Acute Lower Extremity Ischemia

Raymond W. Liu, Hani H. Abujudeh, David W. Trost and Krishna Kandarpa

Acute lower extremity ischemia (ALEI) is a serious condition with substantial morbidity and mortality. ALEI refers to recent onset of lower extremity pain; long-standing lower extremity ischemia is dealt with elsewhere in this book. If ALEI is severe and prolonged, the patient may develop progressive paresthesia, motor dysfunction, and eventually tissue infarction in the lower extremity. The rapidity plus severity of the onset of symptoms is dependent on the location, extent, and degree of collateral pathways around the obstruction. The estimated incidence of ALEI is approximately 1.5 cases per million each year. The two principal causes of ALEI are (1) embolic, in which an artery may become occluded when an embolus becomes dislodged from a proximal source, and (2) thrombotic, in which occlusion of a native artery occurs in the setting of severe atherosclerotic disease. Patients who have an embolic etiology to their presentation often present early (within hours of the embolic event) owing to lack of collateral flow, whereas patients with a thrombotic etiology may present more slowly over a day or so. The clinical presentation of ALEI has classically been stated as the six Ps: pain, pallor, pulselessness, paresthesia, paralysis, and poikilothermia (inability to regulate body temperature).

An acute profoundly ischemic limb is a surgical emergency. Cell death begins within 4 hours of total ischemia and is irreversible after 6 hours. Revascularization in this setting may result in sudden tissue reperfusion and lead to a systemic acid-base disorder and impaired cardiopulmonary function.¹ In the late 1970s, Blaisdell et al. documented mortality rates in excess of 25% after open surgical repair of ALEI.² Operative mortality remains high despite advances in surgical technique and management.³ Amputation rates can vary from 10% to 30%.⁴

Treatment generally begins with early anticoagulation with heparin to limit propagation of the thrombus. This has traditionally been followed by surgical thromboembolectomy and correction (patch angioplasty or bypass graft) of the culprit lesion to restore arterial flow.⁵

Thrombolytic therapy provides an attractive alternative to open surgery because it offers several advantages. It is a less invasive procedure, since it not only dissolves the primary arterial thrombus but also helps clear the microcirculation, thereby resulting in gradual reperfusion and averting the release of anaerobic metabolites and thus helping reduce the potential for sudden reperfusion and compartment syndrome.¹

In the 1970s, intravenous thrombolytic agents (e.g., streptokinase) were shown to restore patency in acutely occluded arteries in 75% of cases.⁶ However, systemic infusion of thrombolytic agents carries a high risk of remote bleeding complications and has largely been abandoned in favor of catheter-directed local thrombolytic therapy. Local intraarterial thrombolytic therapy has gained popularity over the past 20 years and in many cases, barring contraindications, is the initial intervention of choice. Thrombolytic agents are infused directly into the occluding thrombus in a concentrated fashion so systemic drug concentration and the total dose required for the procedure are reduced. As flow is restored, the underlying culprit lesion is usually unmasked and managed by interventional or surgical techniques.

Indications

A classification system was devised by the Society for Vascular Surgery (SVS, United States) and updated by The TransAtlantic Inter-Society Consensus (TASC) II guidelines in 2007 for describing the degree of acute limb ischemia (Table 33-1). The main objective of this categorization is to stratify the acuity of limb ischemia into defined groups for decision-making purposes. The TASC II guidelines also suggest an algorithm for the diagnosis and treatment of acute limb ischemia (Fig. 33-1).⁷

TABLE 33-1

Society for Vascular Surgery Clinical Categories of Acute Limb Ischemia

Category	Definition	Prognosis	Physical Examination		Doppler Signals
Category	Definition	Prognosis	Sensory Loss	Muscle Weakness	Arterial	Venous
I	Viable	Not immediately threatened	None	None	+	+
II	Threatened
II-a	Marginally	Salvageable with prompt treatment	Minimal (toes)	None	Occasional +, frequently −	+
II-b	Immediately	Salvageable with immediate treatment	More than toes, pain at rest	Mild to moderate	Rare +, usually −	+
III	Irreversible	Major permanent tissue loss	Anesthetic	Paralysis	−	−

Modified from Rutherford RB, Baker JD, Ernst C, et al. Recommended standards for reports dealing with lower extremity ischemia: revised version. J Vasc Surg 1997;26:517–38. ^©The Society for Vascular Surgery and the North American Chapter of the International Society for Cardiovascular Surgery.

Percutaneous intraarterial thrombolysis (PIAT) is indicated in patients who have acute-onset claudication (SVS I, the limb is generally viable) or limb-threatening ischemia (generally SVS II-a, but also SVS II-b) due to thrombotic or embolic arterial occlusion.5,8 McNamara et al. described occlusion patterns and found that all patients with a single occluded segment but normal inflow and patent collaterals (generally SVS I) successfully underwent PIAT, with no deaths or amputations.⁵ In patients with normal inflow and patent collaterals but tandem occluded segments, PIAT was successful in 90% and had a mortality of 0.7% and a limb loss rate of 8.2%. In patients with irreversible limb ischemia (SVS III), PIAT has unacceptably high morbidity and mortality and is therefore not indicated (see Fig. 33-1). Patients who are considered to have viable or marginally threatened limbs may have imaging performed prior to angiography and thrombolytic therapy. Available modalities include duplex ultrasonography, computed tomographic angiography (CTA), and magnetic resonance angiography (MRA).

Previously thrombolysis was used to clear the acute thrombosis of a popliteal aneurysm to visualize a suitable distal runoff vessel for surgical bypass when the initial diagnostic arteriogram failed to do so.⁹ These days, with the availability of MRA, which has high sensitivity for demonstrating these distal vessels, this practice has been abandoned for the most part.

Indications for salvage of a graft require consideration of the individual case.¹⁰ There are twin goals of removing the clot and correcting the underlying lesion. If the underlying lesion is secondary to diseased inflow or outflow, progression of atherosclerotic disease is usually the primary etiology. In this scenario, treatment with angioplasty/stent or bypass grafting has demonstrated success. If the underlying lesion is secondary to intrinsic graft disease, either intimal hyperplasia or graft stenosis is usually the primary etiology. The type of conduit can guide treatment, since prosthetic grafts will develop intimal hyperplasia, while venous bypass grafts often develop stenosis at the site of a valve. Prosthetic grafts may not have successful long-term results with angioplasty and require surgical graft thrombectomy and patch angioplasty. Venous bypass grafts can be treated successfully by angioplasty and/or stenting.

Contraindications

Relative and absolute contraindications are listed in Table 33-2. Absolute contraindications include active internal bleeding, cerebrovascular events such as a recent (within 6-12 months) cerebrovascular accident or a transient ischemic attack (within 2 months), known intracranial neoplasm, or craniotomy within 2 months.