her lifestyle, the disease is progressive. In addition, most patients with PAD also have coexistence of cerebrovascular or coronary artery disease, which also increases the mortality rate. The outcomes in women tend to be worse than in men, chiefly because of the small diameter of the arteries. In addition, females are more likely to develop complications and embolic events.

• Ischemia/Gangrene
• Amputation
• Infection
• Ulceration
• Heart attack
• Stroke
• Blood clots
• Erectile Dysfunction

Once the diagnosis of PVD is made, lifelong follow up is required. The disorder has no cure and if the lifestyle is not modified, the condition progresses.

Vascular surgeon

Endocrinologist

Interventional radiologist

• Discontinue smoking
• Control of diabetes
• Maintain a healthy weight
• Begin exercise program
• Control of blood pressure and cholesterol levels 

PVD is a systemic disorder and for the most part progressive. The condition is associated with life and limb-threatening complications. Despite many advances in endovascular surgery, amputations of digits and limbs are not uncommon. Thus, the present-day approach is to prevent the disorder in the first place. There is ample evidence that changes in lifestyle can significantly decrease the rate of progression of the disease and improve the quality of life. Besides physicians, nurses and pharmacists have a vital role in preventing PVD. These two healthcare professionals should emphasize the importance of smoking cessation, maintaining a healthy weight and controlling blood sugars. The pharmacist should also ensure that the patient is not on any medications that can lead to vasoconstriction. The patient should be taught about basic foot hygiene and wear protective shoewear. The patient should be educated on signs of vascular disease and seek assistance if any changes occur. Finally, current guidelines indicate that PVD patients should be treated with a statin and either aspirin or cilostazol. An interprofessional approach to patient education and management will improve outcomes. [16][17][18] (Level V)

Outcomes

The outcomes of PVD depend on where the disease is located and gender. Overall, females appear to have worse outcomes compared to males, primarily because they have smaller vessels, which are more likely to become narrowed. When surgery is done in females for peripheral vascular disease, complications are also more frequent and serious. [19][20][21](level V)