ACUTE LIMB ISCHEMIA

Acute limb ischemia (ALI) arises when a rapid or sudden decrease in limb perfusion threatens tissue viability. This form of ischemia may be the first manifestation of arterial disease in a previously asymptomatic patient or may occur as an acute event that causes symptomatic deterioration in a patient with antecedent lower extremity PAD and intermittent claudication (308).

The severity of ALI depends on the location and extent of arterial obstruction and the capacity of the collaterals to perfuse the ischemic territory. Severity may be influenced by the status of systemic perfusion (cardiac output and peripheral resistance). Acute limb ischemia is often associated with thrombosis due to atherosclerotic plaque rupture, thrombosis of a lower extremity bypass graft, or lower extremity embolism originating from the heart or a proximal arterial aneurysm.

When embolic occlusion affects a vascular bed not previously conditioned by collaterals, the resulting ischemic syndrome is typically severe. Collateral development in relation to the severity and chronicity of pre-existing ischemia due to atheromatous obstructive arterial disease lessens the severity of ischemia when acute thrombotic arterial occlusion develops. Arterial embolism is more likely than arterial thrombosis to cause sudden, severe, limb-threatening ischemia.

The hallmark clinical symptoms and physical examination signs of ALI include the 5 “Ps” that suggest limb jeopardy: pain, paralysis, paresthesias, pulselessness, and pallor. Some clinicians would also include a sixth “P,” polar or prostration, to indicate a cold extremity or the patient’s sufferances respectively. In certain clinical settings, however, arterial embolism can occur without symptoms, whereas thrombosis can produce sudden, severe limb ischemia.

The clinical diagnosis of arterial embolism is suggested by (a) the sudden onset or sudden worsening of symptoms, (b) a known embolic source (including atrial fibrillation, severe dilated

cardiomyopathy, left ventricular aneurysm, atheromatous plaque in the aorta or proximal limb arteries, or mural thrombus lining the wall of an aortic or arterial aneurysm), (c) the absence of antecedent claudication or other manifestations of obstructive arterial disease, or (d) the presence of normal arterial pulses and Doppler systolic blood pressures in the contralateral limb.

Arterial emboli typically lodge at branch points in the arterial circulation where the caliber of the arterial lumen diminishes (i.e., bifurcations). Embolism to the aortoiliac bifurcation (“saddle embolus”) may produce bilateral lower-limb ischemia occasionally associated with reversible paraplegia and a high mortality rate (308, 309). Embolic occlusions at sites of arterial bifurcation may cause more

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profound ischemia when collaterals of perfusion are interrupted, as occurs when the profunda femoris artery is compromised by embolism to the more proximal common femoral artery.

Acute limb ischemia may also occur as a result of acute arterial thrombosis superimposed on a stenotic atherosclerotic plaque. A common site of thrombosis is the superficial femoral artery, although occlusion may occur anywhere from the aorta to the digital arteries. Rarely, an extrinsic local factor such as popliteal entrapment, cystic adventitial disease, or repetitive trauma may be the precursor of arterial thrombosis. The location of the obstruction in relation to other axial arteries in the region of the obstructed vessel and the collateral flow they provide also affects the severity of ischemia. The longer the obstructive lesion, the more collateral pathways that are interrupted. Thrombosis tends to

propagate proximally in an artery, up to the next large side branch. The low flow state distal to the obstructing thrombus also encourages distal propagation of thrombus. This is the rationale for treating patients promptly with systemic anticoagulation.

Typically, pulselessness, pallor, paresthesias, paralysis, and coolness characterize acutely ischemic limbs, and assessment of these features is aided by comparison with the contralateral limb.

Evaluation of “capillary” return, which reflects the emptying and refilling of subpapillary venules, is subject to considerable environmental and interobserver variation, but capillary return is usually slow or absent in ALI. Some, but not all, patients with sensory loss describe numbness or paresthesias, but pre-existing sensory deficits in diabetic patients can lead to confusion. Motor deficits indicate

advanced, limb-threatening ischemia, in part because foot movement is produced mainly by more proximal muscles. Dorsiflexion or plantar flexion of the great toe is produced by muscles that originate just below the knee that are innervated by the peroneal nerve that passes through the anterior tibial compartment.

Persistent pain, sensory loss, and toe muscle weakness are among the most important findings that identify the patient with threatened limb loss. Muscle rigor, tenderness, and pain on passive movement are late signs of advanced ischemia predictive of tissue loss.

According to the TASC II guidelines, ALI is defined as a sudden decrease in limb perfusion that causes a potential threat to limb viability (manifested by ischemic rest pain, ischemic ulcers, and/or gangrene) in patients who present within two weeks of the acute event (2). Patients with similar manifestations who present later than two weeks are considered to have CLI, which is by definition chronic.

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The management of acute arterial occlusion remains a challenge for vascular specialists.

Surgical thromboembolectomy and bypass grafting were the mainstays of therapy for many years (310). Subsequently, thrombolytic therapy ± thrombectomy procedures ± PTA ± stenting have become treatment options for selected patients.

Despite these advances, the morbidity, mortality, and limb loss rates from acute lower extremity ischemia remain high. Thus, regardless of the treatment modality used, early diagnosis and rapid initiation of therapy are essential in order to salvage the ischemic extremity.

152 8.1 ETIOLOGIES

Acute arterial occlusion can be the result of emboli from a distant source, acute thrombosis of a previously patent artery, or direct trauma to an artery.

8.1.1 Arterial emboli

Eighty percent of arterial emboli originate in the heart and travel to the extremities; the lower extremities are affected much more frequently than the upper extremities. The majority of these emboli occur in patients with significant underlying cardiac disease; the severity of the patient's underlying cardiac condition may increase the risk of surgery, and limit the options available for restoring blood flow to the ischemic extremity.

Potential sources of emboli from the heart include left ventricular thrombus formation following myocardial infarction, and atrial thrombus in patients with atrial fibrillation. Up to 75% of patients with emboli to the lower extremities have a history of recent myocardial infarction or atrial fibrillation.

Arterial to arterial embolization of thrombus or plaque originating from aneurysms or atherosclerotic lesions is another well described occurrence and accounts for 20% of peripheral emboli.

Emboli typically lodge where there is an acute narrowing of the artery, such as an

atherosclerotic plaque or a point where the vessel branches (i.e., bifurcations): the common femoral, common iliac, and popliteal artery bifurcations are the most frequent locations. In a large series of arterial embolism, for example, the following frequencies were noted:

 Femoral — 28%

 Arm — 20%

 Aortoiliac — 18%

 Popliteal — 17%

 Visceral and other — 9% each

In comparison to clot emboli, atheroemboli are less likely to produce symptoms of acute arterial occlusion. Atheroemboli are typically nondistensible and irregularly shaped; as a result, they tend to

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produce incomplete occlusion with secondary ischemic atrophy. One exception is the blue toe syndrome (see above).

8.1.2 Arterial thrombosis

Thrombosis of a previously patent but stenotic artery is a well-known complication of atherosclerosis. Occlusion of atherosclerotic vessels may occur by two mechanisms:

 Progressive atherosclerotic narrowing of the artery, with resultant low flow, stasis, and finally thrombosis

 Plaque’s rupture with consequent intraplaque hemorrhage and local hypercoagulability leading to thrombosis.

The ischemia resulting from arterial thrombosis in the face of underlying atherosclerosis is usually less severe than that following an acute embolus. This difference is primarily due to the collateral circulation that develops over time in patients with atherosclerosis and chronically narrowed vessels. Collaterals are frequently so extensive that patients notice no change or only a mild increase in their symptoms of chronic ischemia when a major atherosclerotic vessel becomes occluded.

Arteritides, ergotism, and hypercoagulable states can also result in arterial thrombosis, occlusion, and acute extremity ischemia. While these conditions most frequently affect the venous circulation, certain hypercoagulable states favor arterial thrombosis (e.g., antiphospholipid antibodies and hyperhomocysteinemia).

8.1.3 Arterial trauma

Acute arterial occlusion complicating vascular or cardiac diagnostic and interventional

procedures has become a more frequent cause of acute extremity ischemia. The incidence of arterial complications following interventional cardiac catheterization (including hematomas, arteriovenous fistulae, pseudoaneurysms, arterial occlusion, and cholesterol emboli) has been reported to range from 1.5 to 9% (311). Although acute arterial occlusion occurs in less than 1% of interventional catheterization procedures, this complication demands immediate surgical or endovascular management (312). Intimal flaps and dissections are frequently the cause of the occlusion, and an endovascular repair of the vessel is often required. Thromboemboli can also develop at the sheath site or catheter tip, with embolization occurring during sheath removal.

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8.1.3.1 Differential Diagnosis of Acute Limb Ischemia:

The differential diagnosis of ALI involves exclusion of conditions that mimic arterial occlusion, identification of non-atherosclerotic causes of arterial occlusion, and differentiation of ischemia caused by an arterial thrombosis from embolism.

Non-atherosclerotic causes of ALI include arterial trauma, vasospasm, arteritis, hypercoagulable states, compartment syndromes, arterial dissection, and external arterial compression, such as occurs with a popliteal cyst.

Other conditions that may mimic arterial occlusion are acute deep venous thrombosis, especially when associated with features of phlegmasia cerulea dolens; and acute compressive peripheral neuropathy.

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