Lower Limb Peripheral Vascular Disease

Published on 06/06/2015 by admin

Filed under Physical Medicine and Rehabilitation

Last modified 06/06/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 3.2 (19 votes)

This article have been viewed 16912 times

Chapter 56 Lower Limb Peripheral Vascular Disease

Lower limb peripheral vascular disease includes arterial, venous, and lymphatic disorders (Box 56-1). Arterial disease in the lower limb can be caused by atherosclerosis, thrombosis, embolism, vasospasm, arterial dissection, or vasculitis. Venous disease in the lower limb includes venous stasis, deep venous thrombosis, thrombophlebitis, and venous insufficiency. Lymphatic disorders of the lower limb include primary and secondary lymphedema.

Physiatrists work alongside internists, surgeons, and other specialists in the care of patients with peripheral vascular disease. The physiatrist will encounter patients with vascular disorders on the inpatient rehabilitation ward, acute care ward, and in the outpatient clinic. The physiatrist’s goal in the care of these vascular patients is to improve function, increase quality of life, decrease pain, heal wounds, and decrease limb loss.

Arterial Disease of the Lower Limb

Atherosclerotic Peripheral Arterial Disease

Epidemiology and Risk Factors of Atherosclerotic Peripheral Arterial Disease

Atherosclerotic peripheral arterial disease (PAD) causes partial or complete obstruction of the arteries in the legs. It can be proximal or distal, focal or diffuse. PAD is part of a systemic disease process and is a major cause of morbidity and mortality worldwide. Physiatrists must be knowledgeable about PAD because it affects many of the patients who are commonly seen because of its correlation with other vascular disorders like stroke. PAD also fits well in the practice of physiatry because it affects physical function and quality of life.

PAD is common in the United States, affecting around 8 million Americans.25 Men present to physicians more frequently. When screening is performed on asymptomatic individuals, however, women appear to be affected as commonly as men. Blacks are more affected than other races.41 Smoking is the biggest risk factor for PAD. Smokers are at higher risk for PAD, and they develop it at an earlier age than nonsmokers.51 Diabetes is also a major risk factor for PAD. The risk of PAD increases 26% for every 1% increase in hemoglobin A1c.58 Other factors associated with PAD include hypertension, dyslipidemia, chronic renal insufficiency, elevated inflammatory biomarkers, and hyperhomocysteinemia (Box 56-2).

Clinical Presentation of Atherosclerotic Peripheral Arterial Disease

The various clinical presentations of PAD include asymptomatic, intermittent claudication (IC), critical limb ischemia (CLI), and acute limb ischemia, with the most common being asymptomatic (Box 56-3). Only around 10% of people with PAD report symptoms of IC. Around half of PAD patients report leg symptoms other than claudication. Forty percent of people with PAD report no leg symptoms at all.25


The majority of PAD patients do not have the classic symptoms of IC. The absence of symptoms does not suggest a benign course. Complete occlusion of a major leg artery was found in one third of patients with asymptomatic PAD in one study.9 The lack of symptoms is due to low physical activity level rather than mild disease. Functional impairment can be present despite the lack of symptoms.30 Functional decline has been shown to be related to ankle–brachial index (ABI) even in the absence of symptoms.29

Acute Limb Ischemia

Acute arterial occlusion of the lower limb can be caused by thrombosis, embolism, or dissection (Figure 56-2). This is a limb-threatening medical emergency. The incidence is around 140 new cases per million persons per year.41 Patients present with pain, poikilothermia, and pulselessness. They might also have the classic symptoms of pallor, paresthesia, and paralysis. Symptoms are usually present for only hours to days when the patient presents. If symptoms have been present for less than 2 weeks, it is considered to be acute limb ischemia. Acute limb ischemia requires emergent vascular surgery evaluation and treatment. Just as with myocardial infarction and stroke, reperfusion must occur as soon as possible to prevent irreversible tissue loss (muscle, nerve, or limb loss). Embolectomy and thrombolysis can be attempted in appropriate patients. Up to 30 percent of patients with acute limb ischemia will require amputation in the first month of presentation.41

Critical Limb Ischemia

CLI is chronic ischemia (Figure 56-3). CLI is ischemia of the limb for more than 2 weeks causing rest pain, ischemic ulcers, and gangrene. Because so many patients with PAD are asymptomatic, it is not uncommon for the initial presentation of PAD to be CLI. The incidence is around 500 new cases per million persons per year.41

CLI generally begins once the toe pressure falls to less than 30 to 50 mm Hg. Rest pain generally does not occur until the toe pressure falls below 30 mm Hg; however, higher perfusion pressures are needed to heal wounds than are needed to maintain intact skin. A patient with a toe pressure of 40 mm Hg and intact skin can be asymptomatic but then develop a nonhealing ischemic ulcer after minor trauma. Such a patient would meet the criteria for CLI despite having no history of rest pain or IC. All patients with CLI should be urgently referred for evaluation by a vascular surgeon to see whether they are a candidate for revascularization.

Evaluation of Atherosclerotic Peripheral Arterial Disease

History and Physical Examination

A low awareness of PAD is found in the general public and among physicians.14 This lack of awareness, and the fact that most PAD is asymptomatic, leads to underdiagnosis of PAD. Physicians must maintain a high level of suspicion when evaluating patients at risk. Making the diagnosis of PAD is important because it has prognostic significance for impairment of mobility and physical functioning, as well as morbidity and mortality.

When clinically evaluating a patient for PAD, the physician should specifically ask questions to determine whether there is a history of IC or rest pain. Patients frequently do not spontaneously offer this information without prompting. A functional history should be taken to include mobility, activities of daily living, and independent activities of daily living. The presence of risk factors for PAD must be noted.

On physical examination, lower limb pulses should be evaluated, including the dorsalis pedis, posterior tibial, popliteal, and femoral. The presence of pedal pulses has a 90% negative predictive value for the diagnosis of PAD.41 Absent or diminished pulses, however, do not always indicate the presence of PAD but should prompt further investigation. The legs and feet should be examined for changes of skin temperature, color, and evidence of poor vascular flow. Decreased arterial blood flow to the legs can cause muscle atrophy, thin shiny skin, and decreased hair growth. Nails are often thick and brittle. The foot can appear red or purple when in the dependent position (dependent rubor) and show pallor when elevated.

When evaluating patients with leg complaints, the physician needs to remember that many things can cause leg pain, such as spinal disease, arthritis, and other musculoskeletal conditions. The physician must also remember that claudication is reported in a minority of PAD patients and so cannot be relied on as the sole method of diagnosing PAD (otherwise, many cases will be missed). Some patients can have limited activity for other reasons, and therefore do not experience claudication. The absence of pedal pulses and the presence of leg pain cannot be used in isolation to accurately diagnose PAD.

Vascular Testing for Peripheral Arterial Disease

Ankle–Brachial Index

PAD is usually diagnosed with the ABI, which compares the brachial systolic pressure with the ankle systolic pressure (Figure 56-4). An ABI of 0.9 or less is 95% sensitive in detecting PAD compared with angiography. The ABI is inexpensive, simple, and noninvasive, making it an appealing screening test. An ABI should be obtained on all patients over the age of 70, patients aged 50 to 69 who have cardiovascular risk factors, or any patient with symptoms of PAD or an abnormal lower limb vascular exam.40 An ABI of 1.4 or greater is due to incompressible vessel walls at the ankle and is nondiagnostic. Patients with an elevated ABI will need additional testing such as toe pressures to evaluate for the presence of PAD. Patients with a normal ABI but a high suspicion for IC should have the ABI repeated after exercise (Figure 56-5). The ABI is related to prognosis and functional ability, and ABI can be repeated to follow disease progress.


FIGURE 56-4 Measurement of the ankle–brachial index.

(From Hiatt WR: Medical treatment of peripheral arterial disease and claudication, N Engl J Med 344:1608-1621, 2001.)


FIGURE 56-5 Evaluation of patients with suspected peripheral arterial disease: which patients should undergo screening with ankle–brachial index?

(From Hiatt WR: Medical treatment of peripheral arterial disease and claudication, N Engl J Med 344:1608-1621, 2001.)

Transcutaneous Partial Pressure of Oxygen

Measurement of transcutaneous partial pressure of oxygen (TcPO2) is a useful test to predict wound healing. It can also be used to select amputation level. TcPO2 less than 30 mm Hg is associated with poor wound healing.46 TcPO2 above 40 mm Hg suggests adequate skin perfusion for healing. Readings are taken with electrodes attached to the skin. One is placed on the chest as a control, and the other is placed on the area of interest. Readings require proper positioning and temperature and can take 30 minutes to obtain.

Magnetic Resonance Angiography

Magnetic resonance angiography (MRA) is safer than intraarterial angiography. MRA sensitivity and specificity are greater than 90% for evaluating PAD.23,38 For these reasons, MRA has become the preferred imaging technique at many institutions. Contraindications are the same as with magnetic resonance imaging (MRI) in regard to the magnetic field. Some patients are unable to tolerate the procedure because of claustrophobia. Some patients are unable to lie still for the prolonged amount of time required for testing, which can cause motion artifact. There might also be artifact from stents or other hardware in the area of interest. The patient’s renal function needs to be considered before testing because nephrogenic systemic fibrosis is associated with gadolinium administration in patients with impaired renal function.

Multidetector Computed Tomography Angiography

Like MRA, computed tomography angiography (CTA) has a sensitivity and specificity greater than 90% for evaluating PAD.32 CTA is faster than MRA, which makes it more tolerable for some patients. CTA has more risk than MRA but less risk than intraarterial angiography. The risk relates to the use of iodinated contrast and radiation exposure. There can be artifact on imaging from calcium in the vessel wall.

Management of Atherosclerotic Peripheral Arterial Disease

PAD is not only underdiagnosed but it also is undertreated even after being identified.3 When treating patients with PAD, the physician and patient must remember that PAD is part of a systemic vascular disorder. Peripheral, coronary, and cerebral artery diseases are all part of systemic atherosclerosis. Patients with PAD are more likely to have coronary artery disease and cerebral artery disease than patients without PAD. Physicians and patients, however, often do not recognize PAD as an important predictor of cardiovascular morbidity and mortality and do not treat it as aggressively as coronary artery disease or cerebral artery disease.

The goals of treatment are to reduce ischemic symptoms, increase walking ability, improve function, prevent and heal wounds, prevent limb loss, and reduce morbidity and mortality. This is best accomplished using a multidisciplinary approach that includes physiatrists, primary care physicians, vascular surgeons, and the patient. Management involves education, risk factor modification, pharmacotherapy, exercise, and vascular interventions (Figure 56-7).


FIGURE 56-7 Treatment of patients with proven peripheral arterial disease.

(From Hiatt WR: Medical treatment of peripheral arterial disease and claudication, N Engl J Med 344:1608-1621, 2001.)

Risk Factor Modification

Management of patients with PAD should always include risk factor modification. Risk factor modification includes smoking cessation, weight reduction, and control of hyperlipidemia, hypertension, and diabetes. Statins have been shown to reduce mortality, coronary events, and strokes in PAD patients.37 Patients with PAD who do not have coronary artery disease should have as a goal a low-density lipoprotein (LDL) cholesterol level of less than 100 mg/dL. Patients with PAD and coronary artery disease should have a goal LDL cholesterol level of less than 70 mg/dL.41 If patients do not already have a primary care physician, they should be referred to one for aggressive management of glucose, blood pressure, and cholesterol. Patients can also be referred to a nutritionist for diet education.

It should be made clear to patients that smoking cessation can reduce their risk of amputation and cardiovascular events even if it does not improve claudication symptoms. The patient must understand the connection between continued smoking and higher risk of amputation, as well as a higher risk of cardiovascular events.26 Patients should be referred to smoking cessation programs, and the use of nicotine replacements and bupropion should be considered. Patients should be advised to stop smoking at every visit. Varenicline was recently approved for smoking cessation.


Just as with ischemic pain, ischemic wounds are best treated with reperfusion of the limb (Figure 56-8). Wounds can be ischemic or neuroischemic and should be kept clean and free from necrotic debris. Sharp debridement of ischemic wounds must be done with caution because it can increase the area of ischemic necrosis. This is because the surrounding tissue might not have sufficient blood supply to repair itself after the trauma of debridement. Dry gangrene can be allowed to autoamputate as long as there is no evidence of infection and there is adequate perfusion to support healing of the underlying tissue. Appropriate orthoses and off-loading devices should be used to protect the foot from pressure and shear forces. Footwear should cover the foot to protect against trauma and have enough length, breadth, and depth to prevent pressure on the wound.

Dressings should be applied to keep the wound base clean and moist, but there is no good evidence supporting any one type of dressing over another (see Chapter 32). The wound should be monitored for infection and treated immediately if detected. The ischemic foot often has dependent rubor, which can be distinguished from cellulitis by reexamining the limb after a short period of elevation. Dependent rubor should fade with elevation and is not associated with induration or increased warmth. The erythema of cellulitis is often associated with induration, increased warmth, swelling, and does not fully resolve with elevation of the limb.

Patients with ischemic wounds should be evaluated for revascularization. TcPO2 is a useful test to predict wound healing. TcPO2 less than 30 mm Hg is associated with poor wound healing.46 If revascularization is not an option, amputation might be necessary. The physiatrist should be involved preoperatively in determining the level of amputation. The decision should be made based on tissue viability, function, and prosthetic options. Patients who undergo amputation of a limb should receive physical and occupational therapy for transfers, mobility, activities of daily living, and education. Prosthetic limbs should be prescribed for appropriate patients. See Chapter 13, Rehabilitation of People With Lower Limb Amputation, for a more detailed discussion.


Exercise can improve walking time and walking distance in PAD patients with or without claudication symptoms.28 Exercise increases pain-free walking distance in patients with a history of IC.68 All patients should begin an exercise program, except those unable to participate in a walking exercise program because of physical, cardiac, or pulmonary reasons. Patients are encouraged to walk until they experience near maximal leg symptoms. Patient then rest until symptoms subside, and then they walk again until they experience near maximal symptoms. The patient should continue this cycle for 30 to 60 minutes two or three times a week.55 Patients without claudication symptoms should be told to exercise at a moderately hard level. Supervised exercise programs have been more successful than home exercise programs. Despite a proven benefit, supervised programs are not readily available. This is likely the result of problems with reimbursement and low patient interest.


Patients with symptomatic PAD have a 25% 5-year mortality rate.11 An inverse correlation exists between ABI and odds of having a myocardial infarction, stroke, or cardiovascular death.31 The risk particularly escalates once the ABI has decreased to less than 0.50.5 Up to 60% of deaths in PAD patients are from coronary artery disease; up to 20% of deaths are from cerebral artery disease; and another 10% of deaths are from other cardiovascular causes.41 Patients with PAD are at high risk for cardiovascular events and death and should be treated accordingly, with aggressive risk factor modification, cholesterol-lowering medications, and antiplatelet therapy.15

Amputation is not a common outcome for most patients with PAD but is common in certain subsets. The Framingham study found that less than 2% of patients with PAD had amputation as an outcome.20 Patients who are more likely to progress to amputation are those who smoke, have diabetes, have an ABI less than 0.50, have CLI, or have acute limb ischemia. Less than 10% of patients with PAD will develop CLI.13 Patients with PAD and diabetes are more likely to develop CLI. Patients presenting with CLI are at high risk for amputation and death. At 1 year 25% are deceased and 30% of survivors have lost a limb. Those that received a below-knee amputation as the initial primary treatment have 10% perioperative mortality, 30% 2-year mortality, and a 30% risk for further amputation.41

PAD is a serious disease that should not be missed by physicians. Receiving the diagnosis of PAD has important prognostic implications for a patient and places the patient in a high-risk category that impacts the plan of care.

Thromboangiitis Obliterans (Buerger’s Disease)

Clinical Presentation, Evaluation, and Diagnosis of Thromboangiitis Obliterans

Patients typically present with claudication symptoms in the upper or lower limbs. If the patient continues to smoke, the disease will progress to rest pain and ischemic ulcers. Clinically the legs are more involved than the arms. Most patients with TAO, however, will have three or four limbs involved when assessed with angiography, even if they are symptomatic in only one limb.42 There have been case reports of disease in the vascular beds of the heart, lung, brain, kidney, and intestinal tract.17 Although some patients report arthralgias (which can appear long before the ischemic problems and typically resolve spontaneously), there is no erosive arthritis with TAO.

The physician should do a thorough history and physical examination when evaluating a patient suspected to have TAO. A tobacco history should be taken, including smoking and smokeless tobacco use. Pulses should be checked carefully in the upper and lower limbs. When evaluating a patient with leg-only symptoms, the physician can perform an Allen test to assess for asymptomatic involvement of the upper extremities (Figure 56-9). A positive test suggests small artery disease in the upper limbs but is not specific to TAO. Evidence of small artery disease in the lower and the upper limbs places TAO high on the list of differential diagnoses.


FIGURE 56-9 The Allen test.

(From Olin JW, Lie JT: Thromboangiitis obliterans (Buerger’s disease). In Cooke JP, Frohlich ED, editors: Current management of hypertensive and vascular diseases, St Louis, 1992, Mosby–Year Book.)

No diagnostic laboratory tests exist for TAO, but testing should be performed to rule out other diagnoses. Testing for autoimmune disorders and other forms of vasculitis should be performed and are negative in patients with TAO. Erythrocyte sedimentation rate and serum C-reactive protein are normal. Patients should be screened for diabetes, hyperlipidemia, and hypercoagulable disorders, which typically are not present in patients with TAO.42

An echocardiogram should be performed to rule out a cardiac source of emboli. An arteriogram of all four limbs should be obtained. The arteriogram should assess for the presence of atherosclerosis or source of emboli, both of which should not be present in TAO. Arteriogram findings in TAO include small- and medium-sized vessel involvement with corkscrew collaterals. These findings are suggestive of, but not specific to, TAO. They are also seen with other vasculitides or autoimmune disorders, which must be ruled out with laboratory investigation as previously mentioned.

No standard set of diagnostic TAO criteria has been validated, but several criteria have been proposed.33,42,43,59 Commonly accepted criteria are a history of tobacco use, age less than 45, distal limb ischemia, and exclusion of atherosclerosis and autoimmune and hypercoagulable disorders. For diagnostic criteria purposes, patients are considered to have limb ischemia if they have claudication, rest pain, ischemic wounds, or gangrene.

A biopsy should be performed if TAO is suspected, but the clinical picture is not typical. Pathologically the acute phase of TAO shows an occlusive thrombus that is inflammatory but which spares the vessel wall. The vessel wall is not spared in other vasculitides or in atherosclerosis.42

Management of Thromboangiitis Obliterans

Smoking cessation is key to disease management. It must be made clear to patients that to continue smoking means the disease will progress and the risk of amputation will be high (Figure 56-10). Almost all patients who quit smoking can avoid amputation. Patients must understand that they control the outcome of this disease by their choice to continue smoking or not. It has been reported that smokeless tobacco and nicotine replacement patches or gum can cause disease exacerbation and should therefore not be considered as safe alternatives to smoking.24


FIGURE 56-10 Patient with Buerger’s disease.

(From Stone JH: Vasculitis: a collection of pearls and myths, Rheumatic Dis Clin N Am 33:691-739, 2007.)

Revascularization is not usually a successful option for patients with TAO. Because the disease is distal and segmental, there are usually no target vessels for a bypass procedure. Trials for new treatments have been small and limited in the United States. Treatment options that have been or are being investigated either in the United States or abroad include pneumatic compression devices, prostaglandins, thrombolytics, omental transfer, electrical spinal cord stimulation, and angiogenesis. Angiogenesis has been attempted via growth factors by either direct intramuscular injection of the growth factors or gene transfer. Cell therapy has also been investigated using autologous bone marrow injection or stem cell injection. Fenestration of the tibia and intramedullary wire have also been studied.44 Although current research gives hope for the future, the mainstay of therapy continues to be smoking cessation, local wound care, and amputation when required.

Buy Membership for Physical Medicine and Rehabilitation Category to continue reading. Learn more here