Abstract
Peripheral arterial disease (PAD) is atherosclerosis of the abdominal aorta and lower extremity arteries. Diabetes mellitus (DM) increases the risk of PAD and development of diabetic peripheral neuropathy. Persons with DM and PAD are at significant risk for development of non-healing skin ulcers, potentially leading to limb amputation. Risk factor modification, prophylactic foot education, and preventative care are key to reducing the risk of limb loss.
Definition
The incidence of lower limb amputations due to vascular disease in the United States has increased by approximately 20% during the last decade, disproportionately in minorities. Persons with diabetes mellitus and peripheral arterial disease (PAD) should be identified and prophylactic foot education and preventive care instituted to reduce the risk of limb loss.
Diabetes mellitus, a multisystem disease, causes two conditions that place the foot at high risk for amputation: polyneuropathy and PAD. Diabetes affects about 29.1 million Americans or 9.3% of the US population. Another 8.1 million people in the United States with diabetes are undiagnosed. Racial and ethnic differences are observed, with higher percentages in American Indians/Alaskan natives, non-Hispanic blacks, and Hispanic populations. Data from the Framingham Heart Study revealed that 20% of symptomatic patients with PAD had diabetes. The true prevalence of PAD in patients with diabetes has been difficult to determine, as most patients are asymptomatic, many do not report their symptoms, screening modalities have not uniformly been agreed upon, and pain perception may be blunted by the presence of peripheral neuropathy.
Risk factors for diabetic ulcers include male sex, hyperglycemia, and diabetes duration. Foot ulcers often result from severe macrovascular disease, and diabetic neuropathy exacerbates the risk. More than 60% of non-traumatic lower limb amputations occur in people with diabetes, underscoring the need to prevent foot ulcers and subsequent limb loss. Minor foot trauma in a person with poor underlying circulation and reduced sensation can lead to skin ulceration. Non-healing skin ulcers can lead to gangrene and progress to a point such that an amputation becomes necessary. This sequence of events can often be prevented before it starts. Multidisciplinary clinics that identify and manage patients with at-risk feet have demonstrated impressive reductions of 44% to 85% in the incidence of foot ulcers and lower limb amputations.
Numerous studies have further shown that attention to lifestyle modification can dramatically reduce progression to type 2 diabetes. The importance of identifying and treating a core set of risk factors (pre-diabetes, hypertension, smoking, dyslipidemia, and obesity) cannot be overstated.
PAD is an atherosclerotic disease characterized by occlusion or stenosis of the lumen of peripheral arteries, which leads to a reduction in blood flow to the limbs. The American Heart Association estimates that 8.5 million Americans have PAD, becoming more common with aging. Nearly 75% of them are asymptomatic. Despite its association with other cardiovascular conditions including stroke and coronary heart disease, only 25% of Americans with PAD are undergoing active treatment. Major risk factors associated with the development of PAD or that accelerate its progression are age, smoking, diabetes mellitus, hyperlipidemia, hypertension, hyper-homocysteinemia, metabolic syndrome, positive family history, and chronic kidney disease. African American ethnicity is a strong risk factor for PAD. Hypertension is an important risk factor for PAD, conferring a two- to threefold increased risk of developing PAD. The risk of PAD is increased two to four times by diabetes. Because men have more risk factors for PAD, they are more commonly affected than women.
Symptoms
The patient with a diabetic foot may demonstrate no symptoms because peripheral neuropathy can result in a lack of sensation. Peripheral neuropathy can mask painful ulcers and ischemic skin. Foot collapse due to Charcot joints can progress asymptomatically. Alternatively, diabetic patients can have pain sensations in the feet from sensory polyneuropathy, including burning, tingling, and painful numbness. Because of impaired sensation, patients may report imbalance and falls.
Intermittent claudication is the most widely reported symptom of PAD, although a wide range of leg symptoms can occur. Intermittent claudication is often described as pain, ache, or cramp in the calf during walking and other forms of physical activity. Leg pain is usually worse with increased exertion and relieved by rest. Claudication pain associated with walking results from insufficient arterial blood supply to meet the demand of exercising muscles (reversible muscle ischemia). Patients with neurogenic claudication due to spinal stenosis can have similar leg or calf pain with walking but must bend at the waist or sit to relieve the symptoms. When PAD is severe, persons may present with gangrene, ischemic ulcers on the distal foot, or pain at rest.
Physical Examination
The initial clinical evaluation should be as comprehensive as possible, including a complete foot examination. Inspect the skin for redness, pressure points, ulcerations, cracks, callus, or trophic changes (thin, shiny skin; distal hair loss). Probe any ulcers with sterile cotton-tipped applicators or surgical instruments. If bone is reached, this identifies persons with osteomyelitis, and other special bone imaging is unnecessary. Evaluate for any foot deformities predisposing it to abnormal stress distribution (e.g., hammer toes, collapsed foot arches due to Charcot joints, high arched feet due to intrinsic muscle atrophy from polyneuropathy, changes in stress distribution from previous toe or ray amputations).
Assess sensation because persons with loss of protective sensation are at risk for skin ulceration. The instrument most frequently used for detection of neuropathy is the nylon Semmes-Weinstein monofilament. Inability to perceive the 10-g force applied by a 5.07 monofilament is associated with clinically significant large-fiber neuropathy.
Distal pulses, particularly dorsalis pedis and posterior tibial, should be obtained. If they are absent or weak, it suggests the need for further testing for vascular integrity.
Evaluate gait and balance. Peripheral neuropathy predisposes to falls and skin trauma.
Finally, assess shoes for uneven wear patterns, areas of breakdown, and width of the toe box.
Functional Limitations
Persons with diabetes can develop peripheral polyneuropathy with loss of position sense and weakness, leading to gait instability and falls. Persons with PAD are often limited in community ambulation and vocational activities because of pain from claudication. Activities of daily living (ADLs) such as dressing and bathing may need to be completed in a seated position due to impairments in proprioception, strength, and balance. These impairments may lead to the use of assistive devices such as a cane or walker to achieve community mobility and if symptoms are severe enough, they may require the use of a wheelchair to achieve community mobility. Persons with PAD may be more inclined to pursue sedentary jobs, as their pain can limit their ability to stand or walk for prolonged periods of time.
Diagnostic Studies
Diagnosis of PAD requires a thorough history, physical examination, hemodynamic assessment, and potentially vascular imaging. Disease-specific questionnaires such as the Edinburgh Claudication Questionnaire may be used to aid diagnosis of PAD. The ankle-brachial index (ABI), a ratio of Doppler-recorded systolic pressures in the lower and upper extremities, is a convenient, accurate, noninvasive test that provides objective assessment of lower limb vascular status for screening, diagnosis, and hemodynamic monitoring of PAD. In patients with possible PAD, a resting ABI, with or without segmental pressures and waveforms, is recommended to establish a diagnosis. ABI readings are categorized as abnormal (ABI ≤ 0.90), borderline (ABI 0.91 to 0.99), normal (ABI 1.00 to 1.40), or non-compressible (ABI > 1.40). Typically, an ABI < 0.4 indicates more severe disease and is commonly found in patients with rest pain and/or tissue necrosis.
Exercise treadmill ABI testing is useful in establishing the diagnosis of lower extremity PAD in the symptomatic patient when resting ABIs are normal or borderline and can objectively measure functional limitations attributable to leg symptoms. By comparing the resting ABI measurement to the post-exercise ABI measurement, a diagnosis of PAD can be determined.
Toe brachial index (TBI) can measure digital pressure when small-vessel arterial disease is present; it is used to establish the diagnosis of PAD in the setting of non-compressible arteries (ABI > 1.40) and may also be used to assess perfusion in patients with suspected critical limb ischemia (CLI). Arterial imaging (duplex ultrasound, computed tomography angiography, magnetic resonance angiogram, or invasive angiography) is generally reserved for highly symptomatic patients in whom revascularization is being considered.
The 2016 American Heart Association/American College of Cardiology Guideline on the management of lower extremity PAD recommends resting ABIs to establish the diagnosis of lower extremity PAD in patients with exertional leg symptoms, non-healing wounds, age ≥ 65 years, those with other risk factors for atherosclerosis (HTN, DM, smoking history, hyperlipidemia), or known forms of atherosclerosis.
If a person complains of numbness in the legs or feet or has low back pain, electrodiagnostic testing should be conducted to identify whether peripheral polyneuropathy is present or whether lumbosacral radiculopathy is responsible for these symptoms. Nerve conduction study findings may include reduced sensory and motor amplitude, latencies, and slowed conduction velocity. Electromyographic findings in radiculopathy include increased insertional activity, abnormal spontaneous activity, and changes in motor unit morphology; when these electromyographic findings are seen in a myotomal pattern, this suggests radiculopathy.
Nonvascular
Neurogenic claudication from lumbar spinal stenosis
Calf pain due to S1 radiculopathy
Foot pain due to plantar fasciitis
Symptomatic Baker cyst
Ankle or knee pain due to osteoarthritis
Pain in legs and feet due to polyneuropathy
Arthritis of the hips
Restless legs syndrome
Vascular
Arterial embolus
Deep venous thrombosis
Thromboangiitis obliterans (Buerger disease)
Treatment
Initial Risk Factor Modification
Smoking Cessation
Cigarette smoking is the most important risk factor for development of PAD. Observational studies have demonstrated that the risk of death, myocardial infarction, and amputation is substantially greater in those individuals with PAD who continue to smoke. The risk of smoking for vascular disease is even greater for women than men. Intense smoking cessation programs have been shown to be more effective than minimal intervention programs. Intense programs can include verbal advice from a physician to quit, in-person counselor sessions to discuss cognitive-behavioral therapy and pharmacologic options, and a friend or family support system. Minimal intervention programs often include physician verbal advice to quit and providing patients with resources to explore on their own.
Hyperglycemia Management
The presence of PAD is 20% to 30% higher in diabetics than in the general population. Poor glycemic control has been associated with a higher prevalence of PAD and risk of adverse outcomes. Goals for hemoglobin A1c are typically less than 7%. With each percent increase above 7%, there is an associated 28% increased risk of PAD.
Hypertension Control
Management of blood pressure is required. Desired BP range is BP < 140/90, or <130/80 mm Hg if diabetes or renal insufficiency are present. Choice of antihypertensive medication is generally guided by the presence of underlying diseases such as diabetes, chronic kidney disease, or proteinuria.
Statin Therapy
Treatment with a statin medication is indicated for all patients with PAD. Recent guidelines highlight the class 1 indication for statins in all patients with PAD to achieve an LDL-C level <100 mg/dL (level of evidence B). The mechanism of statin-based risk factor modification is by reduction of systemic inflammation, stabilization of atherosclerotic plaques, attenuation of smooth muscle cell proliferation, and improved release of nitric oxide, which acts as a vasodilator and inhibition of platelet aggregation.
Antiplatelet Therapy
Based on the 2016 American College of Cardiology/American Heart Association (ACC/AHA) guidelines, antiplatelet therapy with aspirin alone (range 75 to 325 mg/day) or clopidogrel alone (75 mg/day) is recommended to reduce MI, stroke, and vascular death in patients with symptomatic PAD. In asymptomatic patients with PAD (ABI ≤ 0.90), antiplatelet therapy is reasonable to reduce the risk of MI, stroke, or vascular death. Warfarin is not recommended for this purpose. Cilostazol, a phosphodiesterase inhibitor, is an effective therapy, in the absence of heart failure, to improve symptoms and increase walking distance in patients with claudication. For patients with refractory claudication despite exercise therapy and smoking cessation, in the absence of heart failure, cilostazol 100 mg bid is recommended in addition to aspirin 75 to 100 mg/day or clopidogrel 75 mg/day ( Table 129.1 ).
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