When one discusses vascular diseases, a number of problems or situations may develop and require the patient to seek medical assistance. Most such problems may be readily recognized and many may be treated conservatively and successfully with little effort or risk. Some situations, however, may produce vague or confusing symptoms and thus may be very difficult to sort out or to diagnose. These patients may then see numerous physicians and have extensive evaluation before the correct diagnosis or therapy is appropriately delineated. Such a diagnostic and therapeutic challenge for physicians may be a patient with a steal syndrome (SS).

Patients present with the more classic, cerebral steal symptomatology in which the diagnosis was readily proven or established. We have also seen a number of individuals with vague, perplexing symptoms for evaluation and in whom eventually a steal syndrome was diagnosed. Those patients who have an established, symptomatic steal syndrome need to be provided the therapeutic options, including major invasive procedures or corrective surgery. Patients with asymptomatic incidentally encountered steal findings present a different situation. Many of these situations require little or no treatment and close periodic follow-up. Avoidance of major interventions and their potential complications may thus be minimized. The severely debilitating or acute life-threatening “steal” developments may require urgent or emergent intervention and the accompanying risk to preserve life or limb. Multiple considerations affect the ultimate therapy and prognosis for the patient (Table 47-1).

What is the definition of a steal syndrome? Different authors may ascribe different definitions or characteristics to this syndrome. A simple definition might be the taking of a blood supply from its usual direction and organ to another area as a result of a change in pressure gradient. This phenomenon can then occur in a number of situations. The classic example is where an artery is obstructed and the blood flow is then reversed in a vessel taking origin distal to the obstruction. The flow then travels around the obstruction and into the distal obstructed artery to serve the tissues distal to the obstruction. This may particularly occur when a greater need is recognized distally because of increased exercise or usage.

When this occurs, the blood, which originally flows away from the vessel obstructed, now flows toward the obstructed vessel and reverses the flow of blood into the circuitous route. This then redirects blood away from the original end-organ and provides the blood and nutrients to the ischemic or needy tissues. Thus, the original end-organ may receive a smaller supply of blood or nutrients. If the patient has findings on vascular study of blood flow redirection, or reversal, and the patient is asymptomatic, the process is called a “steal phenomenon” (SP). If the patient becomes symptomatic as a result of their obstruction and flow reversal, the diagnosis of a steal syndrome (SS) is established.

In essence, a steal occurs when blood is syphoned off from one area to another when a demand for blood or tissue nutrition presents at the second site. When this diversion occurs, the patient may develop symptoms relative to the area from which blood is diverted or stolen. The severity of the patient’s problem will then define how severe the steal and thus the steal syndrome. The organ or structure from which blood is stolen from may initiate symptoms such as dizziness, pain, syncope, or weakness.

There are a number of causes for the development of the “steal” in a patient (Table 47-2). The most commonly recognized and understood steal situation develops as a result of arteriosclerotic, occlusive disease. This usually develops in elderly patients who have a propensity to form arteriosclerotic (cholesterol) plaque build up within an artery, which may lead to occlusion of a major vessel. Most commonly, this will involve the cerebral central nervous system (CNS) vasculature-carotid and subclavian arteries. The classic example is the left subclavian artery occlusion with vertebral vessel flow redirection. However, the arteriosclerotic process may also cause obstruction of other vessels such as the iliac arteries, which may lead to the development of a steal. Such a phenomenon may become particularly evident during the correction of an obstructing lesion. Coronary symptoms may even develop as a result of an occlusive process postcoronary bypass using the internal mammary artery.

Atherosclerotic occlusive disease is not the only etiology for a steal development. Iatrogenic causes include vascular surgery for congenital heart lesions, which may obstruct the normal subclavian routing and lead to CNS problems or symptoms. These patients may develop the SP but not the SS for years and their problems may thus be difficult to recognize. Arterial shunting of blood from a high-flow or high-pressure system to a low-resistance vessel may also lead to the steal occurring, e.g., the iliac steal postvascular repair of the iliac occlusion. Another iatrogenic cause is seen by the nephrologists who have noted a steal in a number of their fistula or shunt dialysis patients. When severe, these patients have required additional surgery to correct the problem and prevent tissue loss. Traumatic vascular lesions may also lead to steal through vascular occlusion or fistula formation. Such lesions may require extensive difficult surgical intervention.

Further classification according to the end-organ stolen from is well illustrated (Table 47-3). The end-organ affected may be the brain/brain stem in the subclavian steal. However, the coronary artery and heart may develop ischemia when the subclavian artery occludes postcoronary bypass utilizing the left internal mammary artery. The distal organ “stolen from” may include the hand, gastrointestinal system, or lower extremity and thus the end-organ classification.

Multiple vessels may be involved in the development of the SP. These vessels are usually larger vessels which carry a large volume of blood. Thus, when these vessels occlude, symptoms may be expected. Vessels that may be listed or involved in a “steal” include not only the larger readily recognized but also the smaller tributaries and capillaries (Table 47-4). Some of these steal situations may be recognized by their vessel names, e.g., subclavian or coronary steal.

First described in 1960 by Contorni, a number of additions to our knowledge took place in a short time.¹ The subclavian steal phenomenon (SSP) was shown to be a result of severe stenosis or occlusion of the subclavian artery. One year later, Ravitch demonstrated that the subclavian artery occlusion could be associated with neurologic symptoms.² Fisher then called cerebrally symptomatic patients with subclavian flow reversal the subclavian steal syndrome (SSS).³ Brainstem ischemia could thus be considered a result of the SSS. It should be noted that the SSS occurs only when the subclavian artery occlusion is proximal to the vertebral artery origin and the vertebral artery is patent.

The cerebral-subclavian steal is the most commonly recognized steal in which the subclavian artery becomes occluded and the flow is reversed in the left vertebral artery. This then changes the directional flow so that blood from the circle of Willis flows outward through the vertebral artery to the left upper extremity on demand. In the abdominal (mesenteric) steal, the blood is redirected from one organ to serve another during occlusion of the visceral vessels, or on aortic occlusion, into the iliac system. The dialysis access steal is seen particularly when the brachial artery or large radial artery fistulas are created and the arterial blood flows away from the hand.

Another steal example is the coronary artery steal (CAS). This occurs when the proximal left subclavian artery occludes and the left internal mammary artery has been used to revascularize the coronary vessels. A possible iatrogenic cause may develop when the Blalock-Taussig operation is performed for congenital heart disease. During this surgery, division of the distal left subclavian artery, proximal to the origin of the left vertebral artery, may create a potential SP. With growth and aging, these individuals may develop symptoms, including headaches, as a result of an iatrogenic induced subclavian steal. Cerebral lesions and other anatomic lesions should be sought in order to be sure of the diagnosis, the anatomy, and the possible treatment. With time and growth, collateral circulation may then develop through multiple vessels to provide appropriate tissue nourishment.

The anatomic location of the disease process and the number of lesions varies from patient to patient. When the subclavian artery acutely becomes severely stenotic, such that flow is reduced or totally occluded, the arm distally may become symptomatic caused by ischemia. When the stenosis occurs over a long period of time, collateral circulation may develop and maintain the viability of the distal extremity with or without symptoms. Netter’s textbook of anatomy delineates the cerebral arterial system simply and graphically.⁴ The developing collaterals will include the vertebral artery, arterial branches to the chest wall, the circle of Willis, the carotid artery, and other collateral vessels (Figure 47-1). The blood flow for the subclavian steal will usually take place through the right innominate into the right carotid and the circle of Willis [1]. The blood will then flow down the left vertebral [2] to the distal left subclavian artery [3] and then out to the brachial vessels and the arm and hand (B). Increased arm exercise will demand more circulation through the brachial vessels to the left upper extremity. During this period of time, vertebral basilar and other symptomatology may develop. Some individuals, however, have felt that such symptoms may not be because of a reduction in cerebral blood flow (A). This, however, is not the usual consideration. Of interest is the fact that many patients with the SP remain totally asymptomatic.

We have seen patients with multiple etiologies for what is felt to be a subclavian steal. This includes the individual with Takayasu’s disease, as well as the typical elderly arteriosclerotic obliterans process. However, traumatic occlusion of the subclavian artery as well as the iatrogenic causes for subclavian artery disease have been noted, including those patients who have had an anomalous right subclavian artery originating from the left descending thoracic aorta. Subsequent to ligation or division of the anomalous subclavian artery, patients may develop the SSS years later. After extensive arm usage they may pass out or develop syncope with no other anatomic abnormality except the ligated right subclavian artery.

The steal syndrome may also develop when a blood flow circuit is modified or changed. Such may occur when an obstruction or new connection (bypass) reroutes the blood away from the usual distal end-organ and into a different pathway. When this occurs, the blood may literally take a shortcut and follow the path of least resistances as exemplified in Figure 47-1.

At low flow or reduced need, both organs or areas normally perfused may not initiate any symptoms despite an obstruction, flow reversal, or change in distal resistance. Oxygen and nutrient supply are adequate at this point in time. But with increased demand by the end-organ (B) and decreased flow to organ (A), the blood may be shunted or “stolen” away from the usual recipient of the normally directed blood flow to organ (A). This decreased flow to (A) may then initiate hypoxic and hypovolemic symptoms referral to organ (A) in addition to decreased nutrient symptoms from organ (B).

A parallel phenomenon occurs when a large vessel normally serves both a high-and low-resistance area. The blood will flow away from the higher-resistance area when no obstruction is present to the lower-resistance area or the obstruction has been removed.