Chapter 20 Arterial Disease
Principles of Surgery Companion Handbook
|Peripheral Arterial Occlusive Disease|
|Lower Extremity Occlusive Disease|
|Mesenteric and Renal Occlusive Disease|
|Upper Extremity Occlusive Disease|
|Cerebrovascular Occlusive Disease|
For purposes of study, arterial diseases are more appropriately categorized into five general topics: peripheral arterial occulsive disease, aneurysms, cerebrovascular occlusive disease, nonatherosclerotic arterial disorders, and vascular trauma.
Atherosclerotic peripheral arterial occlusive disease can be split into four categories, specified on the basis of the anatomic distribution of the symptomatic stenoses. These categories are clinically relevant with respect to treatment as well, since the choice of intervention depends on the anatomic location of the problem.
Within each category, patients may present with acute or chronic symptoms. While acute symptoms are encountered most commonly with embolic problems and bypass graft occlusions, chronic symptoms are associated more frequently with stenotic or occlusive disease within native arterial segments.
The symptoms of lower extremity occlusive disease are as follows:
1. Claudication symptoms. Claudication is defined as pain occurring with ambulation. The symptoms are reproducible and subside with cessation of ambulation. The pain is located in the calves in patients with infrainguinal disease. Patients with suprainguinal (aortoiliac) disease also may experience calf claudication, but the symptom progresses to involve the thighs and buttocks with continued walking. Claudication is a marker for generalized atherosclerotic occlusive disease with its well-known complications of myocardial and cerebrovascular events. It is not, however, well correlated with lower extremity complications; limb loss occurs only in a small minority of untreated patients.
2. Limb-threatening symptoms. Limb-threatening signs and symptoms are those complaints which, unlike claudication, are harbingers of limb loss. These include the presence of pain at rest (almost always in the forefoot and not in the calf, relieved by dependency), ulceration, and gangrene. Acute limb ischemia most often presents with limb-threatening symptoms as a result of the paucity of preexisting collaterals. These patients often present with signs and symptoms that begin with the letter p, including pulselessness, pain, pallor, poikilothermia, paresthesia, and paralysis.
The diagnosis of lower extremity arterial occlusion begins with palpation of the pulses in the leg, including the femoral pulse in the groin, the popliteal pulse behind the knee, and the dorsalis pedis and posterior tibial pulses at the ankle level. Noninvasive testing, in the form of Doppler segmental pressure determinations, is useful to localize the involved arterial segment and as a quantitative index to gauge the severity of the problem. Arteriography is employed only after the patient has been deemed an appropriate candidate for open surgical or endovascular intervention.
The treatment of lower extremity arterial disease can take one of three forms:
1. Open surgical intervention. Bypass or endarterectomy can be employed to improve arterial flow. Endarterectomy is limited to occasional patients with disease localized to the aorta and common iliac arteries and rare patients with focal superficial femoral disease at the adductor canal. Bypass of aortoiliac lesions is best accomplished with polyester or expanded polytetrafluoroethylene (ePTFE) bifurcated aortobifemoral bypass grafts. Infrainguinal bypasses are best constructed with autogenous conduits (usually greater saphenous vein), especially if the outflow site is a tibial artery, but ePTFE is an appropriate alternative if the outflow site can be kept above the knee joint.
2. Endovascular intervention. Short stenotic or occlusive lesions of the iliac arteries are well treated with balloon angioplasty, with or without the placement of a stent. Long-term success decreases as the lesion is more distal; excellent results are seen with iliac lesions, but angioplasty of the superficial femoral and certainly tibial arteries is dismal enough that the modality should be reserved for patients in whom open surgery is contraindicated.
3. Thrombolytic therapy. Thrombolysis should be reserved for patients in whom the primary process is that of an occluding, nonorganized thrombus. Generally, this is synonymous with acute occlusion of a bypass graft or embolic occlusion of a native artery. Nevertheless, acceptable results are realized with thrombolysis of an acutely occluded native arterial segment. Urokinase is the agent of choice in the United States today. Successful thrombolysis in most cases, however, must be followed by an appropriate endovascular or open surgical procedure to correct any underlying lesion responsible for the occlusive event.
Mesenteric occlusive disease can present in a chronic or acute form; occasionally, acute mesenteric ischemia develops in the setting of chronic symptoms, probably when a critical stenosis of the superior mesenteric artery undergoes sudden thrombosis. Patients with chronic symptoms present with postprandial abdominal pain and weight loss; the diagnosis is unlikely without a history of both. Therapy is directed at revascularization of the superior mesenteric artery and celiac axis, through either a bypass from the aorta or transaortic endarterectomy of the vessels. Acute mesenteric ischemia can develop from embolism, thrombosis overlying a preexisting stenosis, or nonocclusive problems related to low cardiac output or the use of vasopressors. Patients with acute mesenteric ischemia should undergo urgent arteriography to define the problem, with revascularization (e.g., embolectomy or superior mesenteric artery thrombectomy and reimplantation onto the aorta) undertaken for occlusive lesions.
Renal arterial disease can present with hypertension, renal insufficiency, or both. Arteriography is the mainstay of diagnosis, and selective renal function testing (e.g., renal vein renin determination) may help to identify the symptomatic kidney. Therapy may comprise balloon angioplasty for nonostial lesions, stenting for ostial lesions, or a variety of operative revascularization procedures (e.g., aortorenal bypass, transaortic renal endarterectomy, or hepato/splenorenal bypass).
Atherosclerotic disease of the upper extremity vessels is almost always confined to the origin of the subclavian arteries. More distal disease implies a nonatherosclerotic etiology such as giant cell arteritis or embolism. The left subclavian artery is affected much more often than the right. Symptoms comprise arm claudication from hypoperfusion, but digital ischemia or vertebrobasilar symptoms may result from embolism to the fingers or vertebral circulation, respectively. Identifying a pressure gradient between the right and left arms readily makes the diagnosis. The subclavian steal syndrome is actually the anatomic (arteriographic) finding of reversed vertebral arterial flow ipsilateral to a proximal subclavian stenosis and is rarely symptomatic. Treatment of symptomatic subclavian lesions is directed at bypassing the offending lesion (e.g., subclavian-to-carotid transposition or carotid-subclavian bypass), and one must be sure to exclude the embolic source if the indication for operation is embolism.
Abdominal aortic aneurysms most commonly are confined to the infrarenal segment of the aorta, with suprarenal extension in only 5 percent of cases. Males predominate, with a ratio of 9:1. Aortic aneurysms exhibit a familial tendency, especially when found in female patients. Aneurysmal dilatation of the common iliac arteries is found commonly in association with aortic aneurysms and, rarely, as an isolated finding. Although hypogastric artery aneurysms are observed occasionally, aneurysms of the external iliac artery are virtually nonexistent. Other less common sites of nonthoracic peripheral aneurysms are the following: (1) the popliteal artery (bilateral in the majority of patients and in conjunction with aortic dilatation in over 50 percent of patients), (2) the splenic artery (with a high rate of rupture during pregnancy), (3) the renal arteries, (4) the mesenteric vessels (commonly found in patients with periarteritis nodosa), and (5) the subclavian artery (when distal, in association with a cervical rib and poststenotic dilatation). Most extraaortic aneurysms are repaired with bypass and ligation, e.g., femoropopliteal bypass with saphenous vein and proximal and distal ligation for popliteal aneurysms. The risk of complications outweighs the risk of intervention when the diameter reaches a remarkably constant value of 2 cm, irrespective of the specific anatomic site.
Abdominal aortic aneurysms are repaired to prevent rupture, which, when it occurs, is associated with a mortality rate that approximates 50 percent and is probably closer to 90 percent when one includes those patients who die prior to reaching the hospital. The risk of rupture of abdominal aortic aneurysms is related to size. When the diameter exceeds 6 cm, the risk of rupture is great. Smaller aneurysms, however, also can rupture, especially in smaller patients. A useful paradigm for timing intervention is illustrated in the following table, although treatment must be individualized on the basis of more than the three variables listed:
|Aneurysm Diameter||Medical Status/Life Expectancy||Treatment|
|< 4.0 cm||Favorable or unfavorable||Observation|
|4.04.9 cm||Favorable||Consider repair|
|³ 6.0 cm||Favorable or unfavorable||Repair|
The treatment of aortic aneurysms traditionally was performed though a midline transperitoneal incision, although the use of a retroperitoneal exposure has the advantages of (1) better patient tolerability and (2) facilitation of access to the more proximal aorta. Recently, endovascular techniques have been used to repair abdominal aortic aneurysms, inserting a sheathed stent-graft through the femoral artery, removing the sheath, and allowing the stent to expand within the aorta, effectively sealing the aneurysm sac from the path of blood flow. Although yet experimental, endovascular aneurysm repair holds promise as a less invasive method of aneurysm repair.
Focal carotid bifurcation atherosclerosis is the most common manifestation of cerebrovascular disease, and its main complication is embolization and stroke. Symptoms, when present, include (1) transient ischemic attacks (TIAs), defined as neurologic deficits that clear completely within 24 h, (2) reversible ischemic neurologic deficits (RINDs) that resolve within 3 weeks, (3) completed strokes, and (4) amaurosis fugax (reversible) and retinal strokes (fixed). Occasionally, the etiology of symptoms is cerebral hypoperfusion rather than embolization. In these cases the symptoms are usually global and in many instances referable to the hindbrain (vertebrobasilar symptoms).
The presence of a carotid lesion is best ascertained with duplex ultrasonography, and arteriography is being used less frequently as clinicians gain comfort with duplex scanning as the sole preoperative imaging modality. Treatment of carotid bifurcation lesions is possible with endarterectomy, since the lesions are remarkably well localized to within a few centimeters of the internal carotid artery origin. Carotid stenting is presently being evaluated as an alternative to endarterectomy, but current results suggest that the new procedure is not as safe as traditional endarterectomy in standard patients. Newer stent devices and delivery systems can be expected to improve future results. Presently, patients with recurrent carotid stenosis, those with radiation-associated disease, and those with severe medical comorbidities represent categories that may benefit from carotid stenting in its current stage of evolution.
The risk of stroke appears most closely related to the degree of internal carotid artery stenosis, irrespective of the presence or absence of symptoms. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) found that patients with stenoses greater than 70 percent of the vessel diameter fared better with endarterectomy than with aspirin alone. Similarly, the Asymptomatic Carotid Artery Study (ACAS) demonstrated improved results when asymptomatic patients with carotid stenoses greater than 60 percent were treated with surgical repair. Patients with less severe carotid bifurcation disease should be treated with antiplatelet agents to prevent both carotid embolization and the complications of coexisting coronary artery disease.
Thoracic Outlet Syndrome The thoracic outlet, bounded by the clavicle, first rib, and scalene muscles, is a tight space that the brachial plexus, subclavian artery, and subclavian vein must traverse. As such, compression of any of these structures may result in symptoms. Neurologic symptoms are most common, due to the susceptibility of nerve tissue to compressive injury. Venous symptoms are next in frequency, usually manifested by acute thrombosis of the axillary and subclavian veins associated with trauma, exercise, or protracted shoulder abduction. Arterial symptoms (digital embolization from a poststenotic aneurysm) are infrequent, and when they are observed, one should suspect the presence of a cervical rib. Treatment involves resection of the cervical rib, if present, removal of the first rib in the absence of a cervical rib, and repair of the artery for significant dilatation.
Popliteal Artery Occlusion There exist two entities that are associated with popliteal artery occlusion, adventitial cystic disease and popliteal entrapment. If the artery is stenotic but not yet occluded from adventitial cystic disease, operative evacuation of the contents of the cyst will ameliorate the problem. Similarly, patients with popliteal stenoses from entrapment will benefit from lysis of the medial head of the gastrocnemius muscle. With either entity, however, operative bypass becomes necessary once the popliteal artery occludes.
Vasospastic Disorders The vasospastic arterial disorders affect the fingers more frequently than the toes. The prototypic vasospastic disorder is Raynaud's syndrome, a primary benign or secondary (related to collagen vascular disease) more virulent process. Characteristically, patients describe cold-induced cutaneous color changes of pallor, cyanosis, and finally, rubor accompanied by pain and numbness. Treatment entails avoidance of cold, tobacco, and drugs such as beta blockers. Calcium-channel blockers may provide symptomatic relief. Cervical sympathectomy has been used, but with limited long-term success.
Inflammatory Arteritides A number of vasculitides produce arterial symptoms, including giant cell arteritis (temporal arteritis and Takayasu's disease), Buerger's disease (tobacco-associated arterial and venous angiitis), periarteritis nodosa, systemic lupus erythematosus, and other collagen vascular disorders. The success of operative intervention for these entities has been disappointing, especially when performed during the acute phase of the disease.
Arterial trauma is best handled by understanding a set of caveats relating to the problem:
For a more detailed discussion, see Ouriel K and Green RM: Arterial Disease, chap. 20 in Principles of Surgery, 7th ed.
Copyright © 1998 McGraw-Hill
Seymour I. Schwartz
Principles of Surgery Companion Handbook