Peripheral Arterial Surgery
Michael C. Siah
Gerardo Gonzalez-Guardiola
Khalil Chamseddin
James A. Walker
Melissa L. Kirkwood
INTRODUCTION
Epidemiology
Peripheral arterial disease (PAD) is the chronic manifestation of atherosclerosis in the lower extremity vasculature. Its incidence continues to increase worldwide, with current epidemiologic estimates approaching 200 million people.1 In the United States alone, 8 to 12 million Americans are estimated to be affected by PAD.2 The domestic and global prevalence of PAD is expected to continue increasing as populations continue to age and the prevalence of diabetes grows. The burden caused by PAD has resulted in burgeoning health care costs associated with its care and the management of its complications.
PAD represents a disease process that markedly impairs the quality of patients’ lives and is the primary cause of major amputation in the United States. Patients with PAD often suffer from high rates of cardiovascular death, myocardial infarction (MI), and stroke. It is generally uncommon among younger populations, as its prevalence is less than 5% in individuals less than 50 years of age. Its incidence increases with age, as it is prevalent in 12% to 15% of individuals over 65 years old and approaches 20% in individuals over 80 years of age.2
Risk Factors
PAD shares many of the same risk factors of atherosclerotic conditions affecting other vascular beds, namely the coronary and cerebrovascular arteries. The traditional risk factors for the development of PAD include increased age, gender, cigarette smoking, diabetes, hypertension, dyslipidemia, obesity, alcohol consumption, chronic kidney disease, race/ethnicity, and genetic factors. Additional risk factors include socioeconomic status, autoimmune diseases, and hyperhomocysteinemia.
PATHOGENESIS
PAD primarily occurs as a result of systemic processes. Endothelial dysfunction with atherosclerotic risk factors initiates an inflammatory pathway leading to PAD. Chronic endothelial injury from reactive oxygen species, cigarette toxins, and proinflammatory cytokines leads to increased endothelial dysfunction and permeability. Oxidized low-density lipoprotein (LDL), endothelial growth factors, and chemotactic agents recruit macrophages and promote vascular smooth muscle cell growth. Macrophages migrate into the subendothelial space and aggregate oxidized LDL, which results in foam cell formation. The activated macrophages create a positive feedback loop stimulating vascular smooth muscle cells, which eventually distort the overlying endothelium and arterial lumen. Production of matrix metalloproteinases, platelet-derived growth factor, interleukin-1, transforming growth factor-beta and tumor necrosis factor-alpha contributes to plaque formation and stabilization.
CLINICAL PRESENTATION
Common Signs and Symptoms
The spectrum of PAD can be differentiated into three distinct categories: asymptomatic disease, intermittent claudication (IC), and critical limb threatening ischemia (CLTI). The largest portion of patients with PAD are asymptomatic. Both IC and CLTI are much less common; however, they often represent the primary indication for referral to a vascular specialist for treatment.
IC is a clinical syndrome resulting in symptoms such as cramping, aching, or fatigue in the lower extremity. The symptoms are typically reproducible at certain walking distances and are completely relieved with cessation of the provocative activity. In more advanced PAD, such as those presenting with CLTI, patients endorse symptoms of constant pain at rest and develop ulceration, gangrene, or wounds that fail to heal. Location of the symptoms along the lower extremity may assist in identifying the level of arterial obstruction that is classified as aortoiliac, femoropopliteal, or infrapopliteal disease.
Physical Examination Findings
The initial approach to the physical examination in a patient with PAD requires a well-documented history and physical examination, with focus on the presence and quality of peripheral perfusion. Examination of the extremities is the most critical component of the physical examination from the vascular perspective. In patients with aortoiliac occlusive disease, the constellation of thigh and buttock claudication, impotence, and absent femoral pulses is known as Leriche syndrome.
A proper physical examination begins with inspection for skin changes, edema, atrophied muscles, nonhealing ulcers, and rubor. The pulse examination should identify presence, absence, or diminished pulses at the common femoral artery,
popliteal artery, anterior tibial, posterior tibial, peroneal, and dorsalis pedis arteries while comparing to the contralateral extremity. Diminished femoral pulses or bilateral symptoms may be indicative of aortoiliac occlusive disease. In patients with nonpalpable pulses, Doppler auscultation may assist in the examination. The absence of a palpable pedal pulse generally suggests inadequate perfusion to allow for wound healing. The presence or absence of palpable peripheral pulses provides a general anatomic distribution of areas of atherosclerotic disease on a macroscopic level; however, a simple examination may not reflect the degree of perfusion in the local area of tissue loss.
popliteal artery, anterior tibial, posterior tibial, peroneal, and dorsalis pedis arteries while comparing to the contralateral extremity. Diminished femoral pulses or bilateral symptoms may be indicative of aortoiliac occlusive disease. In patients with nonpalpable pulses, Doppler auscultation may assist in the examination. The absence of a palpable pedal pulse generally suggests inadequate perfusion to allow for wound healing. The presence or absence of palpable peripheral pulses provides a general anatomic distribution of areas of atherosclerotic disease on a macroscopic level; however, a simple examination may not reflect the degree of perfusion in the local area of tissue loss.
Differential Diagnosis
The differential diagnosis of vascular disease encompasses pathologies that cause leg pain. Typically, those include neurogenic (spine disease), venous, joint, and other musculoskeletal disorders.
DIAGNOSIS
In addition to the history and physical examination, noninvasive vascular studies assist in objectively quantifying the degree of PAD. The ankle-brachial index (ABI) is the calculated ratio of the highest ankle systolic pressure divided by the highest brachial artery systolic pressure, with normal value considered as 1.0 to 1.4. A value between 0.4 and 0.9 is considered mild to moderate PAD corresponding to IC, whereas an ABI below 0.4 is associated with severe PAD, which may manifest as rest pain and tissue loss. The 2015 Society of Vascular Surgery (SVS) and 2016 American Heart Association/American College of Cardiology (AHA/ACC) guidelines recommend resting ABI to establish the diagnosis in patients with a history and physical examination suggestive of PAD.3,4 In patients with abnormal ABI (<0.90) and lifestyle limiting symptoms despite guideline-directed medical treatment, further diagnostic imaging is recommended. Individuals with symptoms consistent with PAD and an ABI between 0.90 and 1.40 are recommended to undergo exercise ABI testing. With exercise treadmill ABI, the resting baseline ABI is taken, and the patient then walks on a treadmill at ˜2 mph with 12° inclination for 20 minutes or until forced to stop because of symptoms. Postexercise ABI measurements are taken. A 20% decrease in ABI from baseline, a 30 mm Hg drop in ankle systolic pressure, or more than 3 minutes to recovery of baseline ankle systolic pressure is indicative of PAD.5 With ABI greater than 1.40, the value may be falsely elevated because of the increased cuff pressure needed to occlude the vessels in patients with extensively calcified vessels. This more commonly affects diabetics and patients with renal failure. An ABI above 1.4 in a patient with blunted waveforms, and nonpalpable pedal pulses should be suggestive of calcified vessels.
Other noninvasive studies include toe digital pressures, segmental pressures along the lower extremities, and pulse volume recordings. Digital toe pressures and toe-brachial index (TBI) are most useful in patients with falsely elevated ABI because of calcified tibial disease. A TBI below 0.70 is indicative of PAD. Additionally, a systolic toe pressure less than 40 mm Hg is indicative of inability to heal wounds. AHA/ACC guidelines recommend TBI measurements as the next diagnostic step when the ABI is greater than 1.40.4
Segmental pressures use cuff pressures to measure the systolic pressure at various levels along the lower extremity. A decrease of 20 mm Hg across any level indicates a hemodynamically significant disease at that level, which may assist in localizing the area of obstruction. Similar to segmental pressures, pulse volume recordings obtain arterial waveforms at several levels along the lower extremity to identify the level of arterial disease. Distal to the diseased segments, the waveform becomes dampened with a decrease in amplitude or slope of the upstroke. Example waveforms are displayed in Figure 90.1.
In chronic arterial disease, noninvasive imaging techniques with anatomic data—including duplex ultrasound, magnetic resonance angiography (MRA) and computed tomography angiography (CTA)—have largely replaced catheter angiography for most patients and allow accurate assessment of disease distribution. The hemodynamic significance of a stenosis demonstrated by these techniques can be further evaluated with targeted duplex ultrasound or catheter angiography. The 2015 SVS guidelines recommend use of anatomic imaging studies such as duplex ultrasonography, CTA, or MRA only in patients being considered for revascularization. In our practice, we usually obtain preoperative CTA to guide interventions if there is a clinical indication of CLTI.3 Table 90.1 lists the various diagnostic tools.
Adjunct laboratory studies are aimed at assessing systemic risk factors. This should include a complete blood count, fasting blood glucose, hemoglobin A1c, serum creatinine, and lipid panel.
 FIGURE 90.1 Pulse volume recording showing a decrease in amplitude and slope of the upstroke distal to the diseased segment. |
TABLE 90.1 Diagnostic Studies for PAD | ||||||||||||||||||||||||||||
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MANAGEMENT OF PERIPHERAL ARTERIAL DISEASE
Medical Approach
PAD is a systemic disease caused by multiple cardiovascular risk factors. Thus, managing these comorbidities is critical to the optimal treatment of these patients. Effective medical management of hypertension, hyperlipidemia, diabetes mellitus, smoking, and chronic kidney disease is essential. Medical management should be aimed at risk factor reduction and preventative lifestyle modification. The aggressive pharmacologic treatment of risk factors has been shown to benefit patients with symptomatic PAD; however, they have not shown significant benefit in asymptomatic patients when treated similarly.6 The SVS guidelines provide Class IA evidence for smoking cessation interventions and patient education as primary management in asymptomatic patients.3
Antihypertensive treatment has been shown to reduce the risk of MI, stroke, heart failure, and cardiovascular death in patients with symptomatic PAD.7 Treatment of hypertension should aim at a systolic blood pressure less than 140 mm Hg and diastolic pressure less than 90 mm Hg. For individuals with diabetes or chronic kidney disease, the blood pressure goal should be less than 130/80 mm Hg. Recommended agents for first-line therapy include angiotensin-converting enzyme (ACE) inhibitors. In 2000, the Heart Outcomes Prevention Evaluations (HOPE) study found that ramipril significantly reduced the risk of cardiovascular deaths in high-risk patients (relative risk 0.74, P < .01).8 Caution should be used in prescribing ACE inhibitors to patients with renal artery stenosis.
Similar to hypertension, treatment of hyperlipidemia significantly reduces cardiovascular morbidity in PAD.9 Recent guidelines recommend statin therapy based on estimation of 10-year cardiovascular risk. Because the 10-year cardiovascular risk in PAD patients is greater than 7.5%, statin treatment is indicated.10 Management of hyperlipidemia includes moderate or high-intensity statin therapy to maintain LDL less than 100 mg/dL and less than 70 mg/dL in higher risk individuals.
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