The pathogenesis of acute lower-extremity ischemia has changed over the decades. Traditionally, embolism related to rheumatic heart disease was the most common cause, whereas in most contemporary series, bypass graft occlusion or thrombosis of a native vessel now predominates. This observation is probably related to a decline in rheumatic heart disease and the increased performance of vascular surgical procedures. While embolism from the heart is still observed on a relatively frequent basis, it is most often related to myocardial infarction (MI) or arrhythmia. Emboli typically lodge at branch points of vessels related to diameter change, a finding that, coupled with the absence of pre-existing collaterals, explains the severe ischemia associated with embolic events.

Development of thrombosis of native vessels is usually related to the slow progression of atherosclerotic plaques. Atherosclerotic plaques develop at predictable locations. The most common location for occlusion in the lower extremity is at the adductor canal of the superficial femoral artery. The development of occlusive disease of the lower-extremity vasculature is ordinarily a slow process that allows the development of alternate collateral channels that may limit symptoms to claudication only. However, rapid progression of symptoms may develop in occasional patients, possibly related to an acute disruption of the fibrous cap of the atherosclerotic plaque with exposure of the thrombogenic atherosclerotic core. As such, atherosclerosis can sometimes result in sudden onset lower-extremity ischemia, and often the differentiation between embolism and thrombosis may be difficult or even impossible. Lastly, native artery
thrombosis can occur in the absence of any underlying atherosclerotic lesion and is typically related to an underlying hypercoagulable state. Noting the normal underlying vasculature with a paucity of collaterals in these patients, the symptoms are characteristically sudden and dramatic, with a clinical presentation that can easily be confused with arterial embolism.

The other less common causes of acute lower-extremity ischemia are diverse but must always be considered. They include atherosclerotic arterio-arterial emboli, trauma, aortic dissection, venous gangrene, and popliteal aneurysm thrombosis. Two unusual causes of popliteal artery thrombosis should also be considered—popliteal entrapment and adventitial cystic disease of the popliteal artery.

The changes that occur with acute hypoperfusion are numerous and oftentimes referred to as the “reperfusion syndrome.” The decreased perfusion will eventually result in tissue infarction and cell death. The time necessary for this to occur is highly variable based on tissue type. Muscle, the dominant tissue in the lower extremity, can typically tolerate ischemia for up to 6 hours prior to irreversible changes; this depends on the amount of collateral flow available.

Hypoperfusion is associated with microcirculatory changes in the muscle. These include swelling of endothelial cells and thrombosis of arterioles and venules. In addition, there can be propagation of thrombus within the macrocirculation, and this can occlude collateral channels and increase the severity of the ischemia.

Expeditious reversal of ischemia is the best method to use for avoiding the complications of the reperfusion syndrome and its sequelae; however, reperfusion itself may also result in serious complications. Reperfusion releases oxygen metabolites, acid, potassium, and cardiodepressants into the macrocirculation. These changes can result in cardiac arrhythmias, as well as damage and swelling of the reperfused tissues, a process that can eventually manifest as a compartment syndrome. In addition, the “no reflow” phenomenon is related to thrombosis of the microcirculation, and even with pulsatile arterial flow, tissues may remain ischemic.

Each of these changes compounds the complexity and difficulty of managing the patient with acute lower-extremity ischemia and emphasizes the need for expeditious revascularization and appropriate postoperative care.

Initial evaluation of acute lower-extremity ischemia requires:

When a patient is initially evaluated, the degree of ischemia should be categorized. In 1997 the Society for Vascular Surgery/International Society for Cardiovascular Surgery-North American Chapter created reporting standards of extremity ischemia (Table 56-1). These categories can also be used to guide the urgency of revascularization. In this system, category I is a viable limb; category II is a threatened limb; and category III is irreversible ischemia. Patients with category I ischemia have no motor or sensory loss, and arterial Doppler signals are present. These patients can generally be evaluated and treated in an elective fashion—the ischemia is not critical and does not require emergent treatment. An example of a patient in this category may be one who has developed a superficial femoral artery occlusion on pre-existing atherosclerotic disease. Such a patient will often have new onset claudication, and presentation may even be delayed for weeks or months after symptom onset. Category II (threatened limb) is further divided into IIA and IIB. Patients in IIA have minimal sensory loss (i.e., toes) and no motor loss. These patients have absent Doppler signals. IIB patients have sensory loss more severe than IIA, but more importantly, they have motor function loss of any degree. They also have absent Doppler signals. The distinction between IIA and IIB is critical, because it determines the urgency of the patient’s treatment. A patient with any motor function loss requires rapid revascularization if the limb is to be salvaged and remain functional. The patient with sensory loss only can be managed with a somewhat less urgent approach. Category III includes mottling of the skin, anesthesia, and paralysis of the limb. If this is early (<3 hours), revascularization may still be worthwhile; otherwise the damage is often permanent and amputation may be the best option.

In addition to assessing the degree of ischemia and the urgency of repair, determining the etiology of the ischemia is helpful, because it can have consequences regarding the ultimate management of the patient. The presence or absence of bypass grafts can be determined by examining for appropriate incisional scars. In addition, bypass graft occlusion can be diagnosed with duplex scanning, although this should not unnecessarily delay treatment. Arterial thrombosis of an atherosclerotic artery is usually associated with a past history of claudication and often will have diminished ankle-brachial indices (ABIs) in the contralateral limb. When an embolism of cardiac origin is the cause of the patient’s acute ischemia, often atrial fibrillation or MI will be diagnosed with electrocardiogram or cardiac enzyme elevation. While the contralateral extremity may have a normal arterial exam, the elderly population prone to arterial embolism may manifest coincidental atherosclerotic disease in the contralateral limb. Aortic dissection should also be considered when evaluating the patient with the acutely ischemic lower extremity. These patients have a history of tearing chest or back pain and hypertension. Limb pressure discrepancies may also exist in the upper extremity. Rapid diagnosis is usually available in the form of contrast computed tomographic scanning or transesophageal echocardiogram.

When performing the physical exam, one should document the pulse status and quality as well as Doppler-derived ABIs. The pulse exam can guide one in differential diagnosis and in surgical approach. For example, a common femoral artery embolism will often result in coolness of the extremity from the mid-thigh distally and
severe ischemia of the lower extremity due to occlusion of both the profunda and superficial femoral arteries. In addition, the artery itself might feel rubbery with embolism and have a strong (“water hammer”) pulse proximally. If thrombosis is the cause of ischemia, the common femoral may feel “rocky” hard and ischemic findings may not be as severe. Patients with popliteal trifurcation level thrombosis or embolism will have palpable femoral and popliteal pulse and coolness, and ischemia will begin in the mid-calf distally. These findings are important in guiding subsequent surgery and incisions.