Acute arterial occlusion
Acute arterial occlusion results in sudden, abrupt onset of peripheral ischemic pain. The level of severity is generally extreme, but may be relatively mild in cases of arterial thrombosis superimposed upon chronic peripheral vascular disease (PVD). The most common etiology of acute obstruction (Table 1) is an embolus from the heart which lodges at a major bifurcation in the arterial tree, simultaneously obstructing both the main channel and the most import-ant collateral for that channel. Another dramatic etiology is abrupt thrombosis of a popliteal aneurysm, during which a chronic laminar thrombus lining the aneurysm wall becomes disrupted with peripheral embolization or obstruction at the site of the aneurysm. More rarely, abdominal aortic, iliac or femoral aneurysm may produce acute obstruction by a similar mechanism. In the presence of chronic PVD, underlying arterial stenoses may abruptly progress to total thrombotic occlusion. A notable change in the pattern of chronic ischemic symptoms results, but usually in a less dramatic fashion than in patients with little PVD because of the presence of preconditioned collateral channels.
Table 1 Causes of acute lower extremity arterial occlusion.
Valvular heart disease with vegetation/thrombus on leaflet
Left ventricular aneurysm with thrombus
Atrial fibrillation/left atrial enlargement with thrombus
Left ventricular mural thrombus following myocardial infarction
Paradoxical embolus through patent foramen ovale
Tumor embolus (atrial myxoma, tumor in pulmonary vein)
Aortic aneurysm thrombus disruption
Peripheral (femoral, popliteal) aneurysm
Severe systemic illness (sepsis, cardiovascular collapse, trauma) Iatrogenic arterial injury (catheters, wires)
Peripheral bypass thrombosis
Table 2 Differential diagnosis of arterial embolus vs. thrombosis.
Identifiable source Usually cardiac disease
Severity of ischemia Usually profound
Course over hours Usual improvement
History of leg PVD Less common
Chronic PVD signs Few; other leg normal
Arteriography Scant disease, few collaterals
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Commonly less severe
Common; other leg abnormal
Diffuse disease, many collaterals
PVD, Peripheral vascular disease.
Diagnostic differentiation between embolus and thrombosis is important, though sometimes difficult (Table 2). Historical features of embolus include dramatic onset without antecedent chronic peripheral arterial symptoms and the presence of cardiac valvular disease, recent myocardial infarction or arrhythmia. In addition, patients with acute embolic occlusion will often experience some improvement over the first few hours after onset as new col-laterals are solicited. Acute thrombosis with underlying PVD is associated with a history of chronic arterial symptoms such as claudication. There may be less improvement over the first hours after an abrupt event because collateral has already developed near maximally. Aneurysms are generally asymptomatic without any useful historical clues, though the patient may have been aware of an unusual pulsation in retrospect.
The level of tissue ischemia is reflected in the signs and symptoms. If the symptoms are unilateral, comparison with the more normal contralateral leg is helpful. Pain is the cardinal early symptom of ischemia.
With prolongation, numbness and paresthesia supervene followed by loss of motor function. Physical examination will reveal pallor in the ischemic portion of the limb. Capillary and venous filling times will be prolonged and marked blanching will occur with elevation. A sensory deficit may be present, corresponding to the patient’s symptoms. The distal limb may improve with time as collateral channels are recruited, with most dramatic restoration of capillary filling and warmth in cases of acute occlusion in the absence of underlying PVD. Pulses will be absent below the level of obstruction. Paradoxically, the pulses above the level of obstruction may be abnormally prominent as flow is frustrated at the point of occlusion, a variant of the so-called ‘water hammer pulse’. There may be evidence of abdominal, iliac, femoral or popliteal aneurysm on palpation. Arrhythmia may be evident or there may be other signs of cardiac disease such as peripheral edema, gallops, cardiac enlarge-ment or rales.
The hand-held Doppler probe is an excellent adjunct to extend the usefulness of the physical examination. It can be used in the office to obtain systolic blood pressure at the ankle, which when compared with the brachial pressure yields the ankle–brachial index. More formal non-invasive vascular laboratory confirmation with segmental limb pressures and pulse volume recordings provides a relatively precise measure of the presence and degree of arterial disease, but is generally not necessary to the initial diagnosis, particularly in acute situations when the history and physical usu-ally tell the story so clearly. Ultrasound imaging, computed tomography or magnetic resonance imaging (MRI) can prove the presence of an abdominal or peripheral aneurysm. Arteriography can identify the exact level of obstruction and help plan definitive therapy. Electrocardiogram and echocardiography help elucidate underlying contributory cardiac disease.
The most important step in early management of patients with acute arterial occlusion is making a timely diagnosis. In the absence of contraindications, anticoagulation with intravenous heparin is an appropriate early step to protect collateral from propagation of secondary thrombosis around the acute obstruction and to help protect the patient from repeat embolic episodes. The patient should be postured in the foot down, reverse Trendelenberg position
to take advantage of gravity to augment flow into the distal arterial bed. The heels and forefeet should be protected from mechanical trauma. The fascial compartments should be monitored for development of compartment syndrome with secondary injury to nerve and muscle produced by increased subfascial pressure. Underlying cardiac disease should be aggressively man-aged with appropriate consultation, particularly if a new event such as myocardial infarction or arrhythmia is evolving simultaneously. In virtually all cases, early consultation to general or vascular surgery should be sought. If the limb is restored to a fully sensate and pain-free status, no definitive early therapy may be required. With persistent pain, and most particularly with progressive or persistent numbness, urgent intervention is paramount, using either percutaneous thrombectomy/fibrinolysis, surgery or a combination of the two modalities to establish improved flow.
Chronic arterial occlusion
Though chronic atherosclerotic peripheral occlusive disease can present in patients < 50 years of age, it generally appears later in life and follows a relatively gradual pattern of progression as thickening of the arterial wall eventually produces occlusion. Whether localized to the aortoiliac, superficial femoral or infrapopliteal arteries or to a combination of these three segments, disease is most often initially manifest by onset of intermittent claudication. The critical historical feature of intermittent claudication is repetitive stereo-typical pain brought on after initiation of exercise with relief upon cessation of exercise. Muscle cramping and fatigue develop after a generally reproducible amount of exercise with prompt relief after stopping to stand or sit. With prolongation of exercise, the symptoms may evolve into numbness or even paralysis and relief may be delayed with some residual aching and even tenderness in the muscle. As in angina pectoris, symptoms are aggravated by added demand such as walking rapidly, walking up an incline or carrying heavy bundles.
The most common situation involves unilateral stenosis or occlusion of the superficial femoral artery producing calf muscle pain. The pattern of claudication may extend to the thigh and buttock musculature if the aorta or iliac arteries are diseased, though relatively isolated calf symptoms may predominate if exercise is not prolonged. Male patients with aortoiliac disease may complain of impotence in addition to bilateral buttock, thigh, and calf claudication (the ‘LeRiche syndrome’). In unusual patients with severe involvement of the internal iliac arteries and relative sparing of the main iliac and femoral trunks, impotence may be present with claudication limited to the buttock muscles. A predominance of disease in the tibial segment of the leg can produce claudication limited to the ankle and foot.
With progression to a more severe level, PVD results in ischemic symptoms at rest. Resting symptoms usually imply involvement of either multiple proximal arterial segments, such as combined iliac and femoral disease, or a predominance of isolated distal disease in the tibial vessels. Historically, the first manifestation of resting ischemia is often nocturnal. With recumbency and sleep, heart rate and blood pressure are reduced and flow into the most peripheral portions of the diseased arterial tree is diminished. Typically, a few hours after bedtime the patient will be awakened by numbness, tingling or aching pain in the toes and forefoot. This discomfort is relieved by dependency, produced by sitting at the edge of the bed or by standing or walking around for a short time. Many patients learn that they can sleep most comfort-ably sitting in a chair or with the bed tipped in a foot down position.
It is a short distance between nocturnal symptomatology and a more constant pattern of resting ischemia. Typically, the pain is a combination of aching and a neuropathic syndrome involving paresthesias and numbness. The pain is generally relieved to some extent by leg dependency and aggravated by elevation. Walking and standing will be uncomfortable because of pressure on the ischemic extremity and superimposition of muscular ischemia during muscle contraction. A slight injury, crack or other inadvertent trauma will easily produce an open non-healing lesion with attendant inflammation and potential for secondary infection. These lesions predominate in the most distal portion of the foot and on the areas such as toe tips, bony prominences, and nails subject to contact and injury.
Physical examination reveals reduced or absent peripheral pulses. In rare instances, a patient with mild claudication based on arterial stenosis may have a normal pulse exam at rest. After a period of exercise such as walking or repetitive tiptoe ankle flexion while standing sufficient to bring on claudication, prompt re-examination should reveal reduction or absence of pulses in the involved extremity. With strictly unilateral symptoms it is valuable to com-pare findings with the uninvolved extremity, realizing that the asymptomatic limb may not be entirely normal but simply masked by the more diseased limb. More severe levels of chronic disease produce muscle atrophy on the basis of poor nutrition and lack of use. Similarly, the skin over the foot is cool, shiny, dry, and atrophic with advanced chronic disease. The absence of hair over the ankle and toes is non-specific and never an isolated finding. Profound pallor with elevation with delayed filling of the forefoot veins beyond 20 s on return of the leg to the horizontal position should accompany resting symptoms. Capillary filling time is delayed when elicited by pressing the skin to empty the capillaries and observing the promptness with which the blanching disappears after release of pressure. With leg dependency, rubor over the distal portion of the foot may be striking, indicating loss of vasomotor tone in the subdermal plexus in the face of advanced ischemia. Cyanosis may also occur if there is coincident venous disease or extremely sluggish flow. Open lesions or non-healing minor injuries are distributed generally in the most distal portion of the foot or at contact areas such as the heel or metatarsal heads. Peripheral edema may be present in patients in whom peripheral ischemia is sufficiently severe to require dependency for relief. Such edema may be enhanced when skin breakdown has produced inflammation and infection.
Variants and differential points
Acute manifestations may be superimposed upon a history of chronic disease. For example, abrupt embolization of atheromatous material or small bits of thrombus from a stenotic region of the aorta, iliac or femoral artery can produce the so-called ‘blue toe syndrome’. The typical history involves no antecedent arterial symptoms or mild claudication consistent with proximal stenosis, with abrupt onset of painful mottled discoloration over the distal portion of the ipsilateral foot or one or more toes consistent with abrupt embolic occlusion of a digital artery or the plantar artery by atheromatous debris which has dislodged from a proximal plaque.
Other varieties of chronic arterial disease include Buerger’s disease (Thromboangiitis obliterans) in which pruning of the pedal and tibial vessels occurs. The classic presentation is a young male smoker with ischemic lesions distributed distally, typically with palpable pulses to the level of the popliteal artery but none more distally. A similar distal distribution is common in another variant of PVD seen in patients with diabetes in whom isolated calcific arterial occlusive disease is present in the tibial arteries, usually with relative sparing of the pedal vessels. Many diabetics also have more proximal arterial disease. Peripheral neuropathy is a prominent feature among diabetic patients with or without accompanying arterial occlusive disease, producing mal perforans ulcers over areas of weight bearing such as the metatarsal heads.
Diabetics frequently present with purely neuropathic ulceration with bound-ing pedal pulses. Vasospastic conditions present with a history of cold sensitivity and there may be objective evidence of accompanying systemic collagen vascular disease. It is very uncommon to have tissue loss in the presence of vasospasm alone without arterial occlusion. Vasculitis may result in digital artery occlusion, producing ischemic lesions and digital gangrene. Patients who present at < 50 years are particularly challenging, since the differential diagnosis includes adventitial cystic disease of the popliteal artery, popliteal artery entrapment syndrome and exercise-induced compartment syndrome. In addition, such young patients often harbor a particularly virulent brand of arterial disease which may be associated with hypercoagulable states and multiple risk factors for systemic atherosclerosis.
True intermittent claudication is predominantly of arterial origin. Symptoms very similar to aortoiliac arterial claudication may be produced by spinal stenosis, with a proximal distribution of pain and other historical and physical findings which must be carefully sorted through to make an accurate differential diagnosis. Spinal stenosis generally produces more of a diffuse numbing weakness than a muscular cramping fatigue. Distress may be caused by simple standing or other postures which increase lumbar lordosis and may persist long after walking ceases with best relief by sitting or other maneuvers which allow lumbar spine flexion. Other neuropathic symptoms are often present, such as perineal numbness or tingling. Venous obstruction is also an unusual cause of intermittent claudication (see below).
Confirmatory laboratory consists largely of physiological non-invasive vas-cular studies. At rest, the presence of significant peripheral arterial occlusive disease almost always causes abnormalities in segmental limb pressure and pulse volume recordings. Non-compliant or calcified arteries may be non-compressible, resulting in unmeasurable or falsely elevated segmental limb pressures. The minority of patients complaining of claudication but with normal physical and laboratory findings at rest may need treadmill exercise study to elicit symptoms and associated changes in segmental limb pressures to clarify the diagnosis and differentiate arterial disease from other etiologies such as spinal stenosis. Anatomic imaging with MRI or contrast angiography are rarely necessary to make the diagnosis of PVD and should be reserved until after consultation with vascular specialists for patients with severe dis-ease who may be candidates for intervention.
Early management strategy depends on presentation. In the case of intermittent claudication, the patient should be advised to initiate a daily exercise regimen. Walking to the point of discomfort, with cessation until comfort returns followed by repeat cycles, usually produces improved collateral flow as well as metabolic adaptation of the muscle itself. Symptoms stabilize or improve in as many as 80% of patients. The addition of pentoxyphyllin or cilostazol has been proven to enhance the likelihood of improvement in most studies, though the degree of improvement for any given individual is unpredictable. A trial of pharmacotherapy may be worthwhile in cases where the risk of intervention is substantial or in individuals in whom the ability to walk an additional short distance would make an important difference to lifestyle. Patients should be cautioned about proper foot care and vigorous efforts should be made to address underlying risk factors such as homocysteinemia, hyperlipidemia, hypertension, diabetes, smoking, and obesity. If the history and physical examination suggest the presence of stenosis in the iliac or superficial femoral artery, percutaneous therapy with balloon angioplasty or stent may be a relatively simple and reasonable therapeutic option. In such selected circumstances, early referral for scan or arteriography is appropriate. In most circumstances, referral for intervention is not warranted unless the claudication is truly disabling or progresses to resting ischemia. Only 3–5% of claudicators experience limb loss over a 5-year period.
In the case of resting ischemia there is a much more immediate threat of limb loss. Early management should include consultation with a vascular surgeon or other vascular specialist. Patients with rest pain and no open lesions can be managed initially with conservative protective measures, skin moisturizers, hygiene, posturing of the bed in reverse Trendelenberg (foot down) position, use of sheepskin or foam rubber under the feet as well as a foot board to elevate sheets and blankets off the toes. Podiatric consultation and support may be very helpful. If open lesions are present, these initial measures should be supplemented with topical antibiotic ointment and dressings, in conjunction with oral or intravenous antibiotics if there is evidence of infection involving the surrounding tissue. If there is swelling, purulence or fever, such lesions may need urgent surgical drainage to control infection.
In the great majority of patients with resting ischemia, it is critically important to establish improved circulation. Arterial imaging must precede revascularization, usually using contrast arteriography or MRI. Modern digital techniques have made arteriography relatively safe and comfortable. MRI is an adequate substitute for arteriography in many situations, and is particularly useful in patients with allergy or increased risk of renal dysfunction related to arteriographic contrast dye. Percutaneous therapy of appropriate iliac artery lesions using balloon angioplasty and stents is associated with complications in < 1% of patients and may be expected to produce a cumulative 5-year patency rate of 85–90%. Catheter-based therapy of the superficial femoral artery is similarly safe, though with somewhat less durable 5-year cumulative patency of about 60% under the best circumstances. These percutaneous methods can be repeated in many instances should the need arise.
A number of surgical options are available for treatment of high-grade or diffuse aortoiliac disease, tailoring the surgical procedure to the patient’s needs and associated risk factors. In general, procedural mortality following surgery for aortoiliac disease is < 3%, with 5-year cumulative patency rates close to 90% for aortofemoral, iliofemoral and femorofemoral bypass. Long-term patency rates for axillofemoral bypass are not quite as favorable, averaging 75–80% in most series. Reconstructions below the groin are associated with roughly 2% operative mortality risk. Five year cumulative success rates are 80–85% for patients with claudication and 65–70% for patients with resting ischemia. Following revascularization, major amputation is necessary in less than 10% of patients within 5 years of intervention.