Collateral circulation and pathways

Although symptoms are generally proportional to the extent of disease, it is sometimes surprising to find patients with arterial occlusions but relatively minor symptoms. Conversely, some patients with one or two stenoses can experience significant impairment to their lifestyle. This variability is mainly due to the quality of the collateral circulation. If an arterial segment is severely diseased or occluded, there are often alternative pathways that are able to carry blood flow around the diseased segment, referred to as collateral vessels. In this situation, reverse flow is observed in major branches of arteries just distal to an area of severe disease, where they help to resupply blood flow to the main vessel. One such example is flow reversal observed in the internal iliac artery, supplying blood to the external iliac artery in the presence of a CIA occlusion (Fig. 9.3). It should be noted that it is very difficult to follow collateral vessels for any length using the duplex scanner, especially in the pelvis. This is not really a problem, as it is the length and severity of the disease in the main vessels that the sonographer is attempting to document. However, the quality of the collateral circulation is very important, and this can be determined by assessing the patient clinically and measuring the ankle–brachial pressure index (ABPI). Common collateral pathways are summarized in Table 9.2.

Figure 9.3 An example of collateral flow. The common iliac artery is occluded (O) and reverse flow (blue) is demonstrated in the internal iliac artery, as it supplies flow to the external iliac artery (red).

Table 9.2 Common collateral pathways of the lower-limb arteries

Intermittent claudication

Atherosclerosis is a major health problem in developed countries where lifestyle factors, such as smoking and diet, can accelerate the progression of the disease. It is estimated that intermittent claudication affects approximately 4.5% of the population aged between 55 and 74 years, and there is evidence that persons with claudication have a significantly higher mortality rate from cardiac disease than nonclaudicants (Fowkes et al. 1991). Intermittent claudication is caused by arterial narrowing in the lower-limb arteries, and symptoms develop over a number of months or years. Claudication is typified by pain and cramping in the muscles of the leg while walking, which usually forces the patient to stop and rest for a few minutes in order to ease the symptoms. The severity of pain experienced and the distance a patient is able to walk can vary from day to day but, generally, walking briskly or on an incline will produce rapid onset of symptoms. The location of pain (i.e., calf, buttock, or thigh) is often associated with the distribution of disease. For instance, aortoiliac disease often produces thigh, buttock and calf claudication whereas femoropopliteal disease is associated with calf pain. There are sometimes physical signs of deteriorating blood flow in the lower limb, such as hair loss from the calf and an absence of nail growth. Claudication only occurs during exercise because, at rest, the muscle groups distal to a stenosis or occlusion remain adequately perfused with blood. However, during exercise the metabolic demand of the muscles increases rapidly, and the stenosis or occlusion will limit the amount of additional blood flow that can reach the muscles, so causing claudication.

Many patients with intermittent claudication are treated by conservative methods. This includes reduction or elimination of risk factors associated with atherosclerosis, such as smoking. Patients are also advised to undertake a controlled exercise program to build up the collateral circulation around the diseased vessel, which may ease symptoms over time. If necessary, serial ABPI measurements or exercise tests can be performed to monitor the patient’s progress. Interventional treatment is mainly by angioplasty which involves the dilation of stenoses or occlusions with percutaneous balloon catheters (see Ch. 1). Arterial stents are sometimes used to prevent restenosis, although in-stent stenosis is known to occur in a proportion of cases due to the development of intimal hyperplasia (see Fig. 9.20). Surgical bypass is usually avoided, unless the patient is suffering from severe claudication, as there is a small potential risk of complications occurring during or after surgery, which in extreme cases could lead to amputation or even death.

Chronic critical lower-limb ischemia

Critical lower-limb ischemia occurs when blood flow beyond an arterial stenosis or occlusion is so low that the patient experiences pain in the leg at rest because the metabolic requirements of the distal tissues cannot be maintained (Fig. 9.4). This is frequently typified by severe rest pain at night, forcing the patient to sleep in a chair or to hang the leg in a dependent position over the side of the bed. This improves blood flow due to increased hydrostatic pressure. The Trans-Atlantic Inter-Society Consensus for the management of peripheral arterial disease (TASC II) (Norgren et al. 2007) makes the following recommendation for defining critical lower-limb ischemia:

Figure 9.4 The appearance of critical lower-limb ischemia with gangrene of the small toe.

In addition the documents also states:

The treatment of lower-limb ischemia includes angioplasty or arterial bypass grafting. Unfortunately, some patients are not suitable candidates for any form of limb salvage, and amputation is the inevitable outcome.

Acute limb ischemia

Acute limb ischemia, as the name suggests, is due to sudden arterial obstruction in the lower-limb arteries that may threaten limb viability. The position of the obstruction can be variable. Main causes of acute ischemia are listed in Box 9.1. Acute thrombosis of an existing arterial lesion, a so-called acute-on-chronic occlusion, can occur when the blood flow across a diseased segment of an artery is so slow that it spontaneously thromboses. Long segments of an artery may occlude in this situation. Acute ischemia is more likely to occur if the collateral circulation around the disease is poorly developed. An embolus may be released from other areas of the body, such as the heart or from an aneurysm, and then travels distally down the leg, eventually obstructing the artery when the arterial diameter is less than that of the embolus. An embolus frequently obstructs bifurcations such as the common femoral bifurcation or distal popliteal artery and tibioperoneal trunk. Another example is obstruction of the aortic bifurcation by an embolus projecting down both CIA origins, referred to as a saddle embolus. The body has very little time to develop collateral circulation around embolic occlusions, and the limb may be very ischemic.

The classic symptoms of acute ischemia are shown in Box 9.2. In this situation, emergency intervention by surgical embolectomy, bypass surgery, or thrombolysis should be performed, provided that the patient is fit enough for treatment. Left untreated, acute ischemia can lead to muscle death or necrosis. This can cause swelling of the calf muscle, and eventually the sac, or fascia, surrounding the muscles will restrict any further swelling, leading to a pressure increase within the muscle compartments. This is known as compartment syndrome, and the acute increase in intramuscular pressure can further exacerbate the muscle ischemia. If limb salvage is possible, surgical splitting of the fascia, called a fasciotomy, may be required to release the excess pressure.

Severe muscle ischemia can produce toxins causing systemic symptoms that can lead to organ failure and death. An urgent amputation is usually performed if there is no viable option to restore blood flow to the limb.

Microembolization into the foot is often called ‘trash foot’ or ‘blue-toe syndrome.’ Localized tissue infarction occurs, leading to necrosis. It is not unusual for the patient to have a palpable ankle pulse. The outcome is often poor when a large area of tissue is affected and results in local amputation of toes, forefoot, or leg.