The incidence of ALI is estimated to be 14 per 100,000 with men and women being equally affected. Most patients with peripheral arterial disease (PAD) present with chronic symptoms such as claudication, rest pain, or gangrene rather than ALI. However, patients who have had previous bypass surgery may present with ALI if their bypass graft occludes.

A useful limb ischemia categorization system has been put forth by the Society for Vascular Surgery/International Society for Cardiovascular Surgery joint council (Table 7.1) and is also known as the Rutherford Classification for ALI. Class I represents a viable limb that is not immediately threatened. No sensory deficit or muscle weakness is present, and arterial and venous Doppler signals are audible. Chronic ischemic rest pain is an example of Class I ischemia. Class IIa is a marginally threatened limb, with minimal to no sensory loss, normal motor function, and inaudible arterial Doppler signals, but audible venous Doppler signals are present. Class IIb is an immediately threatened limb that requires rapid revascularization and is associated with sensory loss and muscle weakness with inaudible arterial signals. Class III is irreversible limb ischemia, with major tissue loss or permanent nerve damage and an insensate and paralyzed limb with rigor and inaudible arterial or venous signals. Patients with class III ischemia usually require primary amputation. These categories are a simple and useful way for clinicians to communicate with each other about ALI patients and their urgency and also represent a reporting standard for clinical research.

The most common etiology of ALI is embolization. Seventy five percent of embolic ALI is cardiogenic. In this context, left atrial appendage thrombus developing in the setting of atrial fibrillation and left ventricular mural thrombus formation after myocardial infarction are the most clinical scenarios and may often occur after recent infarction or postcardioversion, but thrombi forming in a left ventricular aneurysm or in the setting of valvular disease (mitral) are also not uncommon. Proximal aneurysm of a major artery or plaque atheroembolization accounts for 25% of embolic ALI. Rarely, embolic material may pass from the right-sided circulation to the left through a patent foramen ovale or may be related to a mechanical valve, endocarditis, or myxoma. Emboli usually lodge at arterial bifurcations, including the aortic bifurcation, the femoral bifurcation, or the tibial trifurcation. The other primary pathophysiologic mechanism of ALI is in situ thrombosis. Whereas in many cases embolization occurs in patients
who may not have preexisting vascular disease, thrombosis is typically seen in patients with underlying PAD who sustain a thrombotic event involving a chronically stenosed axial vessel, a large collateral pathway, or perhaps a previously placed bypass graft. Other less common etiologies of ALI include trauma, for example, popliteal artery disruption with posterior knee dislocation, or dissection, such as in the aorta with propagation of a dissection flap causing occlusion of an iliac artery.

Common presenting features of the two primary entities that cause ALI are listed in Table 7.2. Clinically, the diagnosis of ALI may be obvious, and the six Ps apply: pain, poikilothermia, pulselessness, paresthesias, paralysis, and pallor. However, some patients may present with subtle changes or a primary neurologic complaint such as numbness or acute paralysis without pain. If a careful history and thorough pulse exam are not obtained, this may lead to a fatal outcome as the patient is sent for consultation and other diagnostic measures, delaying reestablishment of limb blood flow.

History and physical examination often will identify the etiology and location of ALI as well as make the diagnosis and, therefore, are critical in directing therapy in the most efficient manner. Patients with embolic ALI tend to have a more abrupt onset of pain and present with a very cold and mottled extremity with a clear demarcation, usually one level below where the embolus is lodged. While some patients with embolic ALI may have preexisting PAD and robust collateral pathways, most do not, and therefore their ischemia is often profound and may fall into the IIb or III category. Other clues that embolism is the cause of ALI may include a recent cardiac event (such as a recent anterior wall myocardial infarction or a recent cardioversion), a recent history of palpitations, recent discontinuation of anticoagulation, a lack of antecedent claudication, and the presence of normal pulses in the unaffected limb.

By contrast, patients with in situ thrombosis may have a vaguer onset of pain, with no recent cardiac events, though typically they do have coronary artery disease. An antecedent history of claudication or other symptoms of PAD is present, the limb is cool and more bluish than mottled, and no distinct demarcation is present. Pulses in the unaffected limb are often not palpable and only can be heard with a continuous-wave handheld Doppler. In situ thrombosis is much more likely if the patient has had a prior surgical or endovascular revascularization. These patients usually fall in the IIa category, as collateral pathways are often already developed, mitigating the effect of acute occlusion of a diseased axial vessel.

The special situation of aortic dissection deserves mention. A severely hypertensive patient or a patient with risk factors for a connective tissue disorder whose initial presentation includes chest or back pain prior to the onset of ALI must expeditiously be worked up for aortic dissection, which dramatically alters treatment if present.