Peripheral Arteriovascular Disease

Chapter 87


Peripheral Arteriovascular Disease






Principles of Disease



Arterial Anatomy


All arteries possess three layers: the tunica intima, tunica media, and tunica adventitia. As peripheral arteries diminish in caliber, these three layers become progressively indistinct and are no longer identifiable at the level of the arteriole (precapillary vessel containing smooth muscle).


The tunica intima has an inner lining of endothelial cells surrounded by subendothelial connective tissue. The single layer of continuous endothelium is a unique thromboresistant layer between blood and the potentially thrombogenic subendothelial tissues. The integrity of the endothelium is a fundamental requirement for maintenance of normal structure and function of the entire vessel wall. Endothelial injury can result in intraluminal thrombosis and may contribute to the initiation of atherosclerosis.


The tunica media is made up primarily of circular or spiral smooth muscle cells arranged in concentric layers. The outer limit of this layer is marked by a well-defined, external elastic membrane. The elastic content of the tunica media gives resilience to medium-sized arteries. With age, the elastic fibers deteriorate and are replaced by fibrous tissue. This loss of elasticity results in stretching and elongation and accounts for the progressive tortuosity and development of arterial aneurysms with aging. Vascular smooth muscle cells may be important in lipid accumulation in the vessel wall during atherosclerosis and participate in vasoconstriction and dilation.


The tunica adventitia is a poorly defined layer of connective tissue in which nerve fibers and small, thin-walled nutrient vessels (vasa vasorum) are dispersed. Medium-sized arteries contain more nerve fibers than larger vessels, reflecting the importance of their role in the autonomic regulation of blood flow.


The peripheral arterial vascular system can be considered as a single end-organ subject to eight basic pathophysiologic processes: (1) atherosclerosis, (2) aneurysm, (3) embolism, (4) thrombosis, (5) inflammation, (6) trauma, (7) vasospasm, and (8) arteriovenous fistula. Two of these—atherosclerosis and thrombosis—are responsible for most peripheral arterial problems.



Pathophysiology



Atherosclerosis: Atherosclerosis is a disease of large- and medium-sized muscular arteries. The basic lesion, the atheroma, or fibrofatty plaque, is a raised focal plaque within the intima; it has a lipid core (mainly cholesterol, usually complexed to proteins and cholesterol esters) covered by a fibrous cap. As the plaques increase in size and number, they progressively encroach on the lumen of the artery and the adjacent media. Atheromas compromise arterial blood flow and weaken the walls of the affected arteries.


The distribution of atherosclerotic plaques is rather constant. The abdominal aorta has more atherosclerotic disease than the thoracic aorta, and aortic lesions are much more common and prominent around the ostia of major branches. Other vessels affected by atherosclerosis are the aortoiliac, femoral, and popliteal arteries; the descending thoracic aorta; the coronary arteries; the internal carotid arteries; and the circle of Willis. Vessels of the upper extremities are usually spared.


As atherosclerosis progresses, atheromas almost always calcify, resulting in hard, brittle vessels. Ulceration of the luminal surface and rupture of the atheromatous plaques discharge debris, producing atheroemboli (cholesterol emboli). Fissured or ulcerated lesions can produce in situ thrombosis, causing acute intraluminal occlusion.


Hemorrhage into the plaque may further compromise the arterial lumen. Although atherosclerosis primarily affects the intima, in severe cases, the tunica media undergoes pressure atrophy and loss of elastic tissue, with sufficient weakening to create aneurysmal dilation.



Aneurysms: A true aneurysm is an abnormal localized dilation of the intact vessel wall. With a pseudoaneurysm the entire wall perforates or ruptures, and the extravasated blood is contained by the surrounding tissues, eventually forming a fibrous sac that communicates with the artery.


Mural and mechanical factors contribute to true aneurysm formation.1 The major cause of aneurysms is a weakness or defect in the integrity of the arterial wall. The only aneurysms that develop in a normal arterial segment are poststenotic aneurysms, such as with coarctation. Acceleration of flow past a narrow point creates slower flow beyond the stenosis lateral to the jet stream, producing increased lateral pressure. Aneurysmal dilation accelerates, increasing the risk of rupture as diameter increases, as predicted by Laplace’s law: tension (lateral pressure) in the wall of a hollow viscus varies directly with its radius (tension = pressure × radius).


The most common cause of aneurysms is severe atherosclerosis resulting from thinning and destruction of the tunica media. Atheromatous ulcers covered by mural thrombi are common within an aneurysm. Such mural thrombi can form emboli that lodge in distal vessels. When an entire aneurysm is filled with thrombus material, arterial occlusion results.


Aneurysms cause clinical symptoms through (1) rupture with subsequent hemorrhage, (2) impingement on adjacent structures, (3) occlusion of a vessel by either direct pressure or mural thrombus formation, (4) embolism from mural thrombus, and (5) presentation as a pulsatile mass.



Arterial Embolism: An embolus is a blood clot or other foreign body that is carried by the blood to a site distant from its point of origin. Most emboli are the result of detached thrombus formation (thromboembolism). Less common sources include debris from ruptured atherosclerotic plaques, tumor debris, or foreign bodies. Unless otherwise specified, the term embolus in this chapter is defined as thromboembolus.



Thromboembolism.: Most arterial emboli (85%) originate in thrombus formation in the heart. Left ventricular thrombus formation resulting from myocardial infarction accounts for 60 to 70% of arterial emboli. Atrial thrombi associated with mitral stenosis and rheumatic heart disease account for only 5 to 10% of arterial emboli.2 Coexisting atrial fibrillation, often without mitral stenosis, is present in 60 to 75% of patients with peripheral arterial embolic events, because atrial fibrillation itself can predispose patients to intracardiac clotting.3


Acute arterial emboli often cause distal tissue infarction. Clinical outcome depends mostly on the amount of collateral circulation present but also on the size of the vessel and the degree of obstruction. Patients with long-standing atherosclerosis have well-developed collateral circulation, whereas sudden occlusion of a normal artery without collateral pathways results in severe ischemia. After acute obstruction, the embolus can propagate proximally or distally, fragment and embolize further to distal vessels, or precipitate associated venous thrombosis by initiating a localized inflammatory reaction.


Because vessel diameters change most abruptly at branch points, embolic occlusion most often occurs at major arterial bifurcations. The bifurcation of the common femoral artery is the most frequent site of arterial embolism, accounting for 35 to 50% of all cases.2 The smaller femoral and popliteal arteries are involved twice as often as the larger aortic and iliac vessels, reflecting the small size of most emboli.


Cell death from arterial ischemia can produce high concentrations of potassium, lactic acid, and myoglobin in the extremity distal to an arterial occlusion. Their sudden release after revascularization can produce life-threatening hyperkalemia, metabolic acidosis, and myoglobinuria. This myonephropathic-metabolic syndrome accounts for approximately one third of the deaths from arterial embolism after revascularization.4



Atheroembolism.: Atheroembolism refers to microemboli consisting of cholesterol, calcium, and platelet aggregates dislodged from proximal complicated atherosclerotic plaques that lodge in distal end arteries. In the central nervous system, atheroemboli cause transient ischemic attacks and strokes. In the peripheral vascular system, atheroemboli characteristically cause cool, painful, and cyanotic toes, or the blue toe syndrome.5


Atheroemboli are caused by a proximally located arterial lesion, usually atherosclerotic plaques or aneurysms. Bilateral distal extremity involvement usually implies an aortic source, whereas unilateral atheroemboli usually arise from sites distal to the aorta. Distal lesions are most common in the femoropopliteal arteries (60%) and the aortoiliac arteries (40%). Aortic lesions (e.g., aneurysms, polytetrafluoroethylene grafts) are a less common source of microemboli.5


Atheroemboli are small and tend to lodge in distal arteries, such as the digital arteries, which are 100 to 200 µm in size. Single atheroembolic events seldom result in tissue loss, but atheroemboli tend to cluster. If unrecognized, repeated events ultimately result in loss of collateral circulation, progressive symptoms, and extensive tissue infarction.5


Infectious emboli from bacterial endocarditis can produce septic infarcts that may convert to large abscesses. Rarely, cardiac and noncardiac tumors or foreign bodies may gain access to the arterial circulation and embolize. Primary or metastatic lung neoplasms, malignant melanoma, and bullet emboli have been reported. In patients with cyanotic congenital heart disease (e.g., patent foramen ovale), venous emboli may pass directly to the arterial circulation (paradoxical emboli). Although rare, this possibility should be considered in any patient with simultaneous arterial and venous emboli, particularly if a source of the arterial embolus is not evident.





Trauma: Different types of vascular injury result in characteristic pathologic syndromes. Partial arterial lacerations continue to bleed because the intact portion of the vessel wall prevents retraction and closure of the arterial wound. This may form an expanding hematoma, causing progressive deformity, pain, and nerve compression. Complete arterial transection usually has only moderate or insignificant bleeding because of arterial spasm of the transected ends of the artery and the formation of a temporary thrombus. Delayed hemorrhage in completely transected arteries may result from relaxation of arterial spasm, eventual liquefaction of the thrombus, or displacement of the thrombus by arterial pressure. Blunt injury may produce partial or complete intimal disruption. Dissection of the distal intima can lead to progressive obstruction and thrombosis. Complete occlusion may not occur for hours or days after injury. Vasospasm can accompany injuries that are adjacent to blood vessels; spontaneous resolution always occurs in the absence of arterial disruption or intimal injury.




Arteriovenous Fistulae: Abnormal communication between arteries and veins may result from congenital defects, rupture of an arterial aneurysm into an adjacent vein, penetrating injuries, and inflammatory necrosis associated with neoplasms or infection. Arteriovenous fistulae can occur in any region of the body. The artery proximal to the fistula becomes distended, tortuous, and aneurysmal. Similar changes occur in the venous side of the fistula. Proximal and distal veins respond to alterations in hemodynamics with intimal proliferation and fibrosis, followed by a decrease in the internal elastic lamina, resulting in distention, tortuosity, and aneurysm formation. The resultant chronic venous hypertension may cause dermatitis and ulceration of overlying skin. The size of the fistula generally increases with time.


Approximately 60% of arteriovenous fistulae are associated with a false aneurysm.7 False aneurysm formation can occur as part of the fistulous tract or as the result of arterial or venous dilation.7


The increase in cardiac output that occurs when blood switches from the arterial to the venous system can result in a widened pulse pressure or high-output cardiac failure.



Clinical Features



History


Patients with peripheral arterial disease have pain, tissue loss (ulceration or gangrene), or a change in sensation or appearance (swelling, discoloration, or temperature change). Because the primary cause of peripheral arterial disease is atherosclerosis, related conditions providing evidence of atherosclerosis are cardiac disease, myocardial infarction, cardiac dysrhythmias (e.g., atrial fibrillation), stroke, transient ischemic attacks, and renal disease. Factors that increase the likelihood of atherosclerosis are cigarette smoking, diabetes, hypercholesterolemia, and hypertension. Intravenous drug use can lead to arterial injury.


Risk factors not related to atherosclerosis include prior injuries or surgeries, major illnesses, a history of phlebitis or pulmonary embolism, the presence of autoimmune disease or arthritis, and a history of prior coagulation abnormalities.



Acute Arterial Occlusion: The patient with acute arterial occlusion usually exhibits some variant of the five Ps: pain, pallor, pulselessness, paresthesias, and paralysis. Paresthesias and paralysis indicate limb-threatening ischemia that requires emergency surgical intervention regardless of the cause. In patients with non–limb-threatening ischemia, accurate differentiation between embolism and in situ thrombosis as the cause of acute arterial occlusion determines management. Arterial embolism is best managed by emergency Fogarty catheter embolectomy. Non–limb-threatening ischemia from in situ thrombosis is often aggravated by emergency surgical intervention and is therefore initially best managed nonoperatively, if possible (Fig. 87-1). Because acute arterial embolism usually occurs in patients without significant peripheral atherosclerosis and without well-developed collateral circulation, it usually manifests as sudden limb-threatening ischemia. Patients describe a sensation of the leg’s being “struck” by a severe shocking pain. Often the patient has to sit or fall to the ground during the sudden event.



In situ thrombosis usually occurs in patients who have long-standing significant peripheral atherosclerosis and well-developed collateral circulation and is often seen subacutely with non–limb-threatening ischemia. A history of claudication is common with in situ thrombosis and rare in patients with arterial embolism.



Chronic Arterial Insufficiency: Chronic arterial insufficiency causes two characteristic types of pain: intermittent claudication and ischemic pain at rest. The location of arterial occlusion determines the location of claudication. Calf claudication is associated with femoral and popliteal disease, typically a cramping pain, reliably reproduced by the same degree of exercise and completely relieved by rest (usually 1-5 minutes). Aortoiliac occlusive disease causes claudication in the buttocks and hips, as well as the calves. The calf pain in aortoiliac disease is generally more severe than the buttock and thigh pain, which is more often described as an aching, discomfort, or weakness. Some patients deny pain, complaining only that the thigh or hip “gives out” with exercise. Aortoiliac occlusive disease severe enough to produce bilateral claudication is almost always associated with impotence in men (Leriche’s syndrome). Even in the absence of impotency, bilateral hip or thigh pain in a man should indicate the possibility of aortoiliac occlusive disease.


Chronic arterial insufficiency may progress so that ischemic pain occurs at rest. Rest pain often begins in the feet and typically involves the foot distal to the metatarsals, awakening the patient from sleep. Ischemic rest pain is a severe, unrelenting pain aggravated by elevation and unrelieved by analgesics, but patients have prompt relief with any activity that involves a standing position. Patients often sleep with the leg dangling over the side of the bed or sleep in a chair to improve perfusion pressure to the distal tissues.



Physical Examination


A systematic assessment of the peripheral vascular system includes palpation of the pulse volume in the pairs of brachial, radial, femoral, posterior tibial, and dorsalis pedis arteries documented on a scale of 0 to 4+. Approximately 10% of the population does not have one of the dorsalis pedis pulses.8 Carotid arteries should be gently palpated one at a time.


The lower extremities should be examined for signs of chronic and advanced ischemia. Muscular atrophy, particularly in the lower extremities, and loss of hair over the toes and feet with thickening of the toenails resulting from slowness of nail growth are common signs of arterial insufficiency. As ischemia becomes more advanced, the skin becomes shiny, scaly, and “skeletonized” from atrophy of the skin, subcutaneous tissue, and muscle.


Areas where ischemia is suspected can be tested by blanching with finger pressure; a delay in return of normal color (compared with that of the unaffected extremity) implies reduced perfusion.


Buerger’s sign provides reliable evidence of severe advanced ischemia. With the patient supine, his or her legs are elevated to 45 degrees to bring the feet more than 12 inches above the right atrium, and any pallor of the feet is noted. If the color does not change, the patient dorsiflexes the feet five or six times; pallor induced by exercise also connotes inadequate arterial flow. The patient is then moved to the sitting position with the feet hanging down. Within 10 to 15 seconds, color should return, and the veins should fill. Typically in the ischemic foot the first color return is cyanotic, transitioning to red as reactive hyperemia occurs. If the veins require more than 20 seconds to become distended, advanced ischemia is present. With severely restricted arterial inflow and chronic dilation of the peripheral vascular bed, the foot turns chalk white on elevation and intensely hyperemic after 1 minute of dependency. Localized pallor or cyanosis associated with poor capillary filling is usually a prelude to ischemic gangrene or ulceration.


Doppler ultrasonography should be used in patients with questionable or absent pulses. The ankle-brachial index (ABI) is made by comparing the systolic blood pressure at the level of the ankle with the brachial systolic pressure. With the patient supine, a blood pressure cuff is applied just proximal to the malleolus, inflated above brachial systolic pressure, and then deflated slowly. Ankle systolic pressure can be accurately measured with a Doppler probe placed over the dorsalis pedis or posterior tibial artery. This pressure is normally 90% or more of the brachial systolic pressure; with mild arterial insufficiency, it is between 70 and 90%; with moderate insufficiency, between 50 and 70%; and with severe insufficiency, less than 50%.


The Allen test is helpful in assessing patency of the radial or ulnar artery distal to the wrist. The patient initially opens and closes the hand and then clenches the fist to expel as much blood from the hand as possible; the examiner then compresses the radial and ulnar arteries. When the patient opens the fist, the hand is pale. The examiner then releases pressure from the radial artery but maintains it on the ulnar artery. If the radial artery distal to the wrist is patent, the hand becomes pink rapidly; if it is occluded, the hand remains pale. The maneuver is then repeated by maintaining pressure on the radial artery while releasing the ulnar artery. A comparison can be made with the opposite hand.



Arterial Embolism: The physical examination can differentiate arterial embolism from in situ thrombosis. The sudden loss of a pulse is the hallmark of arterial embolism but may be difficult to recognize if the prior pulse status is unknown or is abnormal as the result of associated atherosclerosis. A bounding pulse may be felt initially at the location of an embolus from transmitted pulsations through the fresh clot. In general, patients with arterial embolism have few physical findings suggestive of long-standing peripheral vascular disease with normal proximal and contralateral limb pulses. Tenderness to palpation may occur at the site of an embolic occlusion.


If arterial embolism is suspected, the physical examination should be directed toward identifying its source, most commonly a left ventricular mural thrombus secondary to a prior myocardial infarction and a left atrial thrombus in a patient with mitral valve disease. Coexistent atrial fibrillation is common.


The limb distal to an embolic occlusion is initially chalk white. Because of absence of blood from the venules of the subcapillary layer, the demarcation between ischemic and nonischemic tissue is sharp. With time, cyanosis may appear, indicating desaturation of blood with continued ongoing ischemia. Paresthesia or paralysis indicates limb-threatening ischemia. The presence of sensitivity to light touch is often the best guide to viability of the tissue. Complete anesthesia demands immediate surgical intervention. Paralysis represents severe skeletal muscle and neural ischemia, which may be irreversible. Involuntary muscle contracture with woody hardness represents irreversible ischemia.



Arterial Thrombosis: Physical findings of in situ thrombosis are often accompanied by evidence of atherosclerotic occlusive disease. Proximal or contralateral limb pulses are usually diminished or absent. An embolic source, such as mitral valve disease or atrial fibrillation, is usually absent. Because of collateral circulation, demarcation of limb ischemia is less well defined in these patients (Table 87-1).



Carotid, renal, and femoral arteries may have bruits, and there may be an abdominal aortic aneurysm. If an occlusion of the upper extremity vessels is suggested, the subclavian artery should be evaluated by palpating for thrills and listening for bruits in the supraclavicular fossa.


A funduscopic examination may yield evidence of arteriosclerosis or hypertension. Hollenhorst plaques (atheromatous emboli containing cholesterol crystals in the retinal arterioles) may be detected. Roth’s spots (round or oval white spots seen near the optic disk) may be present in patients with infective endocarditis.


Embolic phenomena can cause diverse end-organ damage: hemiplegia from cerebral emboli, flank pain with hematuria from renal emboli, left upper quadrant abdominal pain from splenic infarcts, and pleuritic pain with hemoptysis from pulmonary emboli. Septic pulmonary embolism from right-sided endocarditis may be confused with pneumonia.




Vasospasm: Vasospastic disorders cause a sharp border between ischemic and normal tissue. Raynaud’s disease is characterized by intermittent attacks of triphasic color changes: pallor, cyanosis, and then rubor.9 The most important element is pallor, during which the digits turn chalk white. Attacks last 15 to 60 minutes, and rewarming the hands restores normal color and sensation. Color changes do not occur above the metacarpophalangeal joints and rarely involve the thumb.


Livedo reticularis is characterized by a persistent cyanotic mottling of the skin that has a typical “fishnet” appearance and may involve all parts of the extremities and trunk. Acrocyanosis, the least common vasospastic disorder, is characterized by persistent, painless, diffuse cyanosis of the fingers, hands, toes, and feet. Cyanosis usually intensifies with exposure to cold and decreases with warming. The involved parts are nearly always cold, exhibit excessive perspiration, and have normal arterial pulses.



Arteriovenous Fistulae: Arteriovenous malformations and fistulae, although rare, must be distinguished from vascular bruits or aneurysms. True aneurysms and arterial stenoses are associated with a systolic murmur. Pseudoaneurysms generally have a loud systolic and sometimes a separate faint diastolic murmur. Arteriovenous fistulae have a constant systolic and diastolic (to-and-fro) murmur heard best directly over the lesion and often associated with a palpable thrill, precisely analogous to the findings of a therapeutic dialysis arteriovenous fistula. Unless congenital, arteriovenous fistulae occur at prior operative or trauma sites. The skin overlying the lesion may be warm, but distally the temperature is often decreased. Veins peripheral to the fistula are usually distended and varicose. Large and long-standing arteriovenous fistulae produce high cardiac output and widened pulse pressure. Digital pressure on the artery leading to the fistula or the fistula itself may decrease the tachycardia (Branham’s sign).



Diagnostic Strategies


An accurate diagnosis of peripheral arterial occlusive disease can be achieved in most patients by careful history and physical examination supplemented by bedside testing.



Noninvasive Assessment


Doppler ultrasonography measures blood flow velocity by detecting the frequency shift of sound waves reflected from red blood cells that move toward and away from the transducer. The Doppler signal generates a normal triphasic velocity waveform. Progressive arterial narrowing alters the triphasic waveform to biphasic and finally monophasic shape. Such Doppler ultrasonographic waveform analysis can detect significant arterial occlusive disease, although it is less accurate in determining exact location.


Ultrasound is useful in detecting and evaluating atherosclerotic plaques and mural thrombi and in sizing aneurysms of the abdominal aorta and iliac, femoral, and popliteal arteries.10 B-mode ultrasonography is noninvasive, painless, less expensive than other modalities, and universally available and is the diagnostic procedure of choice for the initial evaluation and determination of the size of peripheral artery aneurysms. Bedside ultrasound can lead to rapid diagnosis of life-threatening conditions and reduce the number of delayed or invasive diagnostic procedures.11 B-mode duplex ultrasonography combines the image of B-mode ultrasonography and sophisticated online computer analysis of accurately sampled Doppler waveforms to allow simultaneous acquisition of both the image of a vascular structure and the characteristics of blood flow velocity within it. Duplex scanning permits noninvasive and accurate diagnosis of peripheral vascular, cerebrovascular, and venous disease.


Color imaging of blood flow combined with duplex scanning is known as color-coded Doppler, Doppler angiography, or angiodynography. The procedure of choice for most conditions, this combination allows noninvasive and accurate detection of atherosclerotic plaques and stenoses, their effect on intraluminal blood flow, and the presence of venous thrombosis.



Contrast Arteriography


Angiography is the definitive test of abnormal peripheral artery anatomy but is often inconclusive about the physiologic condition of the tissues. Adverse effects of contrast media and catheter-related complications must be weighed against the benefits of this procedure. Contrast media have a direct toxic effect on vascular endothelium; can produce renal failure, especially in diabetic patients; may cause peripheral vasodilation with hypotension; may result in seizures and stroke in patients with neurologic conditions; and can cause severe idiosyncratic and allergic reactions. Catheter-related complications, including embolization, catheter breakage, and vascular disruption, vary with operator skill and anatomic location but average 0.5%. The overall mortality rate from angiography is 0.03%.11 Emergency angiography is usually necessary in the following circumstances: (1) acute arterial embolus or thrombosis if the clinical diagnosis is uncertain, (2) consideration of emergency vascular bypass grafting, and (3) characterization of vascular abnormality before emergency surgical correction.



Computed Tomography and Magnetic Resonance Imaging


Computed tomography angiography is the most useful test for evaluation of the abdominal aorta.12 In the peripheral arteriovascular system, CT angiography is useful primarily for atherosclerotic, infected, and false aneurysms and for imaging the cerebral circulation. Magnetic resonance imaging (MRI) has the capability for angiography (magnetic resonance angiography) and has been particularly useful in delineating cerebrovascular problems (see Chapter 101); it is seeing expanded use in the evaluation of peripheral vascular disease. The ability to make axial, coronal, and sagittal sections provides accurate visualization of anatomy. MRI detects changes in the relaxation variables of tissues before obvious structural changes, uniquely differentiating blood, thrombus, fat, and fibrosis.



Management Options


The management of acute arterial occlusion depends on the degree and cause of ischemia. Patients with limb-threatening ischemia from embolism should undergo emergency Fogarty catheter embolectomy.13 Patients with limb-threatening ischemia caused by in situ thrombosis require direct or Fogarty catheter thrombectomy combined with vascular bypass grafting. Thrombectomy alone often fails because of recurrent thrombosis. Patients who have a lesion that cannot be bypassed, who have evidence of irreversible ischemia, or who are too ill to tolerate revascularization are treated with primary amputation.


A patient with non–limb-threatening ischemia from embolism still is treated with Fogarty catheter embolectomy. Non–limb-threatening ischemia from in situ thrombosis is managed nonoperatively with immediate systemic heparinization and possibly with intra-arterial fibrinolytic therapy (see Fig. 87-1).


Elective surgical repair of an asymptomatic atherosclerotic peripheral arterial aneurysm is usually accomplished by excision of the aneurysm with end-to-end anastomosis or graft interposition. Infected true and false peripheral aneurysms require aneurysm resection, débridement of infected tissue, and ligation of the proximal and distal uninfected arteries. Autogenous vein bypass through uninfected tissue planes is attempted, because prosthetic grafts carry a high risk of graft infection. The surgical approach for uninfected false aneurysms is similar to that for peripheral atherosclerotic aneurysms.


Patients with thoracic outlet syndrome who have cervical ribs, arterial involvement, or significant neurologic symptoms require surgical decompression with removal of anomalous fibromuscular bands and resection of the first rib, if present. Subclavian and subclavian-axillary aneurysms can be treated with resection and end-to-end anastomosis, graft reconstruction, or surgical revision. Patients with distal embolic occlusions are treated with Fogarty catheter embolectomy. Axillary and subclavian vein thromboses are best managed with surgical thrombectomy or systemic fibrinolytic therapy. Patients with only brachial plexus involvement and minimal signs and symptoms should be followed closely with conservative treatment.


Surgical treatment of peripheral arteriovenous fistulae requires interrupting the fistula tract and restoring both arterial and venous continuity with end-to-end anastomosis or graft interposition. If the anatomic location precludes surgical intervention, percutaneous transvascular embolization with liquid tissue adhesives (e.g., isobutyl 2-cyanoacrylate) is usually successful.



Noninvasive Therapy




Fibrinolytic Therapy: Low-dose intra-arterial fibrinolytic therapy is increasingly used for acute arterial occlusion. Patients with limb-threatening ischemia are not candidates because clot lysis generally takes 6 to 72 hours. Patients with limb-threatening ischemia cannot tolerate several more hours of ischemia without tissue or limb loss. Fibrinolytic therapy is generally reserved for patients with in situ thrombosis and non–limb-threatening ischemia.


Intra-arterial fibrinolytic agents induce clot lysis in the small, distal runoff vessels, decreasing outflow resistance and enabling the native artery to remain open longer. Fibrinolysis often uncovers a critical stenosis that, untreated, may lead to another episode of thrombosis. After successful fibrinolytic therapy, most patients require secondary bypass grafting or percutaneous transluminal angioplasty. Streptokinase, urokinase, and tissue plasminogen activator have all been used successfully. Intravenous administration of a fibrinolytic agent is less effective than direct administration into the clot. Clots more than 30 days old are more organized and less likely to achieve successful lysis.



Invasive Therapy




Peripheral Percutaneous Transluminal Angioplasty: The initial success and long-term patency achieved with angioplasty depend on the location of the lesion and the extent of atheromatous disease. Proximal larger arteries (e.g., iliac, femoropopliteal) have the best initial and long-term results. Discrete stenotic lesions (<5 cm) have better long-term patency rates than vessels that are diffusely involved or have multiple involved segments. Balloon angioplasty is the accepted treatment for isolated stenotic lesions in the renal, iliac, and superficial femoral vessels.


Transluminal angioplasty with intravascular stent is used in more distal vessels, including the popliteal and tibial circulation, in cases of more diffuse lesions, and for patients who are prohibitive surgical risks, although its value remains to be determined.14


Recanalization devices include the percutaneous atherectomy catheter, percutaneous angioscope, hot-tip laser, excimer laser, and high-speed rotating wire and drill.



Grafting: Vascular grafting is associated with a variety of complications that can be diagnosed in the emergency department. Autogenous vein grafts (usually a reversed greater saphenous vein) provide excellent long-term patency for small arteries. Vein grafts respond to arterial pressure with gradual intimal proliferation and medial fibrosis. They may develop atherosclerosis, which can lead to graft stenosis and thrombosis. False aneurysms can form along the suture line.


Polytetrafluoroethylene (Teflon) prosthetic grafts are widely used in medium and large arteries that are impossible to bridge with smaller vein grafts. Prosthetic grafts have a higher rate of thrombosis than venous grafts. Distal emboli may result from poor fixation of luminal fibrin. If the prosthetic graft has not been adequately covered by viable tissue, it can erode into adjacent structures and hollow viscera. Prosthetic graft infection is a devastating complication requiring removal of the entire graft.


Vascular grafts can be used to bypass arterial occlusions and reconstruct a diseased arterial bifurcation, or can be interposed between sections of resected artery. The two most common complications of both prosthetic and vein grafts are thrombosis and development of a false aneurysm at one or more suture lines. Bypass grafting is most often used as palliative treatment for symptoms of atherosclerotic occlusive disease. Patients with localized unilateral stenosis (<3-5 cm in length) may have a comparable rate of success with percutaneous transluminal angioplasty with or without stent placement.15


Patients with calf claudication from superficial femoral or popliteal occlusive disease can slow progression if they stop smoking and maintain an active exercise regimen. Patients who have progression of disease, significant rest pain, or tissue loss require surgical revascularization.





Specific Arteriovascular Diseases



Diseases of Chronic Arterial Insufficiency



Arteriosclerosis Obliterans


Arteriosclerosis obliterans (atherosclerotic occlusive disease, chronic occlusive arterial disease, obliterative arteriosclerosis) is the peripheral arterial presentation of atherosclerosis. Most often, arteriosclerosis obliterans affects the lower abdominal aorta, the iliac arteries, and the arteries supplying the lower extremities. Upper extremity manifestations are rare.


Arteriosclerosis obliterans is responsible for 95% of cases of chronic occlusive arterial disease. It is most common in persons older than 50 years, but as many as 19% of cases occur in patients aged 30 to 49 years. Men are affected more often than women (5 : 1 to 10 : 1). Approximately one third of patients with arteriosclerosis obliterans have coexistent coronary artery disease. The incidence of diabetes mellitus is 20 to 30%.18


Risk factors for arteriosclerosis obliterans include cigarette smoking, hyperlipidemia, and hypertension. Of patients with arteriosclerosis obliterans, 70 to 90% are smokers when first examined, 75% have hyperlipidemia, and 30% have hypertension.18



Clinical Features and Differential Diagnosis: Acute arterial occlusion from embolism, thrombosis, or trauma is ruled out primarily by history. Atheromatous emboli from proximal ulcerated plaques or aneurysms can cause small scattered ischemic lesions in the toes, feet, or legs, causing blue toe syndrome (Fig. 87-2). The peripheral pulses are present in blue toe syndrome. Exercise-induced claudication must be distinguished from the nocturnal muscle cramps that frequently occur during rest in elderly patients. Aortoiliac occlusive disease must be differentiated from osteoarthritis of the hip, which tends to be more variable from day to day, is not relieved completely with rest, and is not reliably reproduced by the same amount of exercise. Pseudoclaudication from the cauda equina syndrome is caused by narrowing of the lumbar canal from spondylosis, disease of the intervertebral disks, or spinal cord tumor. The symptoms mimic intermittent claudication but are less closely related to exercise and rest than true claudication.


< div class='tao-gold-member'>

Stay updated, free articles. Join our Telegram channel

Jul 26, 2016 | Posted by in ANESTHESIA | Comments Off on Peripheral Arteriovascular Disease

Full access? Get Clinical Tree

Get Clinical Tree app for offline access