CLAUDICATION, CRTICIAL LIMB AND ACUTE LIMB ISCHEMIAS

As previously mentioned symptoms may be classified in three major categories:

 Patients presenting with intermittent claudication,

 Patients presenting with CLI,

 Patients presenting with ALI.

This kind of classification is based solely on the severity of the symptoms and not on the degree of the disease extension. Accordingly, even if there is frequently a strict correlation between symptoms and disease extension, the opposite may also be frequently observed.

As example one should remember that, in case of an acute embolic occlusion of the common femoral artery bifurcation, in a previously disease free femoral arteries, the clinical picture may be extremely severe with a patient presenting with severe pain and an increased risk of limb necrosis.

Conversely patients presenting with chronic extensive arterial occlusion (e.g., Leriche

syndrome, long SFA occlusion) may have developed an extensive collateral circulation (via the lumbar arteries and inferior mesenteric artery in the Leriche syndrome; via the profunda femoral artery in case of SFA occlusion) and therefore present only with mild symptoms.

For these reasons, and especially because the degree of aggressiveness by proposing an arterial revascularization, will depend principally by the clinical status, more then by the disease extension, we have separated the next issues concerning the endovascular options of

revascularization according to principal disabiliting symptom: intermittent claudication, CLI and ALI.

44 3.1 CLAUDICATION

Claudication is defined as fatigue, discomfort, or pain that occurs in specific limb muscle groups during effort due to exercise-induced ischemia. Individuals with claudication have sufficient blood flow so that limb ischemic symptoms are absent at rest. With increased local muscular demand for

metabolic support during exercise, blood flow in individuals with lower extremity PAD and claudication is inadequate to meet this demand, and limb muscular fatigue and/or pain results.

Lower extremity ischemia is usually due to atherosclerotic lower extremity PAD and

occasionally other causes, including emboli, radiation arteritis, Buerger’s disease (thromboangiitis obliterans), other arteritides, coarctation, popliteal entrapment, cystic adventitial disease, FMD, and trauma may the cause of the disabiliting symptoms.

Table 2 summarizes the different pathology’s groups mimicking intermittent claudication:

Pain Localization Pain Characterist Pain at exercise, rest, body position

Arterial Claudication Buttock, thigh, calf, (foot)

Cramping, aching, fatigue

After some degree of exercise, quickly relieved at rest

Venous Claudication

The entire leg:

groin > thigh > calf

Thigh bursting pain

Increased at exercise, relieved by elevation of the leg

Immediate pain onset, remaining longer at rest. Pain may increase by standing and be

relieved according to the body position

Orthopedic disease:

After some degree of exercise but may be present also at rest. Relief by sitting or

changing position

Table 2 : Differential diagnosis of intermittent claudication [modified according to the TASC Guidelines (1, 2)]

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Vascular claudication due to lower extremity PAD is produced by exercise and is relieved with rest and is therefore traditionally referred to as “intermittent claudication,” or simply “claudication.” The pathophysiology of claudication is considerably more complex than can be accounted for by the supply–demand mismatch that results from stenotic disease itself (110). However, diagnosis and treatment can be guided by an understanding of the lower extremity PAD arterial anatomy.

The anatomic site of the arterial stenosis is often associated with specific leg symptoms.

Occlusive disease in the iliac arteries may produce hip, buttock, and thigh pain, as well as calf pain.

Occlusive disease in the femoral and popliteal arteries is usually associated with calf pain. Occlusive disease in the tibial arteries may produce calf pain or, more rarely, foot pain and numbness.

The pathophysiology of claudication is complex; it is not merely a response to limitations in blood flow but also includes a wide range of skeletal muscle (e.g., metabolic), neurological, and inflammatory effects (110).

The severity of the ischemia can be classified according to either the Fontaine or Rutherford categories. These categories are most commonly used in research settings but may also have value in improving the clarity of communication of lower extremity PAD severity within office practices and in referral from primary practitioner to vascular specialist (2).

Vascular claudication must be distinguished from other illnesses that cause exertional leg pain, which have been called “pseudoclaudication.” These other causes include severe venous obstructive disease, chronic compartment syndrome, lumbar disease and spinal stenosis, osteoarthritis, and inflammatory muscle diseases (2).

The clinical history in case of a suspected PAD should also include risk factors for

atherosclerotic disease, such as smoking, diabetes, hypertension, hyperlipidemia, and a family history of atherosclerotic disease. In addition to the historical factors that distinguish intermittent claudication from other causes of leg pain, the physical examination should document the presence of diminished pulses in the femoral, popliteal, posterior tibial, and dorsalis pedis arteries. Signs of systemic

atherosclerosis, as a clue to a vascular cause of claudication, include femoral bruits, which may be present owing to turbulence from focal stenosis (15). Bruits may also be present in the carotid arteries and renal arteries as a sign of systemic atherosclerosis.

Claudication is usually also associated with reduced ankle blood pressures in the affected leg, which causes a diminished ABI. Some patients may have normal ankle pressures at rest with

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abnormal low ankle systolic pressures (and thus low ABI values) detectable only after exercise.

Individuals with long-standing diabetes, patients with chronic renal failure, and the very elderly have densely calcified vessels that are poorly compressible and may have spuriously high ankle pressures and ABI values.

The ABI should be measured in all patients with claudication. For individuals who present with classic claudication and in whom the ABI is borderline or normal (0.91 to 1.30) or supranormal (greater than 1.30), alternative diagnostic strategies should be used, including the toe pressure, toe-brachial index, segmental pressure examination, or duplex ultrasound, to confirm the lower extremity PAD diagnosis. This strategy is necessary to distinguish claudication from pseudoclaudication, provides an estimate of the overall severity of occlusive disease in the extremity, and serves as a baseline to assess temporal changes due to disease progression or intervention.

The ABI correlates only weakly with treadmill-based walking ability for any individual patient. For example, some patients with a low ABI report minimal walking impairment, whereas some with a higher ABI report marked walking impairment (111). This is due at least in part to the wide range of comorbidities that can coexist with intermittent claudication in patients who have PAD (29). Systemic atherosclerotic disease, medical comorbidities, and back, hip, and knee symptoms may have a greater impact on an individual’s quality of life than claudication, such that lower extremity revascularization may not significantly improve quality of life (112).

Because the natural history of claudication is relatively benign (from the limb perspective), with few patients progressing to CLI or amputation (57), decisions regarding revascularization of individuals with claudication should be based on improving quality of life. Patients with a low ABI, a significant walking impairment, and no or mild comorbidities would be expected to benefit the most from any claudication intervention, including exercise, pharmacotherapy, or revascularization (111).

3.1.1 Exercise and Lower Extremity PAD Rehabilitation

A program of supervised exercise may be considered a primary efficacious treatment modality to alleviate claudication symptoms for all patients with intermittent claudication. Regular walking in a supervised claudication exercise program can be expected to result in an increase in the speed, distance, and duration walked, with decreased claudication symptoms at each workload or distance (113-116). These functional benefits accrue gradually and become evident over 4 to 8 weeks and increase progressively over 12 or more weeks.

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Such sustained increases in physical activity, if associated with improvements in cardiovascular risk factors, have the potential to reduce the risk of cardiovascular ischemic events, thereby potentially improving the poor prognosis for survival in this population (117, 118).

Because patients with claudication often have concomitant clinical or occult coronary artery disease, hypertension, and diabetes, adverse cardiovascular and physiological responses during exercise training are possible, and this risk should be evaluated clinically before initiation of the therapeutic program. However, there is no evidence that patients with claudication need to undergo stress imaging or invasive angiographic studies before initiating an exercise program.

A typical supervised exercise program requires the performance of treadmill or track-based exercise for 45 to 60 minutes performed 3 or more times a week for a minimum of 12 weeks. Such exercise is monitored by a physical therapist, nurse, or exercise physiologist. Treadmill exercise appears to be more effective than other exercise modalities, presumably because treadmill walking most closely reproduces walking in the community setting.

Patients are asked to continue to walk at this workload until they achieve claudication of moderate severity. This is followed by a brief period of rest to permit symptoms to resolve. The exercise-rest-exercise cycles repeated several times during the hour of supervision (113, 115, 116).

There are inadequate data to compare such distinct claudication interventions effectively. It is likely that supervised exercise training can serve as a beneficial adjunct to further augment the improvements in walking that can be gained by both endovascular procedures and surgical bypass (119).

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