(1)
Department of Surgery Division of Surgical Oncology, Icahn School of Medicine at Mount Sinai, New York, NY, USA
Introduction
Peripheral arterial disease (PAD) describes the condition in which atherosclerotic plaques deposit in the vessels of the extremities, usually the legs (Fig. 30.1). Predictably, the risk factors for PAD include smoking, hypertension, diabetes, and hyperlipidemia, and this condition typically coexists with coronary artery disease. Many patients with PAD are asymptomatic, however, some will develop intermittent pain in the buttock, thigh, or calf muscles, known as claudication. There are many causes of leg pain unrelated to PAD, therefore it is important to be specific when eliciting potential symptoms. In order to qualify as true claudication, the leg pain must involve a muscle group, be reproducibly caused by exertion, and relieved with rest. The pathophysiology of claudication is analogous to angina; pain occurs when the muscles of the leg experience ischemia because their metabolic needs exceed the inflow of arterial blood. The site of pain usually correlates with the level of disease: calf claudication is usually caused by disease in the superficial femoral artery, where as thigh or buttock claudication indicates more proximal occlusion, typically at the iliac artery.
Fig. 30.1
CT angiogram images of a patient with peripheral arterial disease demonstrating narrowing of bilateral superficial femoral arteries
As PAD progresses, the arterial supply to the lower extremities may become insufficient to maintain even the baseline metabolic needs of the foot, resulting in rest pain. Patients with rest pain classically dangle their affected leg off the side of the bed, because the gravity-induced increase in blood flow to the foot helps to relieve the pain. Another sign of advanced PAD is a non-healing ischemic ulcer of the foot. These ulcers are typically located on the lateral aspect of the ankle or the toes. This distribution is distinct from ulcers caused by venous stasis, which are usually found on the medial aspect of the ankle. Ultimately, peripheral arterial disease can lead to frank gangrene of the toes.
Any patient suspected of having PAD should undergo a complete history and physical, including a bilateral pulse examination with palpation of the femoral, popliteal, posterior tibial, and dorsalis pedis pulses. Diminished or absent pulses should be noted, and a Doppler device can be used to search for signal in sites where pulses are not palpable. The point of transition from normal to absent pulses usually indicates the level of vascular stenosis.
The ankle–brachial index (ABI) is a way to quantify the degree of decreased blood flow to the extremities. The ABI is a ratio of the blood pressure at the level of the ankle over that in the arm (Fig. 30.2). An ABI of 1 means that the blood pressure in the extremities is equal to the systemic blood pressure and therefore no vascular disease is present. An ABI less than 0.9 is abnormal and suggests the presence of peripheral arterial disease. An ABI less than 0.8 is indicative of moderate PAD, and an ABI less than 0.4 indicates severe PAD, usually associated with ischemic ulcers or gangrene.
Fig. 30.2
Ankle-Brachial Index measurement [Reprinted from Petznick AM, Shubrook JH. Treatment of specific macrovascular beds in patients with diabetes mellitus. Osteopathic Medicine and Primary Care 2010; 4:5. With permission from BioMed Central Ltd]
It is important to note that ABI measurements in diabetics are typically unreliable. The calcifications of peripheral vessels that occur in this disease cause them to be less compressible, leading to falsely normal ABIs, or values greater than 1. In such patients, or toe pressures or pulse volume recordings of the leg, which are not affected by calcifications, can be used to diagnose the presence of PAD (Fig. 30.3).
Fig. 30.3
Pulse volume recordings [Reprinted from Raines JK, Almeida JI. Pulse Volume Recording in the Diagnosis of Peripheral Vascular Disease. In: AbuRahma AF, Bandyk DF (eds). Noninvasive Vascular Diagnosis: A Practical Guide to Therapy. London, UK: Springer Verlag; 2013: 303-310. With permission from Springer Verlag]
In the absence of devitalized tissue, PAD should be treated first with lifestyle modifications and pharmacologic therapy. Smoking cessation should be strongly recommended. Antiplatelet therapy and medications for cholesterol reduction are also prescribed. In patients with claudication, exercise therapy can be used for symptom reduction. Patients are instructed to ambulate until claudication occurs, and then to continue walking for several more minutes before resting. This exercise-rest cycle is repeated several times per session. These periods of ischemia are thought to induce muscle remodeling, ultimately allowing a patient to ambulate a greater distance before claudication occurs. Exercise therapy requires a motivated patient since it must be performed several times a week for 1–2 months before the benefits become evident.
The presence of claudication is not in itself an indication for surgery. Intervention should be strictly reserved for those patients with disabling claudication, rest pain, non-healing ischemic ulcers, or gangrene. The reason for reserving surgical treatment until clearly indicated is that revascularization procedures for PAD have a limited period of patency of 5–10 years. Performing bypass prematurely both exposes the patient to unnecessary surgical risk, and limits the surgical options for treatment of recurrent disease.