James H. Black III
The aging process is associated with the development of variable degrees of degenerative arterial disease. Longevity and quality of life may be improved by recognition, evaluation, and appropriate therapy of diseases that affect blood vessels (see also Chapters 62 and 91). The purpose of this chapter is to provide guidelines for recognition and management of the more commonly encountered problems of acute and chronic occlusive peripheral arterial disease (PAD) and of abdominal and peripheral arterial aneurysms.
Acute Peripheral Arterial Occlusion
Acute ischemia occurs when there is a sudden decrease in arterial perfusion of the lower extremities. It demands immediate recognition and management in an effort to minimize morbidity, including limb loss and death, because irreversible changes such as muscle necrosis, extensive arterial thrombosis, and neurologic deficits may occur in the affected extremity as early as 4 to 6 hours after acute arterial occlusion.
Causes
The two major causes of acute arterial occlusion are cardioarterial embolism and in situ thrombosis. Most large arterial emboli originate in the heart. Arrhythmias and mural thrombi are the major risk factors for embolization. Rare sources of emboli include proximal arterial lesions
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such as aortic aneurysms or large ulcerative aortic plaques, which are commonly associated with arterial cholesterol microemboli. These microemboli may cause the “blue toe syndrome” (the acute development of cyanosis and pain of the toes or the distal feet, often in association with strong posterior tibial or dorsalis pedis pulses) (1). Left atrial myxomas, debris from prosthetic heart valves, paradoxical emboli (venous clots passing through a congenital cardiac defect into the arterial circulation), and foreign body emboli have also infrequently been associated with sudden arterial occlusion.
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FIGURE 94.1. Stages of acute ischemia and clinical manifestations. Overlap of symptoms is common, especially early in the clinical course. Those patients with underlying chronic peripheral arterial disease (PAD) may progress more slowly than those patients suffering acute limb ischemia without antecedent disease. |
In situ thrombosis of a chronic preocclusive arteriosclerotic lesion accounts for approximately 85% of acute occlusive events (2). Such thrombotic complications are most likely to occur in segments of severe stenosis such as the aortic bifurcation, the iliac bifurcation, the common femoral bifurcation, and the superficial femoral artery just above the knee.
Upper extremity ischemia is usually secondary to arterial embolism. Acute thrombosis virtually never causes ischemia in the upper extremity because chronic arteriosclerotic lesions are uncommon and collateralization is excellent. Thoracic outlet compression may rarely give rise to subclavian or axillary arterial thrombosis. Concomitant problems such as hypovolemia from volume depletion or hemorrhage, congestive heart failure (CHF), erythrocytosis, or trauma all have profound influences on management.
Clinical Manifestations
More than 90% of the time, acute embolic occlusion may be distinguished from acute thrombotic occlusion on clinical grounds alone. In instances in which doubt exists about the cause, especially in the absence of atrial fibrillation and recent myocardial infarction (MI), arteriography is essential to distinguish embolus from thrombosis (see Laboratory and Radiographic Studies, below).
Emboli lodge at arterial bifurcations, most often in the lower extremities. Multiple emboli can result from a “shower discharge” of clots from the heart. Therefore, although the legs are affected most often, there may also be symptoms and signs of ischemia elsewhere. The development of new abdominal pain, limb pain, or neurologic deficit in a patient with a recent embolic event should invoke an expeditious diagnostic study, if needed, and prompt therapy.
Clinical manifestations vary depending on the adequacy of pre-existing collateral circulation and the site of occlusion (Fig. 94.1). If pre-existing collateral vessels, stimulated by underlying occlusive arterial disease, are present, acute ischemic symptoms may be mild. Total arterial occlusion of a previously normal arterial tree causes severe symptoms. The cardinal features of acute ischemia include the six Ps of arterial occlusion: Pulselessness, pallor, poikilothermia (“coolness”), pain, paresthesias, and paralysis. The latter three Ps reflect neurophysiologic sequelae of ischemia, and the former three result from mechanical occlusion of an artery. Three fourths of patients complain of pain, but 20% note numbness as the first manifestation of sudden arterial occlusion. Initially, the pain may be mild, but as the ischemia progresses, pain worsens, only to subside later as anesthesia and paralysis develop.
Additional findings include absent or faint distal pulses, poor capillary filling, and collapsed or severely sunken veins on the dorsum of the foot. Pedal edema, if present, is not a result of arterial occlusion, but it may be secondary to heart failure or pooling of blood in the extremities of patients who attempt to relieve ischemic pain by maintaining their legs in a dependent position for long periods.
Cardiac examination may reveal atrial fibrillation, a diastolic rumble or the opening snap of mitral stenosis, the click of a prosthetic heart valve, or a third heart sound associated with congestive heart failure. A recent history of chest pain, dysrythymia, or electrocardiographic evidence of MI also suggests a cardiac origin of acute leg ischemia.
Laboratory and Radiographic Studies
Laboratory studies usually are not helpful in making the diagnosis of acute arterial ischemia of the lower extremities. Arterial blood gas measurements and pH should be obtained to serve as baseline studies for subsequent comparative measurement and to identify metabolic acidosis secondary to muscle ischemia. Hyperkalemia may be noted, particularly if prolonged limb ischemia has occurred. A radiograph of the chest may document cardiac enlargement or congestive heart failure. An electrocardiogram
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(ECG) and, if time permits, a transthoracic or transesophageal echocardiogram may be useful in delineating cardiac disease. All these studies should be obtained after the patient is hospitalized. Although noninvasive evaluation by Doppler ultrasonography (US) or by plethysmography is often superfluous, the inability to obtain any arterial Doppler signal in the foot in a patient with an acute occlusion supports the decision for urgent revascularization.
Contrast arteriography is not performed routinely in patients with acute ischemia except in occasional instances of modest ischemia when it is needed to distinguish between thrombosis and embolus (see Differential Diagnosis). Magnetic resonance angiography is being done in some centers as a less invasive alternative technique, especially when there are contraindications to contrast angiography. It is a key management paradigm that arteriographic investigation should not prolong the treatment interval, especially once neurologic sequelae have occurred. Such delays often lead to permanent nerve and muscle damage that may render a limb functionally useless. Evidence of generalized and severe arteriosclerosis, a tapered arterial occlusion, and well-developed collateral vessels suggest acute thrombosis. Normal-appearing arteries with scanty collateral circulation and an occlusion with an inverted meniscus configuration indicate embolic occlusion. However, embolization can occur in patients who also have chronic occlusive disease, and the diagnosis is occasionally still in question after angiography. In any case, the decision for immediate surgery is based on the clinical status of the extremity, not on the arteriogram.
Differential Diagnosis
Every effort should be made to differentiate embolism from thrombosis because the therapy of the two conditions is different. History is often helpful in separating these two entities. A history of intermittent claudication or of rest pain suggests the acute ischemic event is thrombosis. Absence of a history of intermittent claudication usually indicates embolism. However, a minority of patients who suffer acute superficial femoral arterial occlusion secondary to thrombosis have never had symptoms of intermittent claudication before the sudden occlusive event. On physical examination, classic findings of chronic ischemia such as loss of hair on the toes and dorsum of the foot and the leg, along with nail, skin, and muscle atrophy, suggest arterial thrombosis rather than embolism. A laterally pulsatile abdominal mass suggesting an abdominal aortic aneurysm (AAA) from which a mural thrombus may have embolized to the distal arterial tree might be evident. Finally, if the acute ischemic episode involves only one leg, palpating the popliteal and femoral arteries may detect an aneurysm. If the contralateral vessel is vigorously pulsating and aneurysmal, a thrombosis of an aneurysm on the ipsilateral or symptomatic side may have occurred, especially if a nonpulsatile mass can be palpated.
An acute dissection of the thoracic and abdominal aorta may present as unilateral lower extremity ischemia. Under these circumstances, patients may relate a history of severe, searing, ripping thoracic back pain and may provide a history of long-standing hypertension. Concomitant renal hypoperfusion may be noted, and malperfusion to the visceral vessels may cause vague abdominal pain. Chest radiograph may reveal a widened mediastinal silhouette, and a murmur of aortic insufficiency may be present if the dissection originates in the ascending aorta. Computed tomography (CT) scanning (with IV contrast) can usually demonstrate the septum of the dissection within the main aortic channel, and, often, asymmetric enhancement of the renal arteries or iliac arteries may be present and should heighten the suspicion for hemodynamic compromise of the affected territory.
Treatment
Evaluation and therapy must proceed simultaneously in the management of acute arterial ischemia of the extremities (Fig. 94.2). The cornerstone of early management is the immediate intravenous administration (in the clinician's office or emergency department) of 100 to 150 units heparin sodium per kilogram of body weight (3) (although no prospective controlled studies have established its efficacy) and then urgent vascular surgery consultation.
There may be a role for the interventional radiologist or endovascular surgeon to perform intra-arterial infusion of fibrinolytic agents directly into the site of the acute arterial occlusion (2, 3, 4). If that is the case, a multiple purpose polyethylene catheter is imbedded into the occluding clot after the arteriographic study is performed. Protocols may vary, but typically urokinase or tissue plasminogen activator is infused for 30 to 60 minutes and a second arteriogram is performed. Therapy is continued for 24 to 48 hours with clinical and angiographic re-evaluation at 8- to 12-hour intervals. Such therapy is contraindicated when the extremity is in dire jeopardy because the time required for lysis to occur may be longer than the safe interval before necrosis occurs. In patients whose limbs are not immediately threatened, this therapeutic approach can be efficacious, particularly for high-risk patients in whom operation may be contraindicated and in those patients with a diagnosis of a thrombosed surgical bypass graft. Results for thrombolysis in regard to restoration of perfusion or salvage of a thrombosed graft are best if the event is recent (<2 weeks). Untoward bleeding is the major complication of fibrinolytic therapy and may result in significant morbidity. The duration of the infusion and the optimal dosage to be administered to restore circulation are not yet firmly established. Therefore, until further experience is gained with this modality, it should be reserved for highly selected
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patients who are cared for in centers specializing in management of vascular disease.
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FIGURE 94.2. Overview of treatment of limb ischemia. There may be substantial overlap in those patients who present with threatened limbs. It is not uncommon for IV heparinization to improve the clinical examination of patients with immediately threatened limbs such that investigation (usually by angiography) may be performed; however, it is not acceptable for treatment delay to occur while awaiting investigations. ABI, ankle-brachial index. |
Surgical revascularization, can then be performed, if necessary, after blood flow to the ischemic extremity is restored. The introduction of the balloon-tipped embolectomy catheter by Fogarty et al. in 1963 revolutionized the management of acute embolic occlusion and converted a previously complex undertaking into a simple operative procedure that invariably can be performed under local anesthesia with improved survival and limb salvage rates.
After discharge from the hospital, patients are almost always maintained on therapeutic levels of oral anticoagulants for the rest of their lives, although only in patients with embolism associated with atrial fibrillation has efficacy been established (see Chapter 57). Furthermore, they must be evaluated several times a year to ensure that optimal cardiac function is maintained and for continued evaluation of their peripheral circulation.
Results
Despite improved diagnosis, preoperative care, operative management, and postoperative support, mortality from acute lower extremity ischemia continues to be discouraging and is likely related to associated cardiovascular disease. Early operative mortality rates still average 15% or more (2). Virtually all deaths are related to complications of cardiovascular disease, which reinforces the contention that recognition and correction of cardiovascular risk factors for arterial embolism or thrombosis are critical in the acute and long-term management of such patients (5).
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The likelihood of successful limb salvage, which exceeds 95% in most series, is directly related to the time between arterial occlusion and restoration of blood flow. Therefore, it is improbable that a 100% limb salvage rate will ever be achieved.
Chronic Peripheral Arterial Disease
In contrast to the management of acute arterial occlusion, which requires emergent or urgent treatment, chronic PAD can usually be managed electively because of the presence of collateral channels that bypass slowly developing atherosclerotic lesions and maintain a viable extremity. A knowledge of the natural history of chronic PAD is necessary for the appropriate management of these patients.
Causes and Pathophysiology
The most common cause of chronic PAD is atherosclerosis. Atherosclerotic risk factors for chronic PAD are similar to those for coronary artery disease (CAD) and cerebrovascular disease (CVD): age older than 50 years, male sex, tobacco use, diabetes mellitus (DM), hypertension, and hyperlipidemia. Many patients with PAD have associated CAD and 10% have associated CVD (6). Often patients will not succumb to complications of PAD but will present with fatal or nonfatal cardiovascular and cerebrovascular complications. Therefore, significant focus on risk factor modification is needed to reduce the risk of these associated events.
The prevalence of intermittent claudication in patients with PAD is 1% to 2% for those younger than the age of 50 years and increases to 5% for those 50 to 70 years of age (6,7). Men are affected 1.5 to 2 times more often than women until age 70 years, when prevalence rates for intermittent claudication for men and women are nearly equal (6).
Smoking is the single most important modifiable risk factor for the development of PAD. Smokers develop PAD a decade earlier than age-matched nonsmokers, are at increased risk of amputation, and have less successful outcomes after lower extremity revascularization surgery (8). Tobacco use is synergistic with other risk factors for the development and progression of arterial disease (9).
Diabetic patients (see Chapter 79) manifest PAD a decade earlier than nondiabetic patients. In diabetics, PAD often develops in the more distal arteries of the leg earlier than it does in nondiabetics, and options for revascularization are therefore often limited. If a limb neuropathy is present, paresthesias and undetected infections and ulcerations can occur. Diabetics have a sevenfold higher rate of amputation than do nondiabetics (10,11).
Hypertension is a major risk factor for the development of PAD, especially in women (10,12). Observational studies support the practice of aggressive blood pressure control (see Chapter 67) in patients with PAD, although no prospective randomized trials have yet been done.
Hyperlipidemia is prevalent in patients with PAD, but the direct association is controversial. Nevertheless, treating hyperlipidemia is important in atherosclerotic patients in any case and should be undertaken aggressively in this population as well (see Chapter 82).
Although atherosclerosis is a generalized disease, it has a remarkably segmental distribution. Arteriosclerosis is prone to develop at major arterial bifurcations, in areas of arterial fixation, and at points of marked arterial angulation such as the aortic, common iliac, and common femoral artery bifurcations; the infrarenal aorta; and the distal superficial femoral artery as it enters Hunter canal. With gradual development of such lesions, the formation of collateral vessels compensates for segmental obstructive processes. In many instances collaterals are sufficient to provide adequate blood flow even during moderate exercise, so symptoms are minimal. However, as progressive main arterial involvement occurs, collateral channels may become ineffective or occluded, and ischemic symptoms progress from exercise-induced discomfort in the muscles of the lower extremity to rest pain and finally to tissue necrosis.
Thromboangiitis obliterans, or Buerger disease, is a severe chronic panarteritis that leads to fibrosis and obliteration of small vessels at the tibial and pedal arterial levels. The arteries of the forearm and hand can be involved, and superficial phlebitis may be seen as well. Buerger disease is an uncommon cause of lower extremity arterial insufficiency in the United States. This entity affects young men in their 20s and 30s and is almost always associated with severe tobacco addiction. Successful management hinges on cessation of all forms of tobacco usage.
Natural History
Intermittent claudication reflects a relatively benign condition (13, 14, 15). Approximately one third of patients improve, one third remain stable and tolerate their symptoms, and one third deteriorate and require revascularization. Relentless progression of the peripheral atherosclerotic process is unlikely in most nondiabetic patients, particularly if use of all tobacco products is discontinued. Less than 4% of patients will ultimately require amputation, although diabetics are at increased risk (8). On the other hand, patients with ischemic rest pain or gangrene are at very high risk for amputation if revascularization is not undertaken.
The overall 5- and 10-year survival rates among patients with intermittent claudication are approximately 70% and
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40%, respectively, and the most common cause of death (in 75%) is CAD (16).
Clinical Manifestations
Symptoms
Many patients with PAD are asymptomatic. When symptoms begin, they are often described as pain or discomfort that develops in the affected limb with exercise and is relieved within several minutes with rest (claudication). The discomfort is often localized to the calf, although it can also affect the buttocks and thigh as well. The distance a patient walks before developing claudication should be documented. When symptoms advance to pain or discomfort at rest or when supine, it may be assumed that blood flow to the lower extremity is marginal. Gravity can increase blood flow slightly, and patients often learn to alleviate the symptoms by dangling the affected leg over the side of a bed or by standing up.
Physical Examination
A complete vascular examination should routinely be performed, noting the status of all peripheral pulses, the presence or absence of bruits and peripheral aneurysms, and the blood pressure measurements in both upper extremities. In patients with mild intermittent claudication, the skin, hair growth, feet, and toenails may appear normal, and faintly palpable dorsalis pedis and posterior tibial pulses may be present. However, with progressive arterial involvement trophic changes may occur with hair loss and the development of thin parchment-like skin. Lack of pulses below the inguinal ligaments, blanching and pallor with elevation of the extremity, and dependent rubor all indicate advanced ischemia. Gangrenous areas may be evident on the toes. The typical locations of ischemic ulcers are the calcaneus, the lateral malleolus, and the dorsum of the foot.
Laboratory and Radiographic Studies
The distribution and severity of PAD can be determined objectively by noninvasive Doppler flow studies. Doppler signals from the dorsalis pedis, posterior tibial, peroneal, or lateral tarsal arteries are located, and a sphygmomanometer cuff is placed immediately above the malleoli and inflated to above systolic pressure to obliterate the Doppler signal. As the cuff is slowly deflated, Doppler signals return at the systolic opening pressure. The highest pressure recorded is compared with the brachial arterial systolic pressure. A resting ankle-brachial index (ABI) of 1 or greater is normal. For patients with intermittent claudication the mean index is 0.59; for those with rest pain, 0.26; and for those with impending gangrene, 0.05 (17). The accuracy of the measurement is quite high (18). The ABI may be artifactually elevated in diabetic patients and those with advanced PAD because of calcific changes in the arterial wall. In this group, the cuff may not be able to occlude the stiffened vessel, and the ABI may be greater than 1.0. Further corroborative examination, usually by Doppler waveform analysis or pulse volume recording will demonstrate the problem if it is present. In normal patients, a triphasic waveform and pulse volume recording tracing are noted, however, as the PAD worsens, the waveform will progress to biphasic (“sine-wave”) then monophasic (“flat-line”) tracing. A monophasic waveform at any level indicates critical ischemia.
A Doppler study of lower extremity blood flow, although important, is not necessarily required in evaluating all patients with lower extremity arterial occlusive disease. However, noninvasive testing may be helpful in distinguishing vascular insufficiency from other causes of leg pain such as neurogenic claudication secondary to cauda equina compression from spinal stenosis. In the latter condition, Doppler ABI indices are normal at rest and after exercise. Doppler flow studies, with the patient at rest, are almost always sufficient to make the diagnosis of peripheral arterial occlusive disease (19). Rarely, the studies need to be repeated after exercise on a treadmill or even after simply walking the patient to the point of claudication. Noninvasive studies can also document the efficacy of nonoperative therapy and determine whether deterioration of the circulation is progressive (20). Also, comparison of preoperative and postoperative noninvasive data is useful in documenting the effectiveness of operative therapy.
The gold standard study, if it is determined the patient is a candidate for operation, is arteriography. Although risks are very small in experienced hands, arteriography is used only when operation is indicated and agreed to by the patient. Finally, laboratory studies may also reveal hyperglycemia or hyperlipidemia that requires appropriate management.
Treatment and Results
Treatment for arterial insufficiency of the legs may be either operative or nonoperative. Table 94.1 shows indications for operation. Patients should usually be managed nonoperatively unless one of these indications is present
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and medical management has failed. Knowing the natural history of the occlusive process aids significantly in determining whether the patient's symptoms warrant operative intervention in view of associated risk factors and life expectancy. Except for patients who are not considered operative candidates, ischemic rest pain, nonhealing ulcers, pregangrenous changes, and gangrene are unequivocal indications for expeditious revascularization.
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TABLE 94.1 Indications for Operation for Arterial Insufficiency of the Legs |
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TABLE 94.2 Advice That Should Be Given to Patients with Arterial Insufficiency |
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General Measures
An itemized list of recommendations written in nontechnical language should be given to and carefully reviewed with the patient (Table 94.2). Meticulous skin hygiene and avoidance of injury to the foot, however slight, cannot be overemphasized. An otherwise asymptomatic ischemic foot becomes symptomatic when trauma leads to a nonhealing ulcer that may require revascularization. If the patient's feet are cold, particularly at night, a warm pair of socks or a muffler is advised but not the use of heating pads or hot water bottles, which may cause tissue breakdown and ulceration. Patients should inspect their feet every day and should bathe them at least once a day in lukewarm water and thereafter apply lanolin or hand cream to the skin to keep it soft and pliable and to avoid cracking and fissuring and subsequent skin breakdown.
Exercise is the cornerstone of therapy for symptomatic PAD. Supervised exercise rehabilitation programs (e.g., in cardiac rehabilitation centers) using a treadmill have been found to be the most successful at relieving intermittent claudication (10,18). Significant improvement in walking times before onset of intermittent claudication can occur when the program includes up to 30-minute sessions of intermittent treadmill exercise three times a week for 3 to 6 months. These programs require a motivated and compliant patient. During sessions, trained personnel may also reinforce the need for risk factor modification. Patients are also encouraged to continue a walking exercise program at home. Other measures that significantly affect outcome include maintaining satisfactory cardiac function.
Smoking cessation (see Chapter 27) is especially critical for patients with chronic PAD, and the decrease in mortality rates for patients who stop smoking is significant (18,20). Smoking cessation improves symptoms of intermittent claudication in up to 85% of patients and improves exercise tolerance by up to 300%. Patients must clearly understand that nicotine absorption occurs through the buccal mucosa with the use of chewing tobacco, pipes, cigars, and cigarettes and does not require inhalation of smoke.
Diabetic patients with PAD have a high risk of eventual amputation, and the general principles of foot care are especially important for them. Additionally, diabetics should be seen by a podiatrist every 3 months for trimming of their nails and calluses and for close inspection for early signs of infection or ulceration. Intensive hypoglycemic therapy, of value in many diabetics, has not yet been demonstrated to affect the course of atherosclerotic peripheral vascular disease (10) (see Chapter 79).
Management of coexistent hypertension (see Chapter 67) is sometimes challenging, and blood pressure control may be less than ideal because the symptoms of the arteriosclerotic occlusive process may worsen if the patient is returned to a normotensive state. It now seems clear that β-blockers, previously thought to be harmful to patients with PAD, may be used in the treatment of hypertension in this population unless the occlusive disease is severe (21). Angiotensin-converting enzyme inhibitors (ACEIs), may, however, be the antihypertensive agents of choice (22). In patients taking antihypertensive drugs, it is important to check at each visit for orthostatic drops in blood pressure and to adjust the treatment regimen accordingly if orthostatic hypotension occurs.
In order to manage hyperlipidemia (see Chapter 82), a fasting lipid profile should be obtained for all patients with PAD. In PAD, the major risk factors for arteriosclerosis are elevated low-density lipoprotein (LDL) cholesterol and triglyceride levels and low high-density lipoprotein (HDL) cholesterol levels. Appropriate diet (and exercise, if possible) are important but lipid-lowering agents are often required. With respect to LDL cholesterol, the goal is to achieve a level less than 100 mg/dL. Several retrospective trials have demonstrated improved patency of vascular reconstructions (carotid endarterectomy, leg bypass grafts) in those patients taking statin medications (23,24).
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Pharmacologic Management
Antiplatelet Drugs
Aspirin, 81 to 325 mg/day, has been demonstrated to reduce the risk of vascular events in patients with atherosclerotic disease. It has not, however, been shown unequivocally to alter the progress of PAD (25). Nevertheless, its use in patients with PAD is reasonable, especially considering that most of these patients have systemic atherosclerosis. Ticlopidine and clopidogrel, two other drugs that inhibit platelet plug formation, are approved for treatment of patients with PAD. Ticlopidine is prescribed less often because of hematologic side effects. Clopidogrel has fewer side effects (although rare instances of thrombotic thrombocytopenic purpura have been reported [26]) and has been shown to be slightly more effective than aspirin in preventing progression of PAD (27). Nevertheless, aspirin at present is the more cost-effective drug.
Vasodilator Drugs
There is no objective evidence to suggest that vasodilating drugs are beneficial to patients with PAD. Blood vessels in ischemic tissue beds are already maximally dilated. When systemic vessels are dilated by these drugs, blood flow to the compromised extremity may actually decrease. Therefore, these drugs are not recommended for treatment of patients with PAD.
Pentoxifylline
This drug is a xanthine derivative that has been used for many years to treat patients with PAD. It decreases blood viscosity by a direct effect on the red blood cell membrane. Enough data have now accumulated to show that pentoxifylline (typically one 400-mg tablet three times a day) has little, if any, effect in reducing symptoms in patients with PAD and probably should not be prescribed (10).
Cilostazol
This drug is a phosphodiesterase inhibitor that has been approved relatively recently for treatment of PAD. Its mechanism of action is unknown, although it does affect platelet and endothelial function. A number of controlled trials have shown the drug to be effective in improving exercise tolerance (e.g., walking distance improvement of 45% to 100%) in patients with PAD (10,28). A standard dosing schedule is 100 mg (50- and 100-mg tablets are available) twice a day. Because cilostazol inhibits several hepatic drug-metabolizing enzymes, its daily dosage should be lowered if drugs metabolized by those enzymes (e.g., erythromycin or omeprazole) are prescribed concomitantly. The major side effects reported by the manufacturer are headache (up to 34% of patients), diarrhea (up to 19% of patients), and palpitations (up to 10% of patients). Cilostazol is contraindicated in patients with CHF of any severity.
Anticoagulant Drugs
There is no evidence that heparin or warfarin has any beneficial effect in patients with PAD (29) except in reducing the incidence of embolization in patients with atrial fibrillation.
Operative Intervention
It is only upon failure of nonoperative therapy and among patients with clear indications for surgery that arteriographic studies are obtained. It must be understood that arteriography serves as a roadmap for the vascular surgeon when reconstructing the vascular tree. No characteristic arteriographic findings distinguish between patients with intermittent claudication, those with ischemic rest pain, and those with gangrene and ulceration. As a generalization, however, patients who have intermittent claudication usually have hemodynamically significant proximal arterial occlusive lesions affecting the iliofemoral or the femoral–popliteal system. Characteristically, such patients have reasonably good outflow with two or more tibial vessels patent. Patients with advanced ischemic changes are found to have diffuse multisegment involvement and none or only one patent tibial vessel in the lower leg or foot. However, there is considerable overlap between groups, and no single arteriographic finding consistently characterizes any one symptom complex.
Arteriography occasionally demonstrates a distribution of advanced arterial involvement without reasonable runoff vessels for bypass. Under these circumstances, nonoperative therapy is all that may be offered, and there is a significant risk of subsequent amputation. Indications for operation among patients with intermittent claudication relate mainly to significant limitation of activities of daily living. Nonlimiting claudication and mild ischemic rest pain that is controlled by non-narcotic analgesics are not indications for operation, particularly in high-risk patients. A trial of conservative management is especially important if other risk factors, such as recent MI, are present.
When it is determined that the condition of the patient warrants operative intervention and when arteriography documents adequate outflow vessels, a number of options for arterial reconstruction are open to the vascular surgeon, including autogenous vein or prosthetic graft bypass and endarterectomy. There is a definite preference for bypass surgery rather than endarterectomy. Direct reconstructive procedures include aortofemoral bypass, femoral–popliteal bypass, and femoral–tibial bypass. Extra-anatomic reconstruction includes axillounifemoral bypass, axillobifemoral bypass, and femoral–femoral bypass.
The operative mortality rate for aortofemoral bypass grafting is less than 5% with a patency rate of 80% to 90% at 5 years (8). Operative mortality for extra-anatomic reconstructions is slightly less than for aortofemoral bypass,
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but the outlook for graft patency is not as good. Operative mortality for autogenous vein femoral–popliteal and femoral–tibial bypass procedures ranges from 0.5% to 1% depending on the general condition of the patient; 5-year patency rates for such procedures vary between 60% and 70% (8,30). It should be emphasized that patency varies directly with adequacy of the vein used and the extent of the disease in the vessel being reconstructed.
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FIGURE 94.3. Percutaneous transluminal angioplasty (PTA) of superficial femoral artery (SFA) atherosclerotic disease in a patient with severe claudication. A,B: Diagnostic study reveals diffuse severe disease of the SFA with serial severe stenoses. C: PTA balloon demonstrating recalcitrant lesion with tight “waisting” of the balloon. D: Final angiographic result with minimal residual stenosis (<20%) and no flow-limiting dissection. The patient had a significant clinical improvement. (James Black, MD) |
Generally, in contrast to aneurysmal disease, arterial reconstruction for occlusive disease is palliative and does not significantly increase the patient's life expectancy because most patients have significant coincident CAD. However, the quality of life may be vastly improved by surgery, particularly for those who would have undergone amputation if successful arterial reconstruction had not been feasible.
Patients with aortofemoral arterial occlusive disease who do not have CAD or DM have survival rates that equal those of the normal age- and sex-adjusted population. It appears that the presence of CAD reduces life expectancy by approximately 10 years, and the presence of DM reduces life expectancy by an additional 15 years (31).
Angioplasty
Percutaneous transluminal arterial dilation (angioplasty) is used as an alternative to surgical reconstruction for highly selected patients with arterial occlusive disease or those with significant surgical risk. It is a technique that uses a catheter with an attached balloon to dilate the stenosed artery. Advantages include lower morbidity, lower mortality, and possibly lower cost compared with arterial reconstruction. Patients who are not candidates for surgery, if subjected to percutaneous transluminal angioplasty (PTA), could conceivably require operation if complications occur after the percutaneous procedure. Therefore, a cooperative approach between the interventional radiologist and the vascular surgeon is mandatory (Fig. 94.3).
The best results with PTA are obtained typically in patients with short segment stenoses of the iliac arteries, in which success rates range from 76% to 93% at 1 year and from 66% to 92% at 2 years. The reported results of angioplasty for femoropopliteal disease range from 51% to 80% at 1 year and from 46% to 75% at 2 years. There is general agreement that results are less satisfactory if the arteriographic runoff is poor. In the properly selected patient, the probability of early success of PTA is high if the involved vessel is the iliac artery, there is a short segment of stenosis and not occlusion, and the runoff is good (32). Results are less satisfactory when multiple dilations are required. Unsatisfactory results of a peripheral angioplasty may require placement of metallic stents to improve the technical result if restenosis or dissection is noted.
Patients with longer stenoses and total occlusions have less favorable outcomes, but in very poor-risk patients, angioplasty may be the only alternative to operative
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reconstruction. In particular, if an adequate length of autogenous vein cannot be harvested (because of prior coronary or leg bypass), a long segment angioplasty may be the only viable therapeutic option. Occlusions more than 5 cm long and stenoses more than 10 cm long appear to be associated with significant restenosis rates (10% to 30% per year) and a regular surveillance program is indicated for such interventions.
Amputation
In debilitated patients with frank gangrene or unremitting ischemic rest pain in whom arterial reconstruction or transluminal angioplasty is not indicated or feasible, amputation is the only alternative. The goal of amputation is to relieve the patient of disabling pain, remove nonviable and potentially infected tissue, and select a level that will provide the greatest chance of healing with maximal prosthetic rehabilitation.
If the gangrenous process is dry and does not involve the great toe, autoamputation may be allowed to occur or formal surgical amputation may be performed. If pulses are palpable in the foot and the ischemic process affects the tips of the digits, primary healing usually occurs after toe amputation. Nonischemic neurotrophic ulcers on the plantar aspects of the foot in diabetic patients often heal if the head of the metatarsal is removed to relieve the pressure necrosis that occurs as a result of the diabetic neuropathy.
Mortality for amputation is directly related to the preoperative condition of the patient and to other complicating diseases. Mortality rates for amputations performed for occlusive arterial disease have been reported to be as high as 30%, with higher mortality rates recorded in the more proximal amputations.
After successful amputation, which includes primary healing that results in a stump amenable to prosthetic fitting, the most important aspect of therapy is rehabilitation. Prosthetic mobility requires almost twice as much energy with an above-knee amputation than with a below-knee amputation, and mobility is further inhibited by increased age, infirmity, obesity, and a poorly fitting prosthesis. Population studies demonstrate that only 50% of patients undergoing below knee amputation because of PAD will be fully ambulatory on a prosthesis; only 10% to 20% of patients with an above-knee amputation become ambulatory. It is difficult to predict successful rehabilitation in the atherosclerotic population, but cooperation between the surgeon and the rehabilitation team is pivotal to a satisfactory outcome.
Abdominal Aortic Aneurysms
An aneurysm, a blood-filled dilatation of a blood vessel, is generally defined as a 50% increase in diameter of a blood vessel. In the infrarenal abdominal aorta, a diameter of greater than 4 cm is also considered diagnostic of an aneurysm. The recognized incidence of AAAs has increased with the advent of sensitive and specific diagnostic noninvasive tests such as US, CT, and magnetic resonance imaging (MRI).
The most common site of an arterial aneurysm is the abdominal aorta. AAA is encountered two to three times more often than the second most common type, the popliteal artery aneurysm, and has been found in almost 2% of consecutive postmortem studies (33).
Etiology and Natural History
An AAA results from disease of the media characterized by degeneration of extracellular matrix proteins, which maintain the integrity of the vessel wall. AAAs are most often infrarenal (75%). Only 5% involve the suprarenal aorta, and 25% involve the iliac arteries (34).
The highest prevalence of such aneurysms is in white males older than 65 years of age (35). Age-adjusted incidence is fourfold to sixfold higher in men than in women for both asymptomatic and ruptured AAAs. Tobacco use is the risk factor most strongly associated with AAA (36). Smokers with small AAAs (4 to 5.5 cm) have been found to have an increased risk of rupture (1.9% per year versus 0.5% per year for nonsmokers) and poorer long-term survival.
The relationship between AAA and atherosclerosis is not clear. It is not known why some patients develop atherosclerosis and calcification of the abdominal aorta and some develop aneurysmal dilatation. Recently, genetic factors have been found to play a role (37). The prevalence of AAA is 1% in elderly siblings of subjects without AAA and increases fourfold in siblings of subjects who have AAA (38).
Our understanding of the natural history of AAA is clouded by early studies (39) that documented high risks of rupture but included more patients with large aneurysms than patients with smaller ones. This is important, because the risk of rupture is related to the size of the aneurysm (40). The advent of noninvasive screening techniques has allowed the detection of small asymptomatic aneurysms and improved our understanding of the rate of growth and risk of rupture of AAAs. Studies that have prospectively followed AAA size indicate that the average rate of expansion is 0.3 to 0.4 cm per year, with a range of 0.24 to 0.9 cm per year (41, 42, 43). The risk of rupture is negligible for AAAs less than 4.0 cm but increases significantly when the aneurysm reaches a size of 5.0 cm or more or when the rate of expansion is more than 0.5 to 1.0 cm in 6 to 12 months (44) (Fig. 94.4). Thus, whereas early studies demonstrated improved life expectancy with surgical treatment of AAA (45), more recent studies have suggested that early surgery may not offer a long-term survival advantage for patients with small
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asymptomatic aneurysms, who can be followed with serial ultrasound examinations (41) (see Treatment and Results, below).
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FIGURE 94.4. Sagittal reconstruction of a CT scan demonstrating a ruptured 10 cm abdominal aortic aneurysm. Note the fat stranding created by retroperitoneal blood apparent immediately inferior to left kidney. The patient was hemodynamically stable and underwent endovascular AAA repair (James Black, MD). |
Screening
The U.S. Preventive Services Task Force (USPSTF) recommends one-time screening for AAA by US in men age 65 to 75 years who have ever smoked (46). Although the USPSTF makes no recommendation for or against screening in men 65 to 75 years old who have never smoked, it acknowledges evidence that an invitation to such men to participate in screening reduces aneurysm-associated mortality (47). Screening for women and for men younger than 65 or older than 75 years is not recommended. Other expert groups have recommended screening all men age 60 to 85 years, women in the same age group with risk factors for atherosclerotic disease, and all patients older than 50 years of age with a family history of AAA. The Center for Medicare and Medicaid Services and the U.S. Congress are considering whether to provide Medicare coverage for screening for AAA by abdominal ultrasound.
Clinical Manifestations
History
The presentation of an AAA depends on whether complications have occurred. More than 50% are asymptomatic when first discovered during routine examination by a caregiver, by the patient who complains of a second heart in the abdomen upon palpating a pulsatile epigastric mass, or serendipitously during radiographic or ultrasonographic abdominal studies in the pursuit of another diagnosis. The patient may complain of abdominal, flank, or back pain as the aneurysm expands and becomes symptomatic, a harbinger of rupture. The most common misdiagnosis of a ruptured AAA is renal colic, thus, a patient suspected to have renal colic should be examined for a pulsatile mass or a confirmatory study should be performed (CT or ultrasound).
Most aneurysms that rupture bleed into the retroperitoneal space, affording life-saving tamponade. Under these circumstances, the patient presents with a history of syncope or of flank or back pain in a hypovolemic, but not necessarily a hypotensive, state. On the other hand, the patient with an uncontained intraperitoneal rupture of an AAA typically presents in shock secondary to blood loss and requires immediate operative intervention. Aneurysms may rupture into adjacent structures and cause large arteriovenous fistulas, such as an aortocaval or aortorenal fistula with high-output cardiac failure, or into the gastrointestinal tract, usually the duodenum, causing an aortoenteric fistula with massive hematemesis or hematochezia.
Other Complications
If aneurysms are large enough, they may produce symptoms due to compression of adjacent structures such as the ureter, duodenum, vena cava, or vertebral column. Dislodgment of laminated clots from the wall of the aneurysm occasionally may cause peripheral embolization to femoral, popliteal, or distal vessels. When emboli occur, patients may complain of symptoms of sudden leg ischemia as the first indication of AAA (see Examination section). If emboli are small and distal vessels are patent, small areas of tissue necrosis in the toes or skin of the lower extremities are seen.
After seeking specific historical information regarding the aneurysm, the patient should be questioned about other symptoms so that an estimate of the extent of atherosclerotic involvement is obtained. This information often influences recommendations for or against surgical
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therapy. Symptoms of transient cerebral ischemia or previous stroke, angina pectoris or previous MI, or cardiac decompensation such as significant shortness of breath, dependent edema, orthopnea, and paroxysmal nocturnal dyspnea are especially important in determining the risks in this group of patients.
Physical Examination
Abdominal palpation is only moderately sensitive and specific in the diagnosis of an AAA (48). As previously noted, most patients with asymptomatic AAAs are discovered on routine physical examination to have an epigastric or left upper quadrant pulsatile mass. However, a pulsatile mass may not be palpable in obese patients or in those with very small aneurysms.
It is important to palpate the epigastrium because the bifurcation of the abdominal aorta is at the level of the umbilicus. Only rarely when palpating inferior to the umbilicus will one identify an AAA unless both common iliac arteries are also aneurysmal. The laterally pulsatile nature of an aneurysm is a clue in differentiating it from the anteriorly transmitted aortic pulsation through viscera or from a mass overlying the aorta. Conditions confused with aneurysms include pancreatic pseudocyst, horseshoe kidneys, neoplasms of the stomach or transverse colon, and retroperitoneal soft tissue tumors. Often, a normal but prominently pulsatile abdominal aorta in a healthy person and an undilated but tortuous aorta in an elderly person may simulate an AAA. In this circumstance, the pulsatile mass is felt to the left of the midline but not to the right. One should palpate the abdomen by approaching the midline both from the right and from the left to identify the laterally pulsatile characteristic of an aneurysm. Risk of rupture correlates best with the size of the aneurysm as determined by US and not by physical examination alone (see Fig. 94.5).
One fourth to one third of patients have significant associated occlusive arterial disease as well as the AAA, so a systematic evaluation should be performed. Systemic blood pressure should be measured in both arms. Carotid bruits can be detected by listening with the bell of the stethoscope over the carotid bifurcations at the angle of the mandible with the patient supine and holding his or her breath. Examination of the lower extremities should be directed to the character of the femoral, popliteal, and pedal pulses and to the presence or absence of femoral and popliteal bruits and aneurysms. In less than 10% of patients with AAA, there may be coexistent peripheral aneurysms involving the popliteal or femoral arteries.
Laboratory and Radiographic Studies
The presence or absence of an AAA must be confirmed by US. The accuracy of sonographic diagnosis of AAAs approaches 100% (49). Anteroposterior and cross-table lateral plain radiographs of the abdomen also document AAAs in 70% to 80% of cases because the aneurysm wall is often calcified. Ultrasonography is simple, safe, and cost-effective and is recommended as the method of choice for verifying or excluding an AAA and for serial followup every 6 months to assess aneurysmal size for patients being treated nonoperatively.
CT and MRI are more expensive and should be used only as an adjunct to US for confirming unusual situations, such as a suspected leak in an otherwise stable patient, extent of visceral artery involvement, inflammatory change, or the presence and characteristics of horseshoe kidney. Generally, the cost of a CT is about double that of a sonogram. The MRI costs twice as much as the CT and rarely provides additional information.
Objective measurement of peripheral pulses in the lower extremities and baseline Doppler blood flow studies are of value during long-term followup. Because atherosclerotic disease may be progressive, the patient should be followed on a yearly basis after convalescence from surgery.
Treatment and Results
Whereas patients with symptomatic AAAs require operative intervention, it is not clear that early surgery improves mortality in patients with small asymptomatic aneurysms in whom a strategy of “watchful waiting” may be reasonable. In one study, 1090 patients age 60 to 76 years with asymptomatic AAA between 4.0 and 5.5 cm in diameter were randomly assigned to undergo elective surgery or serial ultrasonographic surveillance every 6 months. Surgery was recommended to patients randomized to the surveillance strategy if the AAA diameter exceeded 5.5 cm. After an average of 4.6 years, there was no difference in mortality between the groups (41). The decision about when, and if, to recommend surgery to patients with asymptomatic AAA depends on the assessment of the risk of rupture compared with the risk of elective operative repair (50). The risk of rupture, in turn, is most closely related to AAA size and rate of expansion. Patients with an AAA less than 5.5 cm in diameter may be followed by serial ultrasound examinations performed at 6-month intervals. If the aneurysm exceeds 5.5 cm or if the rate of expansion exceeds 0.5 cm in a 6-month interval, the risk of rupture should be considered high and elective surgery should be strongly considered. When surgery is not recommended, therapy with β-blockers should be considered in an effort to reduce the rate of AAA expansion. This recommendation is based largely on a single study of 121 patients with AAA (approximately two thirds of whom received β-blockers) who were monitored with serial ultrasound examinations approximately every 8 months for an average of 43 months. Among patients with AAA 5 cm or greater, β-blockers
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significantly reduced the expansion rate from 0.68 to 0.36 cm per year (42). Figure 94.5 shows an approach to the management of AAA.
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FIGURE 94.5. An approach to AAA. The risk of rupture is weighed against the mortality associated with AAA repair (by both endovascular and open means). |
Routine use of preoperative aortography among patients with AAAs is very rare. With the advent of multislice CT, outstanding definition can be achieved. A standard protocol CT angiogram with three-dimensional reconstruction can provide all necessary information on the size of the aneurysm as well as anatomic features and suitability for stent-grafting. The procedure requires the administration of 100 to 120 mL of iodinated contrast material. For patients with renal insufficiency, magnetic resonance angiography (MRA) may provide an alternative diagnostic modality. Although surgeons rarely recommend aortography, and most use aortographic studies selectively, under certain circumstances abdominal aortography is helpful and even mandatory. Indications for aortography include the possibility of anomalous renal or visceral vasculature or occlusive disease involving these same vessels that would alter the operative approach. It is important to determine the extent of reconstruction necessary so that the anomalous vessels are not violated and the occlusive lesions are addressed. Drug-resistant renovascular hypertension is an indication for aortography to document renal artery stenosis that can be corrected at the time of abdominal aortic aneurysmectomy. Aortography is essential for delineation of the anomalous circulation of the rare horseshoe kidney initially detected by US.
It is essential to inform the patient of various risks of operative versus nonoperative treatment. Equally important is explaining complications that may occur in the postoperative period. Although this is primarily the responsibility of the operating surgeon, it is appropriate for the primary clinician to discuss with the patient what is likely to occur. The patient should know that a Dacron or polytetrafluoroethylene prosthesis will be used to replace the abdominal aorta and that such arterial grafts are very durable. Fortunately, complications are rare and include (but are not limited to), renal failure, amputation, graft infection, ischemic colitis, paraplegia from spinal cord ischemia, and aortoenteric fistula. It should be stressed to the patient that postoperative complications of abdominal aortic aneurysmectomy are magnified by the urgency of the operative procedure. Proper cardiac risk stratification by noninvasive evaluation (that is, but are not limited to, exercise or nuclear stress test or stress echocardiogram), prior to open AAA repair may identify those patients who may benefit from preoperative coronary angioplasty.
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Endovascular stent-grafting of AAAs is gaining favor as the preferred approach for repair of AAA, especially in those patients of advanced age or with significant co-morbidity. This technique uses an endoprosthesis that is delivered percutaneously through the femoral artery and deployed in the area of the aneurysm. The endograft is secured with metallic expandable stents and thrombosis of the external surrounding aneurysm, in theory, reduces the risk of rupture. Three Food and Drug Administration (FDA)-approved devices are available for implantation.
Results with each are largely equivalent, with only minor technical differences in device insertion. Randomized trials have demonstrated that endovascular stent-grafting of AAAs is equivalent to open AAA repair for prevention of aneurysm-associated mortality (51).
To date, the most common adverse long-term problem with the current devices is “endoleak,” which represents persistent filling of the AAA from either the anastomotic site or through other collateral blood vessels (44). Endoleaks may occur at the interface of the device and the aorta or iliacs, between device junctions, or most commonly from lumbar vessels that back-bleed into the aneurysm sac via collaterals. These endoleaks occur in 10% to 20% of patients per year who have undergone endovascular stent-grafting of AAAs. If associated with expansion of aortic diameter, such endoleaks may require additional procedures to investigate their source.
Patient Experience with Endovascular AAA Repair
Patients are often enticed by the minimally invasive nature of endovascular stent-grafting of AAAs. A standard expected course of endovascular stent-grafting of AAAs is admission on the same day of surgery (if no preoperative overnight hydration for prevention of contrast nephropathy). Patients may have epidural anesthesia (and be kept awake) or general anesthesia. Using bilateral groin incisions, the endovascular implant is introduced via the femoral arteries into the aorta and sealed below the renal arteries to shield the aneurysm sac from the aortic blood flow/pressure. Separate pieces are introduced from either groin to complete the bifurcated device, seal the device at the common iliac arteries bilaterally, and provide passage of blood to pelvis and legs. Transfusion of red blood cells is uncommonly required unless preoperative anemia is present. Patients are monitored in the recovery room or intensive care unit and then convalesce in the hospital for 1 to 2 days prior to discharge. Oral analgesics easily control the pain of the groin incisions, and most patients return to work 2 weeks after endovascular stent-grafting of AAAs. Standard surveillance using CT angiograms of the abdomen and pelvis are required at 1, 6, 12, 18, and 24 months and then yearly to monitor for “endoleaks.” Although recovery time is clearly less with EVAR, patients are often frustrated by the intense postoperative surveillance and the potential necessity for additional procedures to eliminate any endoleak. Nonetheless, even with the trade-off of the imposition of regular surveillance versus the extensive incision and recovery of open AAA repair, endovascular stent-grafting of AAAs is often preferred by patients.
If operation is not recommended or accepted, the patient should be evaluated every 3 to 6 months by interval history, physical examination, and US. The warning signs of a rupturing or symptomatic aneurysm, especially steady dull abdominal, flank, or back pain, should be described to the patient. If such pain occurs or if a change in existing symptoms is noted in a patient being followed with an AAA, the patient should be instructed to seek surgical attention promptly.
Peripheral Arterial Aneurysms
Peripheral arterial aneurysms may involve the carotid, subclavian, brachial, iliac, femoral, and popliteal arteries. More than 90% of peripheral aneurysms involve either popliteal or femoral arteries. Popliteal arterial aneurysms predominate. Tortuous vessels presenting as serpiginous pulsations under the skin may be mistaken for peripheral aneurysms. The most noted example of this is a tortuous subclavian or common carotid artery in an elderly hypertensive patient that may be confused with a carotid or subclavian artery aneurysm. The pathogenesis of peripheral aneurysms is unknown. There is a male predominance (30:1 ratio, men versus women) and up to 50% are bilateral (52).
Most peripheral arterial aneurysms are arteriosclerotic in origin; mycotic, traumatic, and syphilitic aneurysms are rare. Peripheral arteriosclerotic aneurysms are localized manifestations of a generalized disease process. This is underscored by noting that among a group of 37 patients with common femoral aneurysms, 95% had another aneurysm elsewhere, and 92% had associated aortoiliac aneurysms (53). Femoral aneurysms can be bilateral in up to 60% of cases. Similarly, among 36 patients with popliteal arterial aneurysms, almost 80% had an aneurysm elsewhere, two thirds had aortoiliac aneurysms, and bilateral popliteal aneurysms occurred in 50% of these patients (53). Therefore, when a peripheral aneurysm is found, the clinician should be aware that multiple and bilateral aneurysms can occur, and that the popliteal, femoral, and aortoiliac areas should be carefully assessed by physical examination and US.
Femoral and, particularly, popliteal arterial aneurysms are associated with a high incidence of distal thromboembolism and eventual limb loss. Approximately 75% of untreated peripheral aneurysms may eventuate in limb loss from either distal embolization or acute thrombosis.
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On the other hand, rupture with exsanguinating hemorrhage is not a major risk with femoral or popliteal arterial aneurysms, as it is for AAAs.
Clinical Manifestations
Most patients with peripheral arterial aneurysms are elderly, and many are asymptomatic. Femoral arterial aneurysms are usually evident, particularly when they measure 4 or 5 cm in diameter. Similarly, popliteal aneurysms, if they are large, are easily identified. However, popliteal aneurysms may be overlooked because many clinicians do not routinely palpate the popliteal fossa during a physical examination. Approximately 50% of femoral and popliteal aneurysms present with limb-threatening complications of thrombosis, embolization, or rupture. Hence, the discovery of an asymptomatic aneurysm in these anatomic areas is a clear indication for timely repair. Once complications of peripheral aneurysms develop, there is a 25% risk of limb amputation.
An enlarged artery with a very prominent femoral or popliteal pulse to physical examination is characteristic of a femoral or popliteal aneurysm and should be confirmed by US. Diagnosis of femoral aneurysm is easily made on clinical examination alone, but the diagnosis of popliteal aneurysm may be more difficult. When the popliteal fossa is palpated, the patient's leg should be relaxed while the examiner passively flexes the knee with the fingers, compressing the popliteal artery in the fossa, with the thumbs on the patella providing counter-compression. If an unusually prominent popliteal pulsatile mass is palpated and the examiner suspects aneurysm, the patient may be placed in the prone position and the lower leg supported by the examiner's arm to facilitate popliteal arterial palpation. US should be obtained if there is any suspicion of an aneurysm, because diagnosis and treatment before the occurrence of complications are exceedingly important. Occasionally, the only manifestations of a popliteal aneurysm are small punctate necrotic areas of skin over the anterior tibial region or small gangrenous areas of the tips of toes. This “blue toe syndrome” is a result of microemboli from the aneurysm that have showered to the periphery.
Once the diagnosis of a peripheral arterial aneurysm is made, the patient should be referred to a vascular surgeon. Arteriography is mandatory to confirm the anatomy and patency of the femoral–popliteal and tibial arteries when planning operative intervention.
Treatment and Results
Treatment of symptomatic peripheral aneurysms is indicated in all instances. Because the natural history is eventual limb loss, it is important to offer surgical therapy in most cases to maintain or improve quality of life by avoiding amputation. Surgical correction includes replacement of femoral aneurysms with prosthetic or reversed autogenous saphenous vein grafts (SVGs). Similarly, popliteal aneurysms are managed by bypassing the diseased segment with autogenous saphenous vein.
Operative mortality for management of peripheral aneurysms is approximately 1% to 3%. Limb salvage is obtained in more than 90% of cases and is related to the degree of arterial involvement peripheral to the aneurysm. In almost all series of repair of popliteal arterial aneurysms, amputations in the postoperative period have been associated with severe occlusive arterial disease manifested preoperatively by gangrene and rest pain.
Specific References*
For annotated General References and resources related to this chapter, visit http://www.hopkinsbayview.org/PAMreferences.
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