Ann Guttendorf Peripheral arterial insufficiency is the condition that results when there is insufficient blood flow to the extremities. It is much more likely to occur in the lower extremities, although the use of catheter interventions has made the incidence of upper extremity problems more common. In the United States it is estimated that 8 to 10 million people have arterial occlusive disease, and the incidence is more prevalent in those 50 years of age and older.1 The incidence in this population is estimated to be 1 in every 20 individuals.1 When defining peripheral artery disease disease (PAD), if the symptoms have been present for weeks or months, the condition is defined as chronic. If the symptoms develop during hours or days, it is referred to as acute. Chronic arterial insufficiency is a disease that has increasing prevalence as the population ages. Because the major cause of PAD is atherosclerosis, the risk factors are the same as those for coronary artery disease. Diabetes, hypertension, hyperlipidemia, hyperhomocysteinemia, and tobacco use are all independent risk factors. Smokers are twice as likely to develop claudication.2 Vascular disease is one of the most common complications of diabetes. Genetic factors have also long been recognized as playing a role in the development of PAD, and an increased level of homocysteine has been shown to be associated with atherosclerosis.2 Even in younger patients, premature atherosclerosis is the most common cause of chronic arterial insufficiency, although rare causes also include entrapment syndromes and adventitial cystic disease of the popliteal artery. Numerous studies have confirmed that most patients with clinically obstructive arterial disease have underlying coronary artery disease or diabetes. These patients have a 40% increased risk of stroke and a 20% to 60% risk of myocardial infarction (MI), with a twofold to sixfold increase in the risk for cardiac death.2 In cases of severe obstructive disease and acute limb ischemia, the risk for amputation is determined by disease severity, sudden appearance of limb ischemia, and the timeliness and ability to restore limb circulation, not by the mere appearance of claudication.2 The occurrence of acute limb ischemia carries with it a 30-day amputation rate of 10% to 30% regardless of whether thrombolysis has been used.3 Chronic arterial insufficiency results from diverse systemic conditions that can affect the arteries in various parts of the circulatory system, even in the absence of clinical symptoms in more than one arterial system.2 The disease entities that result in arterial insufficiency include degenerative diseases (collagen abnormalities found in Marfan or Ehlers-Danlos syndrome), dysplastic disorders (e.g., fibromuscular dysplasia), and vascular inflammatory processes (e.g., arteritis). Arterial insufficiency can also be a result of thrombosis, thrombotic embolism, radiation-induced arteritis, autoimmune conditions, and, the most common cause, arteriosclerosis.2 In patients without atherosclerosis, the pathophysiology of chronic arterial insufficiency involves loss of structural integrity of the artery wall. This loss of structural integrity produces arterial dilation and favors aneurysm formation with its associated risk of rupture or occlusion as a result of aneurysmal dissection.2 This loss of structural integrity can affect arteries in the carotid, renal, and iliac circulation most commonly, but is not restricted to those circulatory beds.2 In patients with underlying arteriosclerosis, the atherosclerotic plaque causing leg ischemia is identical to that seen in coronary artery disease and carotid disease. The plaque is an intimal lesion that may affect any of these vessels. The blockage may build up slowly, allowing collateral vessels to develop and thereby minimizing symptom progression until such time as the flow is inadequate to support the metabolic needs. Alternatively, intraplaque hemorrhage and thrombosis may lead to sudden expansion and acute symptoms.2 The infrarenal aorta and iliac arteries are classified as the inflow arteries, whereas the femoral, popliteal, and tibial vessels are classified as the outflow vessels. Obstruction of the aortoiliac and femoral arteries is often seen in smokers, whereas disease in the smaller vessels such as that seen in tibial artery disease is much more common in patients with diabetes. There is evidence that the presence of reduced ankle-brachial index (ABI) and diabetes are associated with the development of rest pain and ulcerations from inadequate perfusion. Certain groups of patients are at risk for PAD. This includes patients who are older than 65 years (21% had asymptomatic or symptomatic PAD in one study),2a patients who are older than 50 with a history of diabetes or smoking, and patients younger than 50 who have diabetes and another risk factor for atherosclerosis (e.g., smoking, dyslipidemia, hypertension, hyperhomocysteinemia). It also includes patients with exertional leg symptoms suggestive of claudication or with ischemic rest pain, patients with abnormalities of lower extremity pulses, and patients with known atherosclerotic coronary, carotid, or renal artery disease. All of these patients should undergo a comprehensive vascular review of symptoms (Box 125-1).2 It is imperative to recognize that each patient with PAD is unique; the reported discomfort associated with PAD includes “tiredness,” “giving way,” “soreness,” or “pain.”4 Although the classic or “textbook” symptom of peripheral arterial insufficiency is claudication, patients report two or more symptoms in two or more locations.4 Primary care providers must take a careful history of each symptom, including the impact of each symptom on work, activities of daily living, and recreational activities; the symptoms should be interpreted in the context of patient comorbidities and the presence of previously discussed PAD risk factors.3 When present, claudication is a tightening or cramping pain that is precipitated by exercise and is relieved by rest. These symptoms most frequently occur in the calf muscles but also can occur in the thighs or buttocks depending on the location of the stenosis. Claudication occurs with exercise because of an increased demand for blood that cannot be met by the stenotic vessels. Subsequently, lactic acid and other metabolites build up in the muscle, causing discomfort. Claudication is assessed by how far a patient can walk before pain ensues. Although the distance may be reduced by an incline, cold weather, or a recent meal, it tends to be fairly consistent. Pain is always relieved immediately by stopping the activity and never occurs when the patient is at rest. The thigh or buttock muscles are sometimes affected first. This is indicative of iliac artery obstruction (Leriche syndrome). As the obstruction becomes more severe, the patient may develop pain at rest because circulation to the feet is impaired. Characteristically, the patient will go to bed and be awakened after a couple of hours by pain in the toes that is relieved only by gravity to enhance peripheral blood flow (e.g., getting out of bed or hanging the feet over the side of the bed). The patient may resort to sleeping in a chair to avoid the pain. Ischemic rest pain tends to be consistent; it occurs every night, unlike the intermittent leg cramps seen so often in older adults, which are not related to arterial insufficiency. For effective, collaborative care of the patient with suspected vascular insufficiency, there must be a standard set of measurements. The American College of Cardiology (ACC) and American Heart Association (AHA) guidelines recommend components of the vascular physical examination supplemented by vascular testing (see the section on diagnostics, later). Components of the vascular physical examination include measurement of blood pressure; palpation for pulse, quality, and amplitude; abdominal aortic pulsation assessment; auscultation for bruits; estimation of pulse intensity; and full foot examination and lower extremity skin assessment (Box 125-2).2 On physical examination, inspection of the limbs may reveal muscle wasting and loss of hair. With more severe disease, there is not enough blood to sustain viability, and tissue loss ensues, usually beginning in the toes or heels. Tissue loss may manifest as ulceration, dry gangrene, or wet gangrene. Reduced temperature in an affected limb may be noted. Careful pulse examination is important. Absent femoral pulses suggest inflow disease, whereas the absence of popliteal pulses implies isolated tibial disease. One physical sign that can be helpful in the diagnosis of peripheral vascular disease is dependent rubor. If the ischemic leg is elevated for 30 seconds, it becomes pale because blood is unable to travel uphill. This renders the tissue ischemic, and the capillaries vasodilate. If the leg is then made dependent, blood travels down to those dilated capillaries, and a deep red color ensues. The longer the rubor takes to develop, the worse the ischemia. A careful history and physical examination will allow a good assessment of the functional severity of the obstruction and the likely location. The severity of the patient’s peripheral arterial insufficiency can be graded based on the vascular history and physical examination findings. Fontaine’s stages or Rutherford’s categories are the most widely used tools to provide a standardized system of classifying the severity of peripheral disease, based on symptoms, gangrene, or ulcerations.3 The distances that define mild, moderate, and severe claudication is part of the Fontaine classification and is based on a distance of 200 meters (650 feet). It is not specified in the Rutherford classification of symptoms. In addition, there is a separate Rutherford scale for acute limb ischemia.5,6 Any patient with intermittent claudication, leg pain at rest, or nonhealing wounds in the lower extremity that persist for 4 weeks or more warrants an evaluation for PAD. There is a role for noninvasive testing to supplement the history and physical examination depending on the clinical scenario and the urgency of the patient’s condition. The level of testing should be limited initially to those studies that confirm the presence of arterial disease and those that will alter the course of treatment. The main reason for physiologic testing is to verify a vascular origin for the patient’s complaints and to localize the level of the lesion. In addition, it can be used to assess the adequacy of tissue perfusion and wound healing potential. Lower extremity PAD is diagnosed by the resting ABI in patients with one or more of the following: exertional leg symptoms, nonhealing lower extremity wounds, history consistent with PAD in patients 65 years and older, or symptoms in patients 50 years and older with a smoking history or diabetes.3 The most useful tools in assessing peripheral arterial insufficiency in the office are a portable Doppler instrument and a sphygmomanometer cuff. With these tools, it is possible to compare the systolic pressure at the brachial artery with that in the dorsalis pedis and posterior tibial arteries. This measurement is expressed as the ABI and should be lower in the affected extremity than in the normal one. An ABI of 0.9 or less is indicative of PAD. An ABI of 0.75 to 0.5 is consistent with claudication, and an ABI below 0.5 is consistent with rest pain and/or tissue loss. An ABI of higher than 1.4 is also considered abnormal and can indicate the potential for noncompressible calcified vessels. Along with low ABI, high ABI is also associated with higher cardiovascular risk.3,7–9 Patients with mild claudication may have palpable pulses at rest but lose them with exercise. This is best demonstrated in the vascular laboratory with an exercise noninvasive study. During this test, the patient is placed on a treadmill and ABIs are measured at rest, while exercising, and on recovery. Related medical conditions, such as obesity and peripheral edema, sometimes make it impossible to assess the pulse status. In these situations, the pocket Doppler instrument may be invaluable. A normal pulse is triphasic but becomes increasingly monophasic with proximal obstruction. With practice, it is relatively simple to distinguish these pulses. If Doppler ultrasonography reveals good triphasic pulses in the feet, there is not likely to be significant ischemia in that extremity. A variety of tests are now available to accurately assess vascular status. Patients should be referred to the vascular laboratory for formal evaluation if there is concern for arterial insufficiency or to ascertain the location and severity of occlusive lesions. Once arterial disease is confirmed, the level of the disease and the extent of the severity can be further assessed with segmental limb pressures. This testing is also done with specialized equipment in the vascular lab and can be performed on both the upper and lower extremities. Vascular laboratory evaluation will provide the ABIs, the level at which the pulse becomes monophasic, the pulse volume recording (a plethysmographic test that records the volume of the pulse in the extremity with each heartbeat) and other important measurements (see Diagnostics box). The forefoot tracing is helpful for the vascular surgeon to determine whether there is enough circulation to heal a foot lesion. This is particularly important in patients with diabetes, in whom ABIs are often inaccurate.10 Other tests are available but are used less often except in research protocols. Chief among these is the measurement of transcutaneous oxygen (TcPO2), which reflects the metabolic state of the target tissues. Unfortunately, variants such as ambient temperature make this test impractical as a routine part of the evaluation. The level at which TcPO2 indicates tissue healing remains controversial and will vary in the setting of diabetes and tissue edema It also can be affected by skin temperature and emotional state.11 An analysis from pooled data from the women in the Nurses’ Health Study (1990 to 2010) and from men enrolled in the Health Professionals Follow-Up Study (1994 to 2008) found that elevated levels of β-macroglobulin are associated with increased risk for symptomatic PAD and are indicative of the presence of atherosclerosis promoting kidney disease.12 Instead of a treadmill test, it is possible to use reactive hyperemia as a marker of disease severity. This is obtained after inflation of a pressure cuff to a suprasystolic pressure to produce vasodilation; however, this is somewhat uncomfortable and is not currently used routinely. The presence of peripheral neuropathy in diabetes makes the diagnosis of peripheral insufficiency difficult. Damage to the peripheral nerves may mask the symptoms of arterial insufficiency. Thus, if patients have no feeling in their legs, they may simply complain that their legs get tired of walking. Without sensation, there may be no rest pain, and patients may be initially seen with nonhealing ulcers and possibly painless gangrene. Other conditions that should be considered include cauda equina syndrome, Buerger disease, leg cramps, and musculoskeletal disorders. Spinal stenosis causing pressure on the nerve roots may result in symptoms of claudication from the hip downward, which can easily be confused with Leriche syndrome. This is becoming increasingly common as the population ages and progressive degenerative joint disease becomes more prevalent. Patients with spinal stenosis will often not have relief until they sit down, and usually they have to wait longer for relief than patients who have claudication. The correct diagnosis can be made by ordering noninvasive exercise studies. In cauda equina syndrome, there will be no pressure drop when the patient exercises on a treadmill. Magnetic resonance imaging of the lumbar spine will reveal the arthritic changes. Buerger disease is an inflammatory occlusive disease involving primarily the medium and smaller arteries of both the upper and lower extremities. Although it is less common in the United States, it is seen more often in the Middle East and Asia and appears to be directly related to the effects of smoking. Patients manifest the signs and symptoms of chronic arterial insufficiency but apart from smoking have no other risk factors for atherosclerosis. Bypass surgery is rarely indicated because disease is more distal, but patients will experience remission if exposure to nicotine is avoided. It is important not to forget about the upper extremities in evaluating patients with known or suspected arterial disease. Patients with compromised flow to the upper extremities can have typical ischemic pain of one or more muscle groups but also may have atypical pain or no symptoms at all. The presentation may be only a difference in the systolic blood pressure between one arm and the other. In other cases, patients may report dizziness during arm exertion that can be indicative of disease in the subclavian artery. Subclavian steal syndrome implies the presence of significant symptoms caused by arterial insufficiency in the brain (vertebrobasilar insufficiency) or the upper extremity, which is also supplied by the affected subclavian artery.13 A review of symptoms and upper extremity vascular examination need to be performed in all patients at risk for or with documented PAD. Further testing would be determined based on examination findings and on patient symptoms. This may include duplex ultrasound, transcranial Doppler studies, magnetic resonance angiography, or computed tomography (CT) angiography.14–16 Management of chronic arterial insufficiency depends on the severity of the symptoms. If the patient has stable claudication and is managing without much difficulty, it is reasonable to treat the patient conservatively. Patients with mild, recent-onset claudication are likely to improve with conservative measures alone. These include lifestyle modifications as indicated, particularly tobacco cessation. Hypertension, hyperlipidemia, and diabetes must be treated aggressively to reduce long-term risk. Compression stockings may be used in selected PAD patients to treat leg swelling and reduce deep venous thrombosis (DVT) risk, providing the ABI is 0.8 or higher and the use of the compression stockings does not compromise circulation to the extremity or increase claudication symptoms.17 Studies comparing exercise with angioplasty have shown that a daily exercise program involving walking to the point of pain as often as possible is as effective as angioplasty in providing relief of symptoms.18 Components of a structured exercise program to relieve claudication include (1) an initial session of treadmill or track walking of 30 minutes, with an increase of subsequent sessions to reach 1 hour per session, three times a week; (2) in each session, walking at a speed and grade that produce moderate claudication pain within 3 to 5 minutes; (3) resting until claudication resolves; and (4) repeating the exercise and rest cycles until the session duration is achieved.3 Because the ABI does not change, it is believed that this beneficial effect is produced by training the muscles rather than by increasing flow to the foot. These patients are at high risk for coronary artery disease, so it is prudent to start them on a daily aspirin dose as well. The literature on the role of aspirin, dipyridamole, and ticlopidine in peripheral vascular disease is extensive and confusing.3,19 There is much disagreement as to whether aspirin confers benefit either preoperatively or postoperatively in patients with peripheral vascular disease. There is agreement, however, that low-dose aspirin (325 mg/day) reduces the incidence and mortality of subsequent MI in patients older than 50 years. There has never been a study demonstrating a benefit of adding dipyridamole to that regimen. Ticlopidine, another antiplatelet agent, is at least as effective as aspirin, but it is expensive and has significant side effects. Clopidogrel can be used as an alternative to aspirin or in combination with aspirin (reserved for high-risk patients not at risk for bleeding).3 Any antiplatelet regimen needs to be based on an individual patient’s clinical characteristics (risk of PAD, risk of bleeding) and tolerance for the medications in conjunction with cost and future guidance from regulatory bodies.3 It has been shown that statin therapy helps stabilize plaque and lowers the low-density lipoprotein (LDL) level, and studies have suggested that bypasses are more durable if the patient is taking a statin.20,21 Pentoxifylline (Trental) has been shown to increase the distance that 30% of patients with claudication can walk, although the effect has been small. Trials of cilostazol (Pletal), a phosphodiesterase type 3 inhibitor, have demonstrated significant improvement over both placebo and pentoxifylline in distance walked without symptoms for patients with claudication.21 The main contraindication for using cilostazol is a history of congestive heart failure. Lower extremity ulcers may result from neuropathy, arterial insufficiency, infection, or a combination of these. Infection such as cellulitis, or ulcers with extensive involvement may result in osteomyelitis. The presence of infection can also disturb blood glucose control, complicating diabetes management. Peripheral neuropathy is associated with the development of calcification of the arteries. This is not directly related to the atherosclerotic lesion, which is an intimal lesion, but it does render the vessels relatively incompressible. This means that the ABI may be artificially elevated and less helpful in assessing the degree of ischemia. In these cases, the pulse volume recording can be particularly helpful. Thirty percent of patients with neuropathy also have an autonomic neuropathy, which is sometimes called an autosympathectomy. This condition results in diversion of blood from the nutrient vessels to the skin, making the skin unnaturally warm. Thus it is possible to see a diabetic patient with a minor skin lesion but with no symptoms and a warm foot that is critically ischemic. Failure to recognize this may result in further loss of tissue. Diabetic neuropathy is a polyneuropathy and has a motor component. The paralysis of the intrinsic muscles results in clawing of the foot, and the patient tends to develop traumatic lesions over the metatarsal heads and on the tops of the toes. Healing may be impaired by relative arterial insufficiency. Any infection requires treatment with appropriate debridement and antibiotics. Bed rest is indicated to minimize damage that may go undetected if neuropathy is present. If the ulcer is superficial, it can be treated on an outpatient basis, with non–weight bearing, dressing care, and a first-generation cephalosporin. If the ulcer is deep or has significant cellulitis, hospitalization is advised, and broad-spectrum antibiotics are instituted. Failure to heal with treatment suggests arterial insufficiency and merits referral to a vascular surgeon or vascular medicine specialist for possible arteriography.
Peripheral Arterial and Venous Insufficiency
Peripheral Arterial Insufficiency
Immediate physician or vascular surgeon referral is indicated for suspected arterial occlusion or dissecting aneurysm.
Chronic Arterial Insufficiency
Definition and Epidemiology
Pathophysiology
Clinical Presentation
Physical Examination
Diagnostics
Differential Diagnosis
Diabetic Peripheral Neuropathy
Cauda Equina Syndrome
Buerger Disease
Upper Extremity Arterial Disease
Management
Complications of Peripheral Arterial Disease
Diabetic Foot Ulcer
Infection
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Peripheral Arterial and Venous Insufficiency
Chapter 125
