What Are The Distal Extremities
Marie Ota
Peripheral arterial disease (PAD) is a circulatory problem causing a reduced blood flow through the arteries. This typically reduces blood flow to the extremities manifesting as thigh or calf pain during walking or exertion. This activity describes the evaluation and management of peripheral arterial disease and reviews the role of the interprofessional team in improving care for patients with this condition.
Objectives:
- Outline the risk factors for developing peripheral arterial disease.Explain the role of atherosclerosis in the pathophysiology of peripheral arterial disease.Identify the use of the ankle-brachial index (ABI) in the evaluation of peripheral arterial disease.Review the importance of improving care coordination among the interprofessional team members to advocate for lifestyle changes to improve outcomes and prevent the progression of peripheral arterial disease.
Making the diagnosis of PAD even in asymptomatic patients still, has a significant clinical impact because PAD acts as a marker for systemic atherosclerosis. Patients with PAD have an equivalent cardiovascular risk to patients with previous myocardial infarction and require aggressive risk factor modification to improve their long-term survival. The management of PAD varies depending on the disease severity and symptom status. Treatment options for PAD include lifestyle changes, cardiovascular risk factor reduction, pharmacotherapy, endovascular intervention, and surgery.[1][2][3]
PAD affects over 200 million adults worldwide and the incidence of PAD increases to as high as 20% in people over the age of 70. Although PAD has traditionally been perceived as a disease affecting men, the prevalence of PAD appears to be equal among senior men and women. Under-diagnosis of PAD in the primary care setting may be a significant issue, as most patients with PAD do not present with stereotypical claudication symptoms described in textbooks. Smoking increases the risk of developing PAD fourfold and has the greatest impact on disease severity. Compared to non-smokers, smokers with PAD have shorter life spans and progress more frequently to critical limb ischemia and amputation. Additional risk factors for PAD include diabetes, hyperlipidemia, hypertension, race, and ethnicity.[5]
PAD usually involves atherosclerotic disease in the abdominal aorta, iliac, and femoral arteries. The pathophysiology of atherosclerosis involves complex interactions between cholesterol and vascular cells the details of which are beyond the scope of this article. Atherosclerotic plaque builds up slowly 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. Eventually, the artery cannot dilate any further, and the atherosclerotic plaque starts to narrow the arterial flow lumen.
In some cases, the cause of sudden ischemia may be emboli either of cardiac origin or from atherosclerotic disease of the aorta. Emboli tend to be most common at sites of arterial bifurcation or where vessel branches have an abrupt takeoff. The femoral artery is the most common site for emboli, followed by the iliac arteries, aorta and the popliteal arteries.
Patients with PAD usually have enough collateral blood flow that they only have symptoms during activities that increase energy demand such as walking. Rarely, the PAD becomes progressively more severe, and the blood flow cannot meet the resting metabolic demands of the lower extremity. Poor perfusion to the nerves can result in ischemic rest pain which is often described as an intractable, burning pain in the soles of the feet. Non-healing wounds and ischemic ulcers represent tissue loss due to poor blood flow. In the most severe cases, the toes or entire forefoot can become black and mummified as gangrene develops. [6]
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.
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.
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.
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]
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.
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)
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)
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Methods: Clinical features and laboratory findings were recorded for all 245 residents of Olmsted County, Minnesota who developed PMR over a 22-year period (1970-1991). Those who exhibited > or = 1 episode of diffuse distal extremity edema with pitting were selected for this study, and were evaluated further.
Results: Thirteen women and 6 men in this incidence cohort of PMR had > or = 1 episode of distal extremity swelling with pitting edema. Giant cell arteritis was also identified in 5 patients. In 11 patients, the swelling and edema development concurrently with proximal PMR symptoms. In 2 patients, the distal swelling was the initial manifestation, and in 6 patients, the distal symptoms developed during relapses or recurrences of PMR. Both upper and lower extremities were affected, usually in a symmetric manner. Other peripheral manifestations were also common. The distal swelling and pitting edema responded promptly to corticosteroids, and slowly or incompletely to nonsteroidal anti-inflammatory drugs; a similar response was observed in the proximal symptoms. The distal swelling appeared to represent tenosynovitis and synovitis of regional structures.
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