INTRODUCTION AND EPIDEMIOLOGY
Acute limb ischemia requires rapid recognition and therapy for limb salvage. Critical limb ischemia occurs in chronic progressive peripheral arterial disease when pain at rest, ulceration, or gangrene exists. Despite improvements in the management of peripheral arterial disease, current 1-year mortality after the onset of critical limb ischemia is 25%, and 25% of survivors require amputation.1,2
The prevalence of peripheral arterial disease (defined as an ankle-brachial index of <0.9) in="" the="" united="" states="" is="" 4.3%="" for="" those="">40 years old and 15.5% for those >70 years old.3 This prevalence increases to 29% in high-risk populations in those >70 years old and those >50 years old with diabetes or a smoking history.4 In the elderly, both sexes are affected equally, although symptoms are present two to four times more commonly in men. Smoking and diabetes are the most important risk factors for arterial insufficiency.5 Additional risk factors include hyperlipidemia, hypertension, hyperhomocysteinemia, and an elevated C-reactive protein level.
Between 40% and 60% of patients with occlusive arterial disease have either coronary or cerebrovascular disease.6 The severity of peripheral vascular disease is closely linked to the risk of myocardial infarction, ischemic stroke, and death from vascular disease.7 The most frequently diseased arteries leading to limb ischemia are, in order of occurrence, the femoropopliteal, tibial, aortoiliac, and brachiocephalic vessels.
Acute limb ischemia results from a lack of blood supply to meet tissue oxygen and nutrient requirements. As time proceeds, cell death or irreversible tissue damage occurs. Peripheral nerves and skeletal muscle are more sensitive to ischemia, and irreversible changes occur in these tissues within 6 hours.
After restoration of the blood flow, reperfusion injury can occur, noted by the presence of muscle pain and swelling, renal failure, and peripheral muscle infarction. Often, hyperkalemia, myoglobinemia, metabolic acidosis, and an elevation in creatine kinase level exist. The extent of reperfusion injury depends on the duration and location of the arterial blockage, the amount of collateral flow, and the previous health of the involved limb. Approximately one third of all deaths from occlusive arterial disease are secondary to metabolic complications after revascularization.8
Disorders that can lead to arterial occlusion are compared in Table 61-1.
TABLE 61-1Disorders Associated with Acute Arterial Occlusion |Favorite Table|Download (.pdf) TABLE 61-1 Disorders Associated with Acute Arterial Occlusion
|Disorder ||Cause ||Symptoms/Signs ||Management |
|Thrombus ||Atherosclerosis or thrombosis of bypass grafts ||Intermittent claudication ||Medical first, then consider interventional |
|Embolism ||Cardiac source: atrial fibrillation, rheumatic heart disease, mechanical valves, post–myocardial infarction thrombus, atrial myxomas and leaflet vegetations ||Sudden onset of territorial arterial symptoms ||Preventative anticoagulation, embolectomy |
|Catheterization complication (brachial or femoral) ||Can occur during standard angioplasty, angiography, or arterial blood gas ||Expanding hematoma, pain, temperature and pulse changes ||Conservative vs. operative repair |
|Trash foot or blue toe syndrome ||Cholesterol/platelet aggregate emboli ||Painful cyanotic ...|