Acute limb ischemia (ALI) occurs in the setting of inadequate blood flow and therefore, oxygen delivery to an extremity. This state of hypoperfusion leads to systemic acid–base abnormalities and electrolyte disturbances that ultimately affect cardiopulmonary and renal function in patients managed in the intensive care unit (ICU). Revascularization of an ischemic limb leads to an additional host of metabolic problems as toxic byproducts that build up in the ischemic tissue bed and inflammatory mediators are released. ALI is a vascular emergency with 30-day mortality rates of 15% and amputation rates of 10% to 30% reported in the literature [1]. This chapter outlines common etiologies, diagnosis, and treatment strategies to manage acute lower extremity ischemia in patients that are often critically ill.

The most common etiologies of ALI can be separated into two categories consisting of either embolism or thrombosis. Embolic events result from the detachment of thrombus or atherosclerotic plaques from proximal sources and often result in extreme peripheral ischemia as emboli may become lodged in a previously normal artery without significant collateral vasculature. Cardiac sources of emboli constitute 80% to 90% of peripheral emboli [2]. Myocardial infarction and cardiac arrhythmias such as atrial fibrillation lead to stasis and dilation of the left atrium and ventricle resulting in the formation of a cardiac thromboembolic source [3,4]. The presence of valvular heart disease and prosthetic heart valves are additional sources of cardiac emboli. Noncardiac sources of emboli include arterial aneurysms, ulcerated atherosclerotic plaque, and paradoxic emboli from venous thrombi. Additional noncardiac sources of emboli may occur with recent vascular interventions such as aortic surgery, percutaneous interventions with the passage of wires and catheters or balloon pump placement. The contribution of noncerebral emboli to the development of acute limb ischemia is illustrated by the observance that two-thirds of emboli travel to the lower extremity vasculature. One-half of these emboli obstruct iliofemoral arteries and the remaining half obstructs the popliteal and tibial vessels [5].

Thrombotic occlusions may occur in either native arteries or bypass grafts. Thrombosis of a native artery occurs with progression of an atherosclerotic lesion or rupture of an unstable plaque. Thrombotic occlusions occur most frequently at the site of arterial bifurcations or at areas of anatomic compression such as the superficial femoral artery at the level of the adductor canal [6]. Arterial trauma from fractures, dislocations, blunt injury, bullet wounds, or catheter access may result in pseudoaneurysms, intimal flaps, or dissections and may progress to acute thrombosis of a native artery. Femoral or popliteal aneurysms may also be responsible for ALI by either embolism of thrombus from the aneurysm or thrombosis of the aneurysm itself and occlusion of distal perfusion in the setting of inadequate collateral formation. More commonly,
thrombosis in situ occurs with occlusion of bypass grafts. Occlusion of a bypass graft in the immediate postoperative period is typically secondary to a technical defect. Occlusions of bypass grafts at later time periods may be due to intimal hyperplasia, progression of distal disease, low flow states experienced by critically ill patients, or acquired hypercoagulable states. In general, ALI secondary to thrombosis in situ or bypass graft occlusion may manifest as an acute-on-chronic process with less profound ischemia due to collateral formation not seen with acute embolic events. Therefore, management may not require immediate surgical revascularization and it is possible to proceed with initial nonoperative management including preoperative imaging such as angiography and thrombolytic therapy.

Other etiologies of ALI include aortic dissection creating malperfusion, intense vasospasm resulting from drugs such as cocaine, ergots or vasopressors, and hypercoagulable disorders. Alterations in coagulability have been attributed to both venous and arterial thromboembolism. Increases in coagulation activity in the arterial system in the ICU population have been observed in multitrauma victims, septic patients, and in the setting of heparin-induced thrombocytopenia (HIT) and disseminated intravascular coagulation (DIC) [7,8]. Likewise, inherited coagulation disorders are associated with arterial occlusions. Circulating antiphospholipids (lupus anticoagulant and anticardiolipin antibodies), gene mutations (prothrombin, factor V Leiden, methylene tetrahydrofolate reductase), alterations in activity levels of protein C and S, deficiencies of antithrombin III, and protein C&S have all been shown to contribute to the pathogenesis of arterial thrombosis [9].

A careful history and physical examination is important in determining the etiology, establishing the extent of ischemia, and determining appropriate treatment of patients with acute lower extremity ischemia. Frequently, patients in the ICU are unable to provide valuable history regarding possible comorbidities that may contribute to the acute onset of their ischemia, coexistence of chronic arterial ischemia, and information concerning the onset of symptoms. Therefore, a careful review of the patient’s medical history including a history of atrial fibrillation, coagulation disorders, recent percutaneous interventions, imaging demonstrating mural thrombus or aneurysmal disease, history of claudication or rest pain, and past lower extremity revascularization procedures should be performed. Risk factors including coronary artery disease, hypertension, diabetes mellitus, hyperlipidemia and history of tobacco use should also be assessed.

A thorough physical examination is necessary to determine the duration and extent of ischemia that will ultimately determine the most suitable algorithm for treatment. Both lower extremities should be evaluated for signs of chronic disease including sparse hair growth, elevation pallor, dependent rubor, dystrophic nail growth, or chronic ulcers. Identifying the 6 “Ps” of acute ischemia including paresthesia, pain, pallor, pulselessness, poikilothermia, and paralysis is a useful tool to help establish the diagnosis and duration of acute ischemia. Initially, patients may experience pain in an ischemic limb that may progress to sensory deficit and eventually to paralysis. In addition, the level of pallor, coolness, or mottling may assist in determining the level of arterial injury of obstruction. Frequently, ischemic findings are most severe one joint distal to the level of obstruction.

A pulse exam may provide important clues about the underlying pathology but may also be misleading secondary to the subjectivity of this physical examination finding. Findings such as a “water-hammer” pulse indicating pulsation against an occlusion may be present following embolism or early thrombosis. A palpable thrill, audible bruit, or hematoma may indicate pseudoaneurysm or arteriovenous fistula in the setting of noniatrogenic or iatrogenic trauma seen with percutaneous interventions. If used correctly, continuous wave Doppler is a crucial tool in the bedside evaluation of the ischemic limb. A normal triphasic signal consists of forward systolic, reverse systolic and forward diastolic flow. A monophasic signal is characterized as a signal without pulsatile variability and signifies a proximal obstruction. Ankle–brachial indices (ABI) may also be obtained at the bedside and consist of calculating a ratio of ankle-to-brachial pressure. Abnormal results (< 0.9) must be interpreted with caution as medial calcification of vessels frequently observed in diabetics yield an ABI > 1. This occurs as calcifications prevent vessels from being compressed by a pneumatic cuff. ABIs may also be decreased at baseline in those patients with chronic lower extremity ischemia. Therefore, in a situation of suspected acute ischemia, ABIs should be compared between limbs and to ABIs obtained before the event if this value was recorded.

Further diagnostic testing may be required for operative planning but institution limitations and the urgency of revascularization should be considered when obtaining additional tests. Arterial duplex ultrasound is valuable for determining occlusive lesions, bypass graft occlusions, and the presence of distal and proximal arterial disease. This noninvasive test is operator dependent but has been shown to correlate with contrast angiography findings [10]. Digital subtraction angiography is considered the gold standard for diagnostic imaging in the acute setting. This testing modality provides anatomical detail concerning the offending lesion, presence of chronic atherosclerotic disease, and the status of distal arterial targets. Findings will assist in planning operative intervention including thrombectomy, bypass, or further percutaneous intervention. In addition to its diagnostic advantages, angiography may also be used as a therapeutic modality with the institution of catheter directed therapies. Adverse effects of contrast angiography include nephrotoxicity from contrast administration, embolization, and access site complications including dissection, pseudoaneurysm, arteriovenous fistula, and bleeding. Further imaging with CT or MRI may be necessary if aortic dissection or aortoiliac occlusion is suspected. Otherwise, these tests are time consuming and may not supply information regarding distal arterial runoff that cannot be obtained by angiography in the patient requiring urgent revascularization.

Planning revascularization of the acutely ischemic limb requires consideration of the patient’s overall medical condition, likely etiology and the viability of the ischemic limb. If the patient is not medically stable to proceed to the operating room or angiography suite, revascularization may be postponed in the interest of preserving “life over limb.” In addition, revascularization of an ischemic limb with permanent ischemic nerve or muscle damage may result in a nonfunctional limb and primary amputation may be the most effective treatment strategy. Predicting the urgency of revascularization required to salvage an acutely ischemic limb is a difficult task and treatment paradigms have evolved with the advent of catheter directed thrombolytic therapy. The goal of the revised Rutherford Criteria proposed by The Society for Vascular Surgery and International Society for Cardiovascular Surgery (SVS/ISCVS) is to stratify levels of severity of ALI (Table 154.1). Category I limbs are considered viable with no sensory or muscle deficits. This category includes limbs that are not immediately threatened and may be managed either without an intervention or after a thorough evaluation. Class II limbs have been stratified into two subcategories. Class IIa limbs are marginally threatened
with minimal sensory loss. This category of ischemic limbs can be salvaged with appropriate revascularization directed by further studies such as angiography. Class IIb limbs are immediately threatened with more profound sensory loss and mild-to-moderate muscle weakness. Salvage of Class IIb limbs should be managed with emergent revascularization efforts [11].