Acute Limb Ischemia: Thrombectomy and Thrombolysis
S. Elissa Altin, MD
Senthilraj Ganeshan, MD
Key Points
Acute limb ischemia is a vascular emergency when viability of limb is threatened, and revascularization is recommended within 3-6 hours for acute presentations.
Clinical symptoms and signs include the 6 P’s: pain out of proportion to examination, diminished pulses, pallor, poikilothermia, paresthesias, and paralysis.
Limb loss at 30 days is reported to be as high as 30%-50%.
Endovascular revascularization with catheter-directed thrombolysis, rheolytic thrombectomy, and aspiration thrombectomy are common treatment options.
Surgical embolectomy and bypass are more invasive treatment methods.
I. Introduction
Acute limb ischemia (ALI) is a vascular emergency that occurs when the viability of an extremity and the life of the affected individual are threatened owing to a sudden interruption in arterial perfusion to a limb. It is most commonly the result of thromboembolic pathology.1 Many patients who develop ALI have occlusive peripheral arterial disease, but in the absence of preexisting atherosclerosis, ALI can still occur from embolic sources. Patients may present with profound symptoms, including disabling pain in the setting of acute vascular and neurologic deficits.2 The systemic release of inflammatory mediators as a result of ischemic injury may result in multiorgan dysfunction, which can become life-threatening.3 Patients with ALI are at high risk of amputation and death, making it crucial that practitioners establish the diagnosis early. Although mortality due to ALI has decreased, it is still estimated at 15% within the 30-day period from diagnosis.4,5 By definition, patients with ALI have a decrease in limb perfusion for less than 14 days. The Rutherford classification has assigned clinical categories useful for determining the severity of the threat to viability, urgency to revascularize, and the optimal approach to management.6
II. Epidemiology
A. Peripheral Arterial Disease
1. Despite the substantial clinical burden, there are limited data evaluating the epidemiology of ALI in a given population of patients with peripheral arterial disease (PAD). A population-based prospective cohort study of approximately 93,000 people in the United Kingdom recently described an incidence of ALI events in 10 per 100,000 per year, which is consistent with the findings of a prior large scale Swedish registry data set.7,8 Importantly, this study population was predominantly white (94%), making it difficult to use the findings to predict outcomes for other ethnic groups. Overall
survival at 30 days was 75.3% and 55.9% at 5 years. Amputation-free survival was 59.1% at 3 months, and future limb loss at 1 year was 7.5%. Among patients with ALI, 41.9% had prior PAD and 69% had a history of one or more forms of atherosclerotic cardiovascular disease. The investigators also found that when compared with the prospective registry data they collected over a 10-year period, routine hospital episode and death coding data missed approximately half of all acute ischemic episodes (combination of ALI, chronic limb ischemia, and acute visceral ischemia) and, in other cases, incorrectly labeled an event as an ischemic episode indicating that the incidence and prevalence rates derived from coding data may be inaccurate.8
2. According to the 2007 Trans-Atlantic Inter-Society Consensus (TASC), 30-day amputation rates have been reported to be 10%-30%, despite use of modern endovascular methods and mortality rates for ALI ranging from 15%-20%. The cause of death is not reported in most studies.9 In the TOPAS trial, 1-year mortality was 13.3% after catheter-directed thrombolysis and 15.7% after surgical revascularization.10
B. Thrombosis Importantly, over the past few decades, rates of thrombosis have risen while rates of embolism have declined without any significant change in the overall incidence of ALI.7,11,12 It is possible that this is partly due to improvements in the treatment of conditions responsible for embolic phenomena, including atrial fibrillation and valvular heart disease. With an aging population and an increase in the prevalence of the metabolic syndrome, peripheral arterial disease is an expanding epidemic, and a continued rise in the rate of thrombosis and the overall incidence of ALI can be anticipated owing to increasing disease burden and as a complication of endovascular and surgical treatment of the disease.
III. Etiology
A. Mechanisms of ALI Thrombosis and embolism are the two major mechanisms of ALI. In-situ thrombosis occurs in patients with underlying PAD or prior bypass grafting.13 Acute thrombosis of a limb artery often occurs at sites of prior stenosis owing to atherosclerotic disease, but can also occur at arterial aneurysms. Venous bypass grafts often develop anastomotic thrombosis, whereas prosthetic grafts may thrombose anywhere along the length of the conduit.13
B. Origin An estimated 85% of acute embolisms are of cardiac origin. Risk factors for embolic ALI include atrial fibrillation, apical myocardial infarction with subsequent ventricular thrombus formation, prosthetic heart valves, patent foramen ovale in association with paradoxical embolism, and thrombophilias. Extracardiac emboli arise from sources including aneurysms, atherosclerotic plaque debris, and venous thromboembolisms which enter the arterial system through intracardiac shunting. Aneurysm walls, due to abnormal or slow flow, often contain thrombus which can embolize distally. In particular, aneurysms of the aorta and popliteal artery are the most common sources of embolic ALI. Hematologic and thrombophilic conditions can additionally predispose to arterial thrombosis, including the antiphospholipid syndrome and heparin-induced
thrombocytopenia.9 Atherosclerotic plaque debris due to dislodgement is a major source of embolism during catheterization, as well as procedural catheter based thromboembolism.9 Emboli most commonly lodge at the bifurcation of the femoral artery, trifurcation of the popliteal, and aortic bifurcation.
IV. Clinical Presentation
A. Presentation
1. A classic presentation of ALI includes a constellation of signs and symptoms described as the classic six “P’s”: acute onset of pain out of proportion to examination, diminished pulses, early skin mottling (pallor), coolness to touch (poikilothermia), distal paresthesias, and paralysis. However, there are many factors which can alter the clinical presentation, including the location and duration of the arterial occlusion, the degree of collateral circulation, the extent of preexisting arterial disease (presence of collaterals), and the metabolic consequences of tissue ischemia.13
2. Patients are often easily able to recall the precise timing of the onset of pain, especially for those whose ALI is due to an embolization. Pain is usually severe but over time can relent because nerve damage ensues as ischemia progresses. Patients with PAD who have arterial thrombosis can present with a more gradual or stuttering presentation, as the severity of clinical ischemia is reduced owing to the formation of collaterals. Pallor or paleness below the level of obstruction occurs, and pulses may be absent or diminished when compared with the contralateral side. Temperature dysregulation occurs, causing the limb to be cool (poikilothermia), as the transfer of heat to the extremity is interrupted by inadequate blood flow. Most commonly these findings are located one joint distal to the level of occlusion. Late symptoms include paresthesias and paralysis which occur secondary to neural and muscular ischemia and death, respectively. Livedo reticularis may be seen if the embolization is to the more distal vessels.
B. Physical Examination
1. A thorough physical examination is necessary in the diagnosis of ALI and determination of its severity and the patient’s prognosis. The initial evaluation should include vital signs, the external appearance of the patient, the temperature of the skin, a detailed vascular examination including palpation of pulses in the femoral, popliteal, dorsalis pedis, and posterior tibial arteries of the affected and contralateral limb, and a neuromotor evaluation for sensation and muscle strength. A Doppler instrument should be used to establish if flow is present in distal arteries when a palpable pulse is absent.
2. In the event of a normal vascular examination on the contralateral limb, an embolic etiology of ALI is likely. In a patient presenting with symptoms consistent with thrombosis but no known history of PAD, physical findings to suggest underlying PAD include diminished extremity pulses, scant hair growth, atrophic skin, hypertrophied nails, and ischemic ulcers.
C. Rutherford Classification of Acute Limb Ischemia Patients should be categorized into a Rutherford stage of ALI based on their clinical presentation and physical findings which can guide decisions on their immediate management. Stage I includes those with typical presenting symptoms, audible arterial and venous Doppler signals, and preserved sensation and muscle strength on examination. Patients categorized as stage I have no immediate threat to limb viability. Stage II indicates that limb viability is threatened. In stage IIa the threat is marginal, with the limb considered salvageable if promptly treated. These patients have minimal sensory loss usually involving the toes, and the arterial Doppler signal is frequently inaudible. In stage IIb, there is an immediate threat to limb viability, and the limb may be salvageable with immediate revascularization. Sensory loss is more extensive and spreads proximally along the feet, muscle weakness is also present at a mild or moderate severity, and the arterial Doppler signal is usually absent. In stage III, the limb is considered irreversibly damaged with major tissue loss or permanent nerve damage. Sensory loss is profound, paralysis is present, and arterial as well as venous Doppler signals are absent.6
V. Diagnostic Evaluation
A. Differential Diagnosis The differential diagnosis for ALI includes direct arterial trauma, vasospasm, extrinsic compression, decreased systemic perfusion, acute neurologic syndromes, deep venous thrombosis, vasculitis, and chronic limb ischemia. The history and physical examination are typically sufficient to arrive at a leading diagnosis of ALI. Once conditions mimicking acute limb ischemia have been excluded, nonatherosclerotic causes of acute limb ischemia should be evaluated. In most cases, with the exception of arterial trauma, dissection, and compartment syndrome, the initial management is often unchanged.
B. Imaging
1. Noninvasive diagnostic imaging available to determine the nature and extent of the occlusion includes duplex ultrasonography, computed tomographic (CT) angiography, and magnetic resonance (MR) angiography. The role of these imaging modalities in patients with Rutherford IIb ALI is limited as revascularization is required within 3-6 hours for limb salvage14; although CT or MR angiography may delineate vascular anatomy and assist in treatment planning, it is important that these tests do not delay intervention.
2. Duplex ultrasound is a useful test to perform preprocedurally on most patients, as it can be done quickly and entails little risk to the patient. In patients planned to undergo surgery, CT or MR angiography is useful to ensure an accurate diagnosis and determine the extent of arterial occlusion.15,16 In patients who are planned to receive endovascular therapies, digital subtraction arteriography can be performed immediately before the procedure to provide the information necessary to plan the intervention.17
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