Acute Arterial Occlusion

Acute Arterial OcclusionAcute arterial occlusion characterized by the abrupt onset of severe pain, coldness, numbness, motor weakness, and absent pulses in the involved extremity. When ischemia persists, motor and sensory paralysis, muscle infarction, and gangrene become irreversible in a matter of hours. If left untreated, a line of demarcation will develop between viable and nonviable tissue. Flow in the distal arteries is reduced progressively by propagating intraluminal thrombus, and surgical restoration of blood flow to the ischemic portion of the extremity eventually becomes impossible.

Acute major arterial occlusion may be caused by an embolus, thrombosis, trauma, or dissection. The heart is the source in 80–90% of episodes, with the remainder from proximal arterial lesions. Aortic aneurysms often contain thrombi but they rarely embolize. In contrast, femoral and particularly popliteal aneurysms embolize frequently. Miscellaneous infrequent sources of emboli include cardiac tumors (including cardiac myxoma) and paradoxic emboli (venous thrombi migrating through a patent foramen ovale).

It may be difficult to differentiate between sudden thrombosis of an atherosclerotic peripheral artery and embolic occlusion. The former patients have preexisting atherosclerotic stenosis and low blood flow, which predisposes to stagnation and thrombosis. One should also keep in mind the clinical setting and a history of preexisting symptoms such as atrial fibrillation (embolus) or claudication (primary thrombosis).

Clinical Findings

Acute arterial occlusion is characterized by the five Ps: pain, pallor, pulselessness, paresthesias, and paralysis. Severe sudden pain is present in 80% of patients, and its onset usually indicates the time of vessel occlusion. Pain is absent in some patients because of prompt onset of anesthesia and paralysis and portends a poor prognosis.

On examination, pallor may be replaced by mottled cyanosis as deoxygenated blood gradually suffuses the extremity. It is important to determine if sensitivity to light touch is maintained. These fibers are highly susceptible to ischemia and their dysfunction heralds the beginning of irreversible ischemic changes. The onset of motor paralysis implies impending gangrene. Early intervention is critical. Swelling with acute tenderness of a muscle belly—usually in the calf following acute femoral artery occlusion—generally denotes irreversible muscle infarction. Skin and subcutaneous tissues have greater resistance to hypoxia than nerves and muscles, which may demonstrate irreversible histologic changes after as little as 3–4 hours of ischemia.

Treatment of Acute Arterial Occlusion

Embolism and Thrombosis

Immediate anticoagulation by intravenous heparin slows the propagation of thrombus and allows time for assessment of adequacy of collateral flow and preparation for operation. If light touch is intact, arteriography may be performed to define the anatomy and assist in planning the operation. Diagnosis of acute embolic occlusion is based upon an abrupt block of the artery with little accompanying arterial disease; conversely, acute in situ thrombosis is associated with extensive atherosclerosis and a well-established collateral network. The operative treatment of an embolus differs from that of preexisting atherosclerosis, which may require bypass.

Nonoperative management is reserved for emboli to major arteries in the upper extremities, where collateral circulation is outstanding, and for the rare event in the lower extremities when skin color improves or neural function returns quickly after an initial ischemic episode. If the initial ischemia recedes, the decision for removal of the embolus is based upon an estimate of the disability that will be produced by chronic occlusion of the involved artery. Chronic occlusion of the axillary or brachial arteries is usually well tolerated, whereas chronic occlusion of lower extremity vessels causes claudication, if not rest pain, and should be removed.

Therapeutic options include catheter-directed thrombolysis, percutaneous mechanical thrombectomy, and surgical embolectomy. For patients with severe acute ischemia, operative therapy is preferable because it is usually associated with the least delay in reestablishing perfusion. Surgical embolectomy may be performed through an arteriotomy at the site of the embolus or, most commonly, by extraction with a balloon (Fogarty) catheter inserted through a proximal arteriotomy. Successful embolectomy requires removal of the embolus and the “tail” of thrombus that extends distally or proximally from it. If operation is not performed within the first few hours, the clot may become adherent and subsequent revascularization is less successful. Intraoperative infusion of thrombolytic agents is often a useful adjunct to embolectomy.

Fasciotomy is normally required after prolonged acute ischemia to treat the compartment syndrome that may accompany the reperfusion injury. Renal insufficiency from myoglobin release should be anticipated after reperfusion of ischemic muscle. Treatment consists of vigorous hydration and alkalinization of the urine. Administration of free radical scavengers may be helpful in this disorder.

Patients with clearly irreversible limb ischemia should undergo amputation without an attempt at revascularization, as revascularization may expose the patient to the serious hazards of the reperfusion syndrome caused by release of acidotic and hyperkalemic venous blood from the dying extremity.

In patients who will tolerate a delay in revascularization, ie, those who do not have neural changes on examination, intra-arterial thrombolysis should be considered. The usual regimen involves selective intra-arterial infusion of low doses of thrombolytic agent (eg, tPA) directly into the clot. This activates thrombus plasminogen efficiently, allows high concentrations in the clot while limiting systemic effect, and has acceptable complication rates. In cases of thrombosis on preexisting atherosclerotic lesions, thrombolysis will reveal the underlying lesions. These should be treated to prevent recurrent thrombosis.

Traumatic Arterial Occlusion

Traumatic arterial occlusion must be corrected within a few hours to avoid development of gangrene. Repair of arterial injury is usually performed in conjunction with repair of other injuries.

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