Peripheral Arterial Surgery



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.


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.




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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May 8, 2022 | Posted by in CARDIOLOGY | Comments Off on Peripheral Arterial Surgery
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