Etiology and Pathogenesis

A large number of pathologic processes result in arterial occlusive and aneurysm diseases. By far the most common etiology is atherosclerotic plaque formation in the vessel wall leading to luminal narrowing, wall calcification, plaque destabilization and hemorrhage with rupture, thrombosis, and end-organ damage or showering of emboli distally with resulting tissue damage and necrosis. In other circumstances, atherosclerosis leads to weakening of the vessel lumen leading to true aneurysms, defined as a vessel diameter greater than 1.5 times its normal diameter involving all layers. Genetic abnormalities and environmental exposures are almost always contributory in individuals with advanced vascular pathology. Specific genetic abnormalities have been elucidated in Marfan’s syndrome (fibrillin-1), Ehlers-Danlos syndrome, William’s syndrome (hypercalcemia), Loeys-Dietz syndrome (transforming growth factor-β receptor), and homocysteinuria. Thromboangiitis obliterans (Buerger’s disease), which is usually associated with heavy nicotine use, is also seen with PVD. Other risk factors for atherosclerosis (e.g., hypertension, diabetes, lipid abnormalities) all accelerate disease progression and may lead to a need for surgical or percutaneous intervention. Extrinsic mass effects or vessel encasement in the case of popliteal artery entrapment by the gastrocnemius muscle, celiac artery by the diaphragmatic crus (median arcuate ligament syndrome), or renal artery by neurofibromatosis may lead to similar occlusive symptoms. Clinical manifestations depend on the location and severity of the vessel disease and presence of collateral circulation (see Chapter 44 for additional information on the pathogenesis of atherosclerosis).

Lower Extremity Peripheral Vascular Disease

Clinical Presentation

Population studies suggest that approximately 15% of the general population older than 55 years have lower extremity PVD. In individuals with a genetic predisposition, diabetes, hypercholesterolemia, or a history of significant cigarette smoking, the prevalence of PVD is higher. Symptoms range from mild, intermittent claudication (pain or discomfort that develops during exercise and is relieved with rest) to constant, severe rest pain. The level of the occlusion typically correlates with the level of pain. Distal aortic (Leriche’s syndrome) and iliac disease cause gluteal, thigh, lower extremity, and occasional back pain and impotence. In these individuals, the femoral artery pulses are usually abnormal, diminished, or absent. Superficial femoral and popliteal artery stenoses result in foot and calf symptoms. Less than 20% of patients with PVD progress to critical limb ischemia that jeopardizes the tissue viability of the extremity. The presence of PVD is evidence of systemic atherosclerosis and is associated with a threefold increase in cardiovascular mortality. Cross referral between cardiology and vascular surgery–interventional radiology services is vital to identify patients at risk for treatable coronary disease.

Diagnostic Approach

Examinations used to evaluate the lower extremity arteries are designed to establish the presence and location of disease, quantify severity, and determine temporal progression.

Ankle-Brachial Index and Segmental Pressure Measurements

The ankle-brachial index (ABI) is the simplest baseline examination used for PVD screening. This examination has a high positive predictive value except in diabetics with noncompressible calcified vessels. As an arterial stenosis increases, there is a progressive decrease in the systolic blood pressure (SBP) distal to the stenosis. The decreased blood pressure can be quantified and localized using pneumatic cuffs and either continuous Doppler or plethysmographic sensors. The ABI is determined by measuring SBP in the tibial and brachial arteries. Normally, SBP is amplified in the distal limb by pulse-wave reflection, and the ABI is greater than 1. An ABI of 0.80 to 0.90 is considered to be mildly diminished; 0.50 to 0.80, moderately diminished; and less than 0.50, severely diminished. These values reflect the degree of proximal PVD.

The ABI is simple and inexpensive to use and is an excellent office-based screening tool to identify individuals at risk for limb ischemia who may warrant further investigation if results are abnormal. Pressure measurements at multiple levels along the leg can estimate the location of an arterial occlusion. Blood pressure cuffs are placed on the upper and lower thighs and calves, and a gradient of greater than 10 to 15 mm Hg between adjacent sites suggests a physiologically significant stenosis. Measurements after treadmill exercise may disclose a hemodynamically significant lesion that is unapparent at rest.

Doppler waveform analysis is an accurate method for defining arterial lesion location and severity (Fig. 45-1). Significant arterial stenoses alter the pattern of flow velocity, as assessed by continuous-wave Doppler analysis. A change in the flow velocity waveform—an increase in peak systolic velocity at the site of the lesion, turbulence, loss of the reverse flow component, or a decrease in pulse velocity distal to the lesion—is diagnostic of a flow-limiting arterial lesion. Color Doppler imaging is able to identify the vessel(s) of interest. A critical stenosis (>50%) is characterized by poststenotic turbulence on color imaging (see Fig. 45-1) and a doubling of the peak systolic velocity on continuous-wave Doppler.