34
Arteries
Joseph H. Rapp, MD
Warren Gasper, MD
Arterial disease can be broadly classified into two categories: occlusive and aneurysmal. The major sequelae of arterial obstruction are tissue ischemia and necrosis, while those of aneurysmal disease are rupture and hemorrhage in the aortic position and thrombosis and embolization in the peripheral arteries.
ARTERIAL OCCLUSIVE DISEASE
Although atherosclerosis is the dominant cause of arterial occlusive disease in Western countries, other etiologies such as congenital and anatomical anomalies, auto immune diseases, and remote thromboembolism can also result in arterial obstruction. Symptoms of occlusive vascular disease primarily are end-organ dysfunction and, in the muscle beds, pain with exercise and tissue necrosis.
ATHEROSCLEROSIS
Atherosclerosis can occur in any artery, with plaques most commonly developing in areas of low shear stress, such as at arterial branch points. Lesions are usually symmetrically distributed, although the rate of progression may vary. Early lesions are confined to the intima. In advanced lesions, both intima and media are involved, but the adventitia is spared. Preservation of the adventitia is essential for the vessel’s structural integrity and is the basis for all cardiovascular interventions.
When the hemodynamically significant disease affects a major artery, a parallel system of collateral vessels may preserve flow to the peripheral runoff bed. Collateral vessels are smaller, more circuitous, and always have a higher resistance than the original unobstructed artery. The stimuli for collateral development include abnormal pressure gradients across the collateral system and increased flow velocity through intramuscular channels that connect to reentry vessels. Adequate collateral vessels take time to develop but often maintain tissue viability in patients with chronic major arterial occlusions.
Generally, arterial insufficiency occurs in medium-sized and large arteries with at least a 50% reduction in arterial diameter. This correlates with a 75% narrowing of cross-sectional area and enough resistance to decrease downstream flow and pressure. Early in the process, compensatory dilation of the vessel wall may preserve lumen diameter as the atherosclerotic lesion develops, but with continued growth, lesions overcome this adaptation and result in flow limiting stenoses. If there is adequate collateral flow, single stenoses or even occlusions are reasonably well-tolerated. Severe ischemia occurs when there are inadequate collaterals or there are multiple levels of disease.
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CHRONIC LOWER EXTREMITY OCCLUSIVE DISEASE
General Considerations
Peripheral arterial insufficiency is predominantly a disease of the lower extremities. Upper extremity arterial lesions are uncommon and confined mostly to the subclavian arteries. Even when present, upper extremity atherosclerosis rarely produces symptoms due to abundant collateral pathways. In the lower extremities, however, obstructive lesions are distributed widely, with lesions of the superficial femoral and iliac arteries the most common (Figure 34–1). Symptoms are related to the location and number of obstructions.
Figure 34–1. Common sites of stenosis and occlusion of the visceral and peripheral arterial systems.
Peripheral arterial disease affects at least 20% of individuals older than 70 years with the incidence increasing with the increasing incidence of diabetes. Although most patients with this disorder do not develop gangrene or require amputations, adverse outcomes of systemic atherosclerosis, including myocardial infarction and/or stroke, are common. Even after adjustment for known risk factors, individuals with peripheral arterial disease exhibit a several-fold higher risk of mortality than the nonaffected population. A low ankle-brachial index (ABI) is one of the strongest risk factors for all-cause mortality. Peripheral arterial disease is more a marker of a more virulent form of atherosclerosis and early death from cardiovascular or cerebrovascular disease than an indicator of imminent limb loss; thus, identifying and treating associated atherosclerotic risk factors is essential (Figure 34–2).
Figure 34–2. Odds ratios for risk factors for all-cause mortality. ABI, ankle-brachial index; CAD, coronary artery disease. (Reproduced, with permission, from TASC Working Group: Dormandy JA et al. Management of peripheral arterial disease: epidemiology, natural history, risk factors. J Vasc Surg. 2000 Jan;31[1 Pt 2]:S1-S296.)
Clinical Findings
Regardless of which arterial segment is involved, claudication most commonly involves the calf muscles because of their high workload with the mechanics of normal walking. Occlusions proximal to the origin of the profunda femoris can extend the pain to involve the thigh. Gluteal pain indicates lesions in or proximal to the hypogastric arteries and is often accompanied by impotence. Leriche syndrome occurs in men with aortoiliac disease and includes claudication of calf, thigh, and buttock muscles; erectile dysfunction; and diminished or absent femoral pulses. Occasionally, patients describe transient numbness of the extremity accompanying the pain and fatigue of claudication as nerves as well as muscles become ischemic.
The two conditions that most often mimic claudication are osteoarthritis of the hip or knee and neurospinal compression due to congenital or osteophytic narrowing of the lumbar neurospinal canal (spinal stenosis). Osteoarthritis can be differentiated from claudication because pain occurs predominantly in joints, the amount of exercise required to elicit symptoms varies, symptoms are characteristically worse in the morning and upon initiating exercise, rest does not relieve symptoms promptly, the severity of symptoms changes from day to day, and anti-inflammatory agents may relieve the pain. Impingement on the spinal canal or nerve root produces neurospinal compression symptoms; therefore, the pain is typically burning in nature and symptoms may occur with sitting or standing. Neurospinal pain often follows a dermatomal distribution, a key factor in differentiating this from claudication.
Uncommon conditions such as coarctation of the aorta, chronic compartment syndrome, popliteal artery entrapment, and vasculitis can mimic symptoms of atherosclerotic arterial insufficiency. Age at presentation and associated findings may aid in diagnosing these conditions.
The correct diagnosis of vascular claudication should be easily established by determining the location of pain with exercise (calf), the quality of the pain (aching or cramping), the length of time required for relief of symptoms after stopping exercise (immediate), the reproducibility of the distance walked before symptoms begin (initial claudication distance), and most importantly, the reduction or loss of pulses with exercise.
Patients with rest pain may give a history of claudication, but rest pain also may occur de novo in diabetics with distal tibial disease, embolic occlusion of the distal tibial arteries, and patients whose walking is limited by other conditions. Differentiating ischemic rest pain from neuropathy in diabetics is critical and may require vascular testing to clarify the diagnosis.
Physical examination is of paramount importance in assessing the presence and severity of vascular disease. The physical findings of peripheral atherosclerosis are related to changes in the peripheral arteries and to tissue ischemia.
Noninvasive assessment is helpful to determine the severity of hypoperfusion and the sites of hemodynamically significant stenoses or occlusions.
The ankle-brachial index is a quick screening test and the cornerstone of the diagnosis of peripheral vascular disease. The ABI is determined by dividing the systolic pressure obtained by Doppler insonation at the ankle by the brachial arterial pressure. Normally, the ABI is 1.0 or greater; a value below 1.0 indicates occlusive disease proximal to the point of measurement. The ABI correlates roughly with the degree of ischemia (eg, claudication occurs with a value less than 0.7 and rest pain usually appears when the ratio is 0.3 or lower). Elderly patients or patients with diabetic vascular disease may have artificially elevated ABI values due to calcified, noncompressible arteries, and toe-to-brachial pressure ratios should be substituted.
Blood pressures can be measured at rest and after exercise in the ankle, and the effect of exercise can be monitored. Exercise testing confirms and quantitates the diagnosis of claudication. To perform exercise testing, the patient walks on a treadmill at a standard speed and grade until claudication pain is experienced or a time limit is reached. With significant arterial occlusive disease, there will be a decrease in the ABI with exercise, usually measured 1 minute after cessation of walking. If the pain is not due to arterial stenosis, no fall in pressure will occur. This test is particularly useful in differentiating neurogenic pain with walking from claudication.
Color duplex ultrasound imaging is a mainstay of vascular imaging. It is a painless, relatively inexpensive, and (in experienced hands) accurate method for acquiring anatomic and functional information (eg, velocity gradients across stenoses). Although the accuracy of this study is operator dependent, it can supply sufficient information to permit intervention in selected cases.
CT angiography (CTA) is useful for imaging the arterial tree and has the advantage of visualizing cross-sections of the vessel lumen. In many instances, this allows for more accurate determination of vessel diameter and stenosis severity than conventional angiography. It does require the administration of nephrotoxic contrast dye, it is less useful for tibial disease, and its images may be obscured by the presence of calcification or metallic implants. MR angiography (MRA) also can be used to obtain images similar in quality to angiography in most cases. MRA does not show calcifications and gives better visualization of tibial vessels than CTA. MRA also can reveal details of composition of atherosclerotic plaque. Gadolinium-associated nephrogenic fibrosing dermopathy limits its use in patients with renal insufficiency. The integrated use of computer workstations with CT and MR image data can provide three-dimensional (3D) images that can be useful in visualizing patient anatomy and planning interventional procedures.
Conventional arteriography provides detailed anatomic information about peripheral arterial disease. It is reserved for patients warranting invasive intervention such as percutaneous transluminal angioplasty (often shortened to PTA) or vascular surgery. Complications of angiography are related to technique and contrast media. Technical complications such as puncture site hematomas, arteriovenous fistulas, and false aneurysms are rare (1%). Contrast agents may precipitate allergic reactions (0.1%). Patients with renal failure, proteinuria, diabetes, and dehydration are at increased risk for contrast-induced renal failure. Adequate hydration of patients before and after angiography, acetylcysteine, and periprocedural infusions of sodium bicarbonate infusions may reduce the incidence of this complication.
Treatment & Prognosis
The objectives of treatment for lower extremity occlusive disease are relief of symptoms, prevention of limb loss, and maintenance of bipedal gait.
In general, patients with peripheral vascular disease have shortened life expectancies because of their severe atherosclerotic disease. Nondiabetic patients with ischemic disease of the lower extremity have a 5-year survival rate of 70%. The survival rate is 60% in patients with associated ischemic heart disease or cerebrovascular insufficiency. Patients with peripheral vascular disease and renal failure have a 2-year survival rate of less than 50%. Most deaths are due to myocardial infarctions and strokes. Only 20% of deaths are due to nonatherosclerotic causes.
Nonoperative treatment consists of (1) medical management of cardiovascular risk factors, (2) exercise rehabilitation, (3) foot care, and (4) pharmacotherapy.
Table 34-1. Summary of risk factor modification in peripheral vascular disease.
In the past, elevated lipids were not usually associated with peripheral vascular disease. Hyperlipidemia, however, is often present, especially in patients with early onset of disease. Elevated triglyceride levels and low high-density lipoprotein (HDL) cholesterol levels are more prevalent than elevated levels of low-density lipoprotein (LDL) cholesterol. Reduction of elevated lipid levels is associated with stabilization or regression of arterial plaques. Statins are extremely effective in reducing LDL cholesterol, and goals of therapy for patients with peripheral vascular disease are to maintain cholesterol levels at less than 100 mg/dL (2.6 mmol/L). Statins have other pleiotropic effects that may reduce inflammation, stabilize plaques, and independently increase walking distance in claudicants. Other antihyperlipidemic medications, including niacin and fibrates (gemfibrozil), may be used to lower hypertriglyceridemia, which can increase HDL cholesterol.
Both type 1 and type 2 diabetes increase the prevalence and severity of cardiovascular disease. Intensive glycemic control reduces the incidence of nephropathy, neuropathy, and retinopathy in diabetes, but it does not correlate with the severity or progression of peripheral arterial disease. In order to reduce all-cause mortality, however, it is recommended that fasting blood sugars should be controlled with hemoglobin A1c levels less than 7%.
Since patients with claudication are at a twofold to fourfold greater risk of dying from complications of generalized atherosclerosis than people without claudication, an additional benefit of exercise in these patients is that an improvement in walking distance as part of an aggressive risk factor modification regimen results in an overall decrease in cardiovascular risk.
Two drugs have been approved by the FDA for treatment of intermittent claudication. Pentoxifylline produces a small improvement in both initial claudication distance (about 20%) and absolute claudication distance (about 10%). Cilostazol is a phosphodiesterase III inhibitor with vasodilator, antiplatelet, and antilipid activity. Randomized, placebo-controlled, blinded trials have shown an increase of about 50% in absolute claudication distance in patients treated with cilostazol. Quality-of-life assessments also improved significantly. Gene therapy for cardiovascular disease is being investigated, but conclusions regarding safety and efficacy are premature.
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Critchley JA, Capewell S: Mortality risk reduction associated with smoking cessation in patients with coronary heart disease: a systematic review. JAMA 2003;290:86.
Dormandy JA, Murray GD: The fate of the claudicant—a prospective study of 1969 claudicants. Eur J Vasc Surg 1991;5:131.
Hamburg NM, Balady GJ: Exercise rehabilitation in peripheral artery disease: functional impact and mechanisms of benefits. Circulation 2011,123:87-97.
McCullough PA: Contrast-induced acute kidney injury. J Am Coll Cardiol 2008;51:1419.
Mills EJ, Wu P, Chong G, Ghement I, Singh S, et al: Efficacy and safety of statin treatment for cardiovascular disease: a network meta-analysis of 170,255 patients from 76 randomized trials. QJM 2011;104:109.
Momsen AH, Jensen MB, Norager CB, Madsen MR, Vestersgaard Andersen T, et al: Drug therapy for improving walking distance in intermittent claudication: a systematic review and meta-analysis of robust randomised controlled studies. Eur J Vasc Endovasc Surg 2009;38:463.
Murphy TP, Cutlip DE, Regensteiner JG, Mohler ER, Cohen DJ, et al: Supervised exercise versus primary stenting for claudication resulting from aortoiliac peripheral artery disease: six-month outcomes from the claudication: exercise versus endoluminal revascularization (CLEVER) study. Circulation 2012;125:130.
Rehring TF, Stolcpart RS, Hollis HW Jr: Pharmacologic risk factor management in peripheral arterial disease: a vade mecum for vascular surgeons. Society for Vascular Surgery. J Vasc Surg 2008;47:1108.
Interventional procedures, open or endovascular, are performed both for limb salvage and for incapacitating claudication. The choice of operative procedure depends on the location and distribution of arterial lesions and the patient’s comorbidities. Recognition of coexistent cardiopulmonary disease is particularly relevant, because many patients with peripheral vascular disease also have ischemic heart disease and/or chronic lung disease associated with tobacco use. Preoperative cardiac functional assessment is sometimes necessary, but preoperative myocardial revascularization is not beneficial in patients with reasonable cardiac reserve. All patients undergoing vascular surgery should have preoperative risk assessment. Randomized trials have shown that perioperative β-blocker, angiotensin-converting enzyme (ACE) inhibitor, and statins may reduce cardiac morbidity in patients undergoing vascular surgery. Evidence is also emerging demonstrating the importance of maintaining statin therapy throughout the perioperative period.
Figure 34–3. Endovascular gear. A: Sheath. Inserted using Seldinger technique into access vessel. Wires, catheters, and devices pass through the sheath. Sheaths provide stable working access points and protect artery. B: Catheter. Variable length, stiffness, coating, and shape (examples: B.1, cobra; B.2, pigtail; B.3, mesenteric selective). Catheters help steer wires through vasculature and also maintain access in vessel. C: Guidewire. Variable diameter, length, stiffness, and shape. Used to gain access into vasculature, cross lesions, and deliver devices. D: Balloon catheter. E: Peripheral stent graft. F:Peripheral nitinol self-expanding stent. G: Aortoiliac stainless steel/Dacron stent-graft.
Figure 34–4. Aortoiliac occlusive disease. A: Aorta. B: Severely stenotic/occluded iliac arteries. B.1: Widely patent iliac arteries following balloon angioplasty and stenting (C).
Both stents and stent grafts are commonly used from the aortic bifurcation to the distal popliteal artery. Stenting is performed less commonly below the knee, but angioplasty of tibial disease is now common with the use of small catheters and wires. As in the coronaries, drug eluting stents may significantly improve patency rates. Percutaneous mechanical and laser atherectomy are other options in removing obstructing lesions in lower extremity atherosclerotic occlusive disease.
For short, stenotic segments in larger, more proximal vessels, the results of endovascular therapies are good with 1-year success rates of 85% in common iliac disease and 70% in external iliac disease. The results with superficial femoral and popliteal lesions are lower (Figure 34–5). The success of endovascular therapy for lower extremity occlusive disease is inversely related to the complexity of the lesion, defined by the number and length of stenoses treated.
Figure 34–5. Superficial femoral artery occlusion, angioplasty, and stent-graft. A: Common femoral artery. B: Occluded superficial femoral artery. B.1: Recannulized, stent-grafted superficial femoral artery. C: Profunda femoris artery. D: Stent-graft.
Close follow-up of patients post endovascular therapy is required since disease may recur more frequently after angioplasty than after bypass surgery. The patient should be closely followed using noninvasive tests. Repeat angioplasty or stenting may be indicated for recurrent disease, but the improvement in morbidity and mortality of endovascular interventions may be offset by the need for multiple repeat procedures. In general, minimally invasive percutaneous treatment of lower extremity occlusive disease is best used in patients of high operative risk and severe, limb-threatening ischemia (Figure 34–6).
Figure 34–6. Comparison of outcomes for surgical and endovascular intervention in lower extremity occlusive disease.
Lower risk procedures may be preferable in high-risk patients. If the clinically important lesions are confined to one side, a femoral-femoral or iliofemoral bypass graft can be used. A graft from the axillary to the femoral artery (ie, axillofemoral graft) can be used for bilateral disease. Unfortunately, these “extra-anatomic” methods of arterial reconstruction are more prone to late occlusion than are direct reconstructions.
The best conduit for femoropopliteal bypass is an autologous greater saphenous vein. The saphenous vein may be left in situ or removed and reversed. Expanded polytetrafluoroethylene (PTFE) may also be used as a conduit, particularly for bypass to the suprageniculate popliteal artery. Below the knee, PTFE conduits produce much lower patency rates than saphenous veins. Operative death rates are low (2%), and 5-year patency rates range from 60% to 80%. Limb salvage rates are higher than graft patency rates.
The profunda femoris artery perfuses the thigh and acts as an important source of collateral flow when the superficial femoral artery is diseased. When there is a stenosis of the profunda, profundoplastyalone can be performed for limb salvages with success rates of 80% when the suprageniculate popliteal artery is patent and 40%–50% when the popliteal artery is occluded. Isolated profundoplasty is rarely helpful for treating claudication.
Bradbury AW, Adam DJ, Bell J, et al: Bypass versus Angioplasty in Severe Ischaemia of the Leg (BASIL) trial: an intention-to-treat analysis of amputation-free and overall survival in patients randomized to a bypass surgery-first or a balloon angioplasty-first revascularization strategy. J Vasc Surg 2010,51:5S-17S.
Hirsch AT, Haskal ZJ, Hertzer NR, et al: ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients with Peripheral Arterial Disease) endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. J Am Coll Cardiol 2006;47:1239.
Norgren L, Hiatt WR, Dormandy JA, et al: Inter-Society consensus for the management of peripheral arterial disease (TASC II). TASC II Working Group. J Vasc Surg 2007;45(Suppl S):S5.
Rooke TW, Hirsch AT, Misra S, et al: 2011 ACCF/AHA Focused Update of the Guideline for the Management of Patients With Peripheral Artery Disease (Updating the 2005 Guideline): A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2011,124:2020-2045.
ACUTE LOWER EXTREMITY OCCLUSIVE DISEASE
General Considerations
Sudden occlusion of a previously patent artery is a dramatic event characterized by the abrupt onset of severe pain and absent pulses in the involved extremity. Tissue viability depends on the extent to which flow is maintained by collateral circuits. When ischemia persists, motor and sensory paralysis and muscle infarction become irreversible in a matter of hours.
Acute major arterial occlusion may be caused by an embolus, primary arterial thrombosis, trauma, or dissection. The heart is the source of embolus in 80%–90% of episodes, with the remainder from proximal arterial lesions. Aortic aneurysms often contain thrombus, but this material rarely causes symptomatic emboli. In contrast, femoral and particularly popliteal aneurysms embolize frequently. Ulceration in atherosclerotic plaques also can lead to formation of thrombus, which may fragment. Miscellaneous infrequent sources of emboli include cardiac tumors (including cardiac myxoma) and paradoxical emboli (venous thrombi migrating through a patent foramen ovale). Up to 5%–10% of spontaneous emboli originate from a source that remains unidentified despite thorough diagnostic interrogation.
It may be difficult to differentiate between sudden thrombosis of an atherosclerotic peripheral artery and embolic occlusion. The former patients usually have preexisting atherosclerotic stenosis and low blood flow, which predisposes to stagnation and thrombosis. One should also keep in mind the clinical setting and a history of preexisting symptoms such as atrial fibrillation (embolus) or claudication (primary thrombosis).
Clinical Findings
The Five Ps
Pain
Pallor
Pulselessness
Paresthesias
Paralysis
Acute arterial occlusion is characterized by the five Ps: pain, pallor, pulselessness, paresthesias, and paralysis. Severe sudden pain is present in 80% of patients, and its onset usually indicates the time of vessel occlusion. Pain is absent in some patients because of prompt onset of anesthesia and paralysis and portends a poor prognosis.
On examination, the key finding is a lack of palpable pulses in a diffusely painful extremity. It is important to determine if sensitivity to light touch is maintained. These fibers are highly susceptible to ischemia, and their dysfunction heralds the beginning of irreversible ischemic changes. The onset of motor paralysis implies impending gangrene. Early intervention is critical. Swelling with acute tenderness of a muscle belly—usually in the calf following acute femoral artery occlusion—generally denotes irreversible muscle infarction. Skin and subcutaneous tissues have greater resistance to hypoxia than nerves and muscles, which may demonstrate irreversible histological changes after 3 hours or less of ischemia.
Treatment & Prognosis
Immediate anticoagulation by intravenous heparin slows the propagation of thrombus and allows time for assessment of adequacy of collateral flow and preparation for operation. If light touch is intact, arteriography may be performed to define the anatomy and assist in planning the operation. Diagnosis of acute embolic occlusion is based on an abrupt block of the artery with little accompanying arterial disease; conversely, acute in situ thrombosis is associated with extensive atherosclerosis and a well-established collateral network. The operative treatment for an embolus, embolectomy, differs from that of preexisting atherosclerosis, which may require bypass. Nonoperative management is rarely indicated except in debilitated patients and patients with emboli to major arteries in the upper extremities, which generally have good collateral circulation.
Therapeutic options include catheter-directed thrombolysis, percutaneous mechanical thrombectomy, and surgical embolectomy. For patients with severe acute ischemia, operative therapy is preferable because it is usually associated with the least delay in reestablishing perfusion. Surgical embolectomy may be performed through an arteriotomy at the site of the embolic occlusion or, most commonly, by clot extraction with a balloon (Fogarty) catheter inserted through a remote arteriotomy. Successful embolectomy requires removal of the embolus and the “tail” of thrombus that extends distally or proximally from it. If operation is not performed within the first few hours, the clot may become adherent, and subsequent revascularization is less successful. Intraoperative infusion of thrombolytic agents is often a useful adjunct to embolectomy.
In patients who will tolerate a delay in revascularization (ie, those who do not have neural changes on examination), intra-arterial thrombolysis should be considered. The usual regimen involves selective intra-arterial infusion of low doses of thrombolytic agent (eg, tissue plasminogen activator) directly into the clot. This activates thrombus plasminogen more efficiently, allows high concentrations in the clot while limiting systemic effect, and has acceptable complication rates. In cases of thrombosis on preexisting atherosclerotic lesions, thrombolysis reveals the underlying lesions that will require treatment to prevent recurrent thrombosis.
If revascularization is successful, a reperfusion injury may develop with significant swelling requiring fasciotomy to treat the compartment syndrome that may accompany the reperfusion injury. Renal insufficiency from myoglobin release should be anticipated after reperfusion of ischemic muscle. Treatment consists of vigorous hydration and alkalinization of the urine. Administration of free radical scavengers such as Mannitol may be helpful in this disorder.
Patients with clearly irreversible limb ischemia should undergo amputation without an attempt at revascularization, as revascularization may expose the patient to the serious hazards of reperfusion caused by release of acidic and hyperkalemic venous blood from the dying extremity.
Traumatic arterial occlusion must be corrected within a few hours to avoid development of gangrene. Repair of arterial injury is usually performed in conjunction with repair of other injuries. Occasionally, temporary shunts are used to restore flow to the injured extremity while other injuries are addressed and repaired.
PERIPHERAL MICROEMBOLI
Microemboli are most dramatic when they occlude a digital artery perfusing a toe or finger. This causes sudden pain, cyanosis, and coldness or numbness in the affected digit. These changes characteristically improve over several days. If there are multiple emboli, these symptoms may reappear in a different area of the hand or foot. In the lower extremity, this clinical entity has been called blue toe syndrome or trash foot. The sudden onset of pain and purple discoloration of a toe in the presence of palpable pulses is recognized as a potentially limb-threatening arterial problem. With each succeeding episode, recovery is slower and less complete.
The most common source of microembolization is cardiac valvular disease. However, if no cardiac valvular lesions are found, a careful examination of the proximal arterial tree must be done to identify an arterial source shedding atheroemboli.
Sudden onset may differentiate peripheral microembolism from other causes of blue toes, such as vasculitis, thromboangiitis obliterans, trauma, or chronic ischemia. If a single toe is affected, it is more likely to be the result of emboli, while multiple cyanotic toes are more likely to be vasculitis or chronic ischemia. It is important to remember that a patent proximal artery is required to serve as a conduit for the embolus, so pulses are intact. Furthermore, a normal blood supply is present in adjacent tissue segments. The appearance of a normally perfused foot with a cyanotic toe is characteristic. However, the waxing and waning symptoms of repeated emboli can make the diagnosis difficult. Unless the syndrome is recognized, alternative diagnoses investigated, and the lesion of origin corrected, survival of the foot or hand may be in peril.
Dean SM: Atypical ischemic lower extremity ulcerations: a differential diagnosis. Vasc Med 2008;13:47.
DIABETIC VASCULAR DISEASE
Atherosclerotic arterial disease in patients with diabetes mellitus is more diffuse and more severe than in nondiabetics. In diabetic patients, the tibioperoneal vessels frequently contain atherosclerotic changes, and the vessels are often heavily calcified. The degree of ischemia may be severe and extensive, and noninvasive tests (ABIs) may be falsely elevated. Fortunately, in many diabetics, the small arteries in the foot are relatively spared, making distal bypass to these arteries possible and allowing foot salvage in cases of threatened limb loss.
Diabetic patients also have a high incidence of neuropathy and are more apt to ignore minor foot injuries, which can develop into ulcerations. Daily foot inspections are essential to avoid progression of minor injuries into limb threatening lesions. Neuropathy is also responsible for loss of tone of intrinsic foot muscles that leads to subluxation of the metatarsal phalangeal joints, resulting in a “rocker-bottom” foot and ultimately producing complete joint destruction termed a Charcot foot. These architectural changes also make skin breakdown more likely to occur and require referral to a foot and ankle clinic.
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Gibbons GW, Shaw PM: Diabetic vascular disease: characteristics of vascular disease unique to the diabetic patient. Semin Vasc Surg 2012;25:89.
Nehler MR, Whitehill TA, Bowers SP, et al: Intermediate-term outcome of primary digit amputations in patients with diabetes mellitus who have forefoot sepsis requiring hospitalization and presumed adequate circulatory status. J Vasc Surg 1999;30:509.
Prompers L, Schaper N, Apelqvist J, et al: Predictors of outcome in individuals with diabetic foot ulcers. Diabetologia 2008;51:747.
NONATHEROSCLEROTIC DISORDERS CAUSING LOWER LIMB ISCHEMIA
Thromboangiitis Obliterans
Thromboangiitis obliterans (Buerger disease) is characterized by multiple segmental occlusions of obliterating tibial and pedal arteries. The most distal arteries are affected making bypass impossible. Migratory phlebitis may be present. In contrast to atherosclerosis, which involves the intima and media, thromboangiitis obliterans is manifested by infiltration of round cells in all three layers of the arterial wall. The disease occurs almost exclusively in young male smokers. Fortunately, the incidence appears to be decreasing. It is essential that the patient stop smoking to avoid progression of the disease. Patients with Buerger disease may have specific cellular immunity against arterial antigens, specific humoral antiarterial antibodies, and elevated circulatory immune complexes, but a precise diagnosis can be made only by tissue histology. Arteriographic findings are distinctive but not pathognomonic. Sympathectomy decreases arterial spasm and is useful in some patients. Amputation is indicated for persistent pain or gangrene and can be performed adjacent to the line of demarcation with satisfactory primary healing.
The disease may become dormant if the patient can stop smoking. Unfortunately, smoking cessation seems particularly difficult in these patients, and many ultimately require multiple amputations.
Popliteal Artery Entrapment Syndrome
This rare cause of popliteal artery stenosis or occlusion occurs as a result of an anomalous course of the popliteal artery. The popliteal artery normally passes between the two heads of the gastrocnemius muscle as it enters the lower leg. In the entrapment syndrome, the artery passes medial to both heads of the gastrocnemius, causing compression of the popliteal artery when the knee is extended. There are five anatomic variants of popliteal artery entrapment, but all produce similar clinical effects. Fibrous thickening of the intima occurs at the site of compression and gradually progresses to total occlusion. Symptoms vary from calf claudication to those of more severe ischemia depending on lesion severity and embolization. Popliteal artery entrapment should be considered when a young, otherwise healthy patient presents with calf claudication. Until the artery becomes occluded, the only finding is a decrease in strength of the pedal pulses, most evident when using provocative maneuvers like foot dorsiflexion and plantar flexion. MRI and CT studies are most useful in confirmation of the diagnosis. Atherosclerotic changes are notably absent. Treatment consists of returning the popliteal artery to its normal anatomic course or bypass with saphenous vein.
Cystic Degeneration of the Popliteal Artery
Arterial stenosis is produced by a mucoid cyst in the adventitia, usually located in the middle third of the artery. Calf claudication is the most common symptom, and the only finding is a decrease in the strength of the peripheral pulses. Rarely, a mass can be palpated. Arteriography shows a sharply localized zone of popliteal stenosis with a smooth concentric tapering. Ultrasound or CT scans can be used to demonstrate the cyst within the vessel wall. The stenosis may be missed on conventional anteroposterior films and may appear only on lateral exposures. The cyst and the affected artery should be excised and bypassed because of recurrence with evacuation of the cyst only.
Abdominal Aortic Coarctation
Coarctations of the thoracic or abdominal aorta are rare. They may be congenital or may result from an inflammatory large vessel arteritis such as Kawasaki or Takayasu disease. These rare disorders may produce symptoms of lower extremity, mesenteric, or renal ischemia depending on the location of the constriction. The congenital variant of this condition is best managed surgically when it is recognized; autogenous repair may be preferable to the use of prosthetic grafts. Surgical repair in the presence of ongoing inflammation is not recommended because those patients do poorly. However, if the disease is quiescent with a normal sedimentation rate, standard surgical operations appear to produce satisfactory results.
LOWER EXTREMITY AMPUTATION
General Considerations
More than 90% of the 110,000 amputations performed in the United States each year are for ischemic disease or infective gangrene. More than half of lower extremity amputations are performed for complications of diabetes mellitus, and 15%–50% of diabetic amputees will lose a second leg within 5 years. This risk is about two times higher for men than for women. Other indications for amputations are nondiabetic infection with ischemia (15%–25%); ischemia without infection (5%–10%); osteomyelitis (3%–5%); trauma (2%–5%); and frostbite, tumors, neuromas, and other miscellaneous causes (5%–10%).
Many patients facing amputation are near the end of life because of systemic cardiovascular disease. Approximately 20%–30% of patients undergoing major amputation (below-knee or above-knee) will be dead within 2 years. The prevalence of many comorbidities in this population is also reflected in the perioperative mortality rates for major amputation, ranging from 5% to 10% for below-knee amputations to 10% or higher for above-knee amputations.
The level of amputation is determined by assessing the likelihood of healing of the limb in association with the functional potential of the patient. Compared with normal walking, energy expenditure is increased 10%–40% with a below-knee prosthesis, 50%–70% with an above-knee prosthesis, and 60% with crutches. The clinical conundrum in patients with limb ischemia is twofold: (1) determining which limbs have adequate blood supply to heal at the below-knee level and (2) determining which patients with vascular disease have reasonable rehabilitation potential. The best predictions are based on clinical assessment by an experienced surgeon, assisted by one of the several techniques such as Laser Doppler or transcutaneous measurement of oxygen tension.
Lower Extremity Amputation Levels
Lower extremity amputations are done most commonly at one of the following levels: toe (called digit amputations, which may be extended to include resection of the metatarsal and called ray amputations), transmetatarsal, below-knee, and above-knee. Amputations at other levels (Syme amputation, Chopart amputation, knee disarticulation, and hip disarticulation) are infrequently performed, usually to treat conditions other than vascular disease.
Figure 34–7. Toe and ray amputations.
For dry, uninfected gangrene of one or more toes, autoamputation may be allowed to occur. During this process, epithelialization occurs beneath the eschar, and the toe spontaneously detaches, leaving a clean residual limb at the most distal site. Although preferable in many patients (and especially frostbit patients), autoamputation sometimes requires months to complete.
Ray, or wedge, amputation includes removal of the toe and metatarsal head; occasionally, two adjacent toes may be amputated by this method. As with toe amputation, there is modest cosmetic deformity and a prosthesis is not required. Ray amputation of the great toe leads to unstable weight bearing and some difficulty with ambulation resulting from loss of the first metatarsal head.
Complications that may require amputation at higher levels include infection, osteomyelitis of remaining bone, and nonhealing of the incision. These complications have been reported in up to one third of diabetic patients.
Transmetatarsal amputation produces an excellent functional result. Walking requires no increase in energy expenditure, and the gait is usually smooth. A prosthesis is not mandatory, but to achieve optimal gait, the shoes must be modified.
Figure 34–8. Below knee amputation.
Above-knee amputation may be performed at several levels, including knee disarticulation. Although it is advantageous to preserve as long a lever arm as possible, knee disarticulation is technically more demanding than transfemoral amputation at a higher level. The technique is straightforward. Short anterior and posterior flaps, sagittal flaps, or a circular incision may be used. The bone is divided substantially higher than the skin and soft tissue to avoid tension when the wound is closed and later when the muscles of the thigh atrophy. A simple dressing is then applied.
SPECIAL PROBLEMS OF AMPUTEES
Thromboembolism
The amputee is at great risk for deep venous thrombosis (15%) and pulmonary embolism (2%) postoperatively because (1) amputation often follows prolonged immobilization during treatment of the primary disease and (2) the operation involves ligation of large veins, causing stagnation of blood, a situation that predisposes to thrombosis. If immediate-fit prosthetic techniques are not employed, an additional period of inactivity follows the operation, further increasing the risk of thromboembolism.
Rehabilitation After Amputation
The rehabilitation goals following amputation are highly variable. Younger patients universally want to regain ambulatory status and frequently return to work. Elderly patients with significant comorbid conditions may remain wheelchair-bound, and much of their rehabilitation is focused on providing wheelchair access in their living situations and working on independent transfers. It is important to understand that amputation in an elderly patient is frequently an event that occurs near the end of life. For these people, relief of pain and provision for modest function may be the most appropriate outcome in the limited amount of time they have left.
The length of the residual limb correlates well with regaining the ability to walk. Cardiopulmonary disease and physical weakness make walking an overwhelming effort for some patients; this emphasizes the importance of preserving a below-knee amputation if possible, so that walking will require the least possible amount of energy.
Pain & Flexion Contracture
Physical Therapy consultation is an important adjunct to prevent flexion contractures of the knee or hip occur rapidly in the painful limb because of the natural tendency to assume a flexed posture. Measures to prevent contracture are indicated preoperatively, and application of a rigid dressing postoperatively decreases the incidence of this complication.
Phantom Pain
Persistent sensations in a residual limb are almost universal. Unfortunately, phantom limb pain also is common. Treatment is difficult; improvement has been reported using tricyclic antidepressants, transcutaneous electrical nerve stimulation (TENS), and calcitonin. The incidence and severity of phantom limb pain are increased if there was prolonged ischemia before amputation and decreased if postoperative rehabilitation is rapid.
Ischemia in the Residual Limb
Progressive vascular disease results in ischemia of about 8% of above-knee amputations and 1% of below-knee amputations. Operations are often required to improve arterial flow when gangrene develops in a residual limb. The mortality rate of this condition is high.
Brown BJ, Crone CG, Attinger CE: Amputation in the diabetic to maximize function. Semin Vasc Surg 2012;25:115.
Fleury AM, Salih SA, Peel NM: Rehabilitation of the older vascular amputee: a review of the literature. Geriatr Gerontol Int 2013;13:264.
Jones WS, Patel MR, Dai D, Subherwal S, Stafford J, et al: Temporal trends and geographic variation of lower-extremity amputation in patients with peripheral artery disease: results from US Medicare 2000–2008. J Am Coll Cardiol 2012;60:2230.
Landry GJ, Silverman DA, Liem TK, Mitchell EL, Moneta GL: Predictors of healing and functional outcome following transmetatarsal amputations. Arch Surg 2011;146:1005.
van Eijk MS, van der Linde H, Buijck B, Geurts A, Zuidema S, et al: Predicting prosthetic use in elderly patients after major lower limb amputation. Prosthet Orthot Int 2012;36:45.
CEREBROVASCULAR DISEASE
General Considerations
Unlike in the other vascular beds, symptoms of extracranial carotid disease are most often caused by embolization. Arterial emboli account for approximately one quarter of strokes in Europe and North America, and 80% of these originate from atherosclerotic lesions in a surgically accessible artery in the neck. The most common lesion is at the bifurcation of the carotid artery. Transcranial Doppler studies have shown that emboli are seen in approximately 20% of patients with moderate (> 50% stenosis) lesions at the carotid bifurcation and even higher rates with more than 70% stenoses. The incidence and frequency of emboli is increased in recently symptomatic patients. It would appear that transient deficits and strokes from emboli may not be single events but the result of multiple small emboli that temporarily or permanently obliterate the collateral reserve of the cerebral cortex.
The neurologic dysfunction associated with microemboli may appear as sudden “short-lived,” or transient, neurologic symptoms that may include unilateral motor and sensory loss, aphasia (difficulty finding words), or dysarthria (difficulty speaking due to motor dysfunction). These are termed transient ischemic attacks (TIA). Most TIAs are brief (minutes). By convention, 24 hours is the arbitrary limit of a TIA. If the symptoms persist, it is a stroke, or cerebrovascular accident (CVA). An embolus to the ophthalmic artery, the first branch of the internal carotid artery, produces a temporary monocular loss of vision called amaurosis fugax or permanent blindness. Atherosclerotic emboli may be visible as small bright flecks (Hollenhorst plaques) lodged in arterial bifurcations in the retina.
Characteristically, lesions of atherosclerosis in the internal carotid artery occur along the wall of the carotid bulb opposite to the external carotid artery origin (Figure 34–9). The enlargement of the bulb just distal to this major branch point creates an area of low wall shear stress, flow separation, and loss of unidirectional flow. Presumably, this allows greater interaction of atherogenic particles and the vessel walls at this site and accounts for the localized plaque at the carotid bifurcation.
Figure 34–9. Cerebrovascular circulation anatomy.
The accessibility of this localized atheroma allows effective removal of the plaque and a dramatic reduction in stroke risk. Without treatment, 26% of patients with TIAs and more than 70% with carotid stenosis will develop permanent neurologic impairment (CVA) from continued embolization at 2 years. The risk of CVA can be reduced to 9% with plaque removal. The risk of CVA is lower for patients presenting with amaurosis fugax.
Clinical Findings
Patients with cerebrovascular disease can be grouped into five categories based on symptoms at presentation.
Auscultation of the carotid and subclavian arteries may delineate the sites of hemodynamically significant disease. However, bruits are nonspecific findings correlating more with overall risk for cardiovascular disease than with stroke.
Figure 34–10. Carotid bifurcation occlusive disease. A: 3D CT angiogram of neck demonstrating carotid bifurcation stenosis. B: Axial CT view demonstrating the lesion.
Treatment
Stroke risk is highest immediately after a TIA, returning to baseline at approximately 6 months. Consequently, in symptomatic patients with carotid stenosis, early intervention is mandatory. Antiplatelet therapy, usually in the form of aspirin or clopidogrel, is particularly important in cerebrovascular patients, although clopidogrel should not be initiated in a patient who is scheduled to have a carotid endarterectomy because of the increased risk of bleeding. Cardiovascular risk factor modification is also imperative in reducing stroke and overall mortality. After a completed stroke, caution must be exercised when planning an intervention.
Carotid endarterectomy, the removal of the atherosclerotic lesion at the carotid bifurcation, is the primary operation performed (Figure 34–11). In the North American Symptomatic Carotid Endarterectomy Trial (NASCET), carotid endarterectomy was shown to reduce incidence of ipsilateral stroke from 26% to 9% at 2 years in patients presenting with either TIA or stroke and carotid lesions of 70% stenosis or greater. The results also favored surgery in patients with moderate carotid stenosis (50%–69%), but less dramatically. The 5-year risk of ipsilateral stroke was 15.7% among patients treated surgically (n = 1108) and 22.2% among those treated medically (n = 1118; P = .045). Patients with stenoses of less than 50% did not significantly benefit from surgery.
Figure 34–11. Technique of carotid endarterectomy.
Large clinical trials have also shown a benefit of surgery for asymptomatic carotid stenosis. Both the Asymptomatic Carotid Atherosclerosis Study (ACAS) in North America and the Asymptomatic Carotid Surgery Trial (ACST) in Europe showed that stroke incidence is halved (12%–6%) by carotid endarterectomy versus best medical therapy, which included antiplatelet agents and statins in the ACST, in patients with substantial carotid narrowing at 5 years of follow-up. While ACAS did not show a benefit for endarterectomy in women, the larger European study did.
Carotid endarterectomy cannot be performed when the internal carotid artery is completely occluded, because complete thrombectomy is difficult and residual clot may embolize, creating additional lesions.
Early studies of carotid angioplasty and stenting (CAS) (Figure 34–12) suggested similar morbidity and mortality rates to carotid endarterectomy. Because of the higher rate of emboli with stenting, cerebral protection devices, either filters placed in the internal carotid or devices that allow a washout of atherosclerotic debris, should always be used. Poststenting, clopidogrel is prescribed for 6 weeks to limit late embolization from the stent.
Figure 34–12. Carotid angioplasty and stenting. A: Conventional arteriogram demonstrating diffuse occlusive disease of common and internal carotid arteries. B: Completion arteriogram following angioplasty and stenting of the lesions.
Two large randomized studies found more strokes after CAS than after endarterectomy, the International Carotid Stent Study (ICSS) and the Carotid Revascularization Endarterectomy versus Stenting Trial (CREST). Conversely, there were more myocardial infarctions after endarterectomy. All women and men over age 70 did worse with CAS. Younger men did well with CAS. Current practice reserves CAS for occlusive lesions of the origins of the arch vessels and for recurrent stenosis after treatment. It is also chosen over endarterectomy in patients with hostile neck anatomy due to prior radiation or “high” lesions not accessible via a neck incision and in patients pre-op for CABG as they are at prohibitive risk for surgery.
The main complication of cerebrovascular interventions is stroke, which occurs in 2%–7% of patients depending on the operative indications and cerebrovascular anatomy. Higher stroke rates occur in the setting of symptomatic stenosis or contralateral carotid occlusion. Lower stroke rates occur with asymptomatic stenosis. The operative death rate for all extracranial cerebrovascular interventions is less than 1%.
Transient cranial nerve injury occurs in about 10% of cases after endarterectomy and may cause tongue weakness, hoarseness, mouth asymmetry, earlobe numbness, and dysphagia. Less than 2% of peripheral nerve deficits are permanent, although this number goes up with surgery for recurrent disease, making stenting attractive for this indication.
Restenosis or occlusion is uncommon after carotid endarterectomy (5%–10% at 5 years) and appears to be equally uncommon after carotid stenting. For endarterectomy, using a prosthetic patch for closure of the arteriotomy can reduce restenosis.
Subclavian Steal Syndrome
The subclavian steal syndrome is characterized by reversal of flow through the vertebral artery due to a more proximal occlusion or stenosis of the subclavian artery (ie, the vertebral artery serves as a collateral to supply blood to the arm). While this anatomic arrangement is often demonstrated on angiograms, clinical sequelae are rare. Symptoms of effort fatigue in the involved extremity are more common than neurologic complaints. When necessary, treatment consists of bypass grafting from the common carotid to the subclavian artery distal to the lesion or transposition of the subclavian artery beyond the lesion to the side of the nearby common carotid artery.
Concomitant Coronary & Cerebrovascular Disease
When patients have coexistent severe coronary and carotid atherosclerosis requiring treatment, there has been controversy as to which lesion should be addressed first. Since most strokes during cardiac procedures are from atheromatous emboli from the aortic arch, not from low flow through a carotid stenosis, our policy has been to perform combined procedures only in patients with simultaneous symptomatic carotid and coronary disease, with critical bilateral asymptomatic stenoses, or with extremely high-grade (99%) unilateral stenosis. We have initiated a program of stenting the carotid stenoses 1 day prior to coronary artery bypass graft and have found this to be quite satisfactory.
Other Causes of Cerebrovascular Symptoms
Other than atherosclerosis, primary disease of the extracranial arteries is rare.
Takayasu arteritis is an obliterative arteriopathy principally involving the aortic arch vessels that often affects young women. The pararenal abdominal aorta and pulmonary arteries also may be affected. High-dose corticosteroids and cyclophosphamide have been shown to arrest and in some cases reverse the progress of the disease. Operative treatment of nonspecific arteritis should be avoided when the arteritis is active, but it may be successful in quiescent disease.
Dissecting aortic aneurysms may extend into the arch branches, producing obstruction and cerebral symptoms. These are discussed in Chapter 19, Part I.
Classically occurring in exercising young adults, dissection originating in the internal carotid artery and localized to its extracranial segment occurs as an acute event that may narrow or obliterate the internal carotid lumen. The primary lesion is an intimal tear at the distal end of the carotid bulb. It may also follow various types of neck trauma or severe hypertension.
Cerebral symptoms are the result of ischemia in the ipsilateral hemisphere. Acute neck pain in association with localized cervical tenderness adjacent to the angle of the mandible is a frequent finding.
Arteriography shows a characteristic pattern of tapered narrowing at or just beyond the distal portion of the carotid bulb. The lumen beyond this point may be obliterated or may persist as a barely visible narrow shadow. If the lumen persists, it resumes a normal caliber beyond the bony foramen.
Because thrombus tends to form in and around the dissected vessel, anticoagulation is the treatment of choice for this disorder. In many patients, the intramural clot will be resorbed, restoring a normal lumen. Intervention is indicated for patients with recurrent TIAs. Stenting is the procedure of choice and will restore the normal carotid contour. If stenting is not successful and symptoms persist, ligation can be performed if the carotid back-pressure exceeds 65 mm Hg. Extracranial to intracranial bypass will be needed if the pressure is low.
Fibromuscular dysplasia is a nonatherosclerotic angiopathy of unknown cause that affects specific arteries chiefly in young women. Symptoms of cerebrovascular disease can occur when the carotid artery is affected. It is usually bilateral and involves primarily the middle third of the extracranial portions of the internal carotid artery. Several pathologic variants of the disease have been described, but in most of them, the primary lesion is overgrowth of the media in a segmental distribution, producing irregular zones of arterial narrowing. The most common result is a series of concentric rings, producing the radiologic appearance of a string of beads in a long internal carotid artery. Approximately one third of patients are also hypertensive due to renal artery involvement.
The prevalence of fibromuscular dysplasia and the portion of patients who develop symptoms are not known. Once symptoms develop, transient neurologic events are the most common manifestation. However, more than 20% of patients have had a stroke by the time of presentation. Because of the high incidence of neurologic disability, the lesion should be corrected by angioplasty with distal protection when patients develop symptoms. Surgery with dilation of the carotid with graduated dilators or balloon dilation has given excellent results.
Brott TG, Hobson RW, Howard G, Roubin GS, Clark WM, et al: Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med 2010;363:11.
Ederle J, Dobson J, Featherstone RL, Bonati LH, van der Worp H B, et al: Carotid artery stenting compared with endarterectomy in patients with symptomatic carotid stenosis (International Carotid Stenting Study): an interim analysis of a randomised controlled trial. Lancet 2010;375:985.
Executive Committee for the Asymptomatic Carotid Atherosclerosis Study (ACAS): Endarterectomy for asymptomatic carotid artery stenosis. JAMA 1995;273:1421.
Fairman R, Gray WA, Scicli AP, Wilburn O, Verta P, et al: The CAPTURE registry: analysis of strokes resulting from carotid artery stenting in the post approval setting: timing, location, severity, and type. Ann Surg 2007;246:551-6.
Ferguson GG, Eliasziw M, Barr HW, et al: The North American Symptomatic Carotid Endarterectomy Trial: surgical results in 1415 patients. Stroke 1999;30:1751.
Fusco MR, Harrigan MR: Cerebrovascular dissections—a review part I: spontaneous dissections. Neurosurgery 2011;68(1):242-57.
Halliday A, et al: Prevention of disabling and fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomized controlled trial. Lancet 2004;363:1491.
Rothwell PM, Mansfield A, Marro J, et al: Prediction and prevention of stroke in patients with carotid stenosis. Eur J Vasc Endovasc Surg 2008;35:255.
Yadav JS, Wholey MH, Kuntz RE, et al: Stenting and angioplasty with protection in patients at high risk for endarterectomy investigators. Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med 2004;351:1493.
RENOVASCULAR HYPERTENSION
General Considerations
More than 23 million people in the United States have hypertension, and renovascular disease is a causative factor in 2%–7% of cases. Atherosclerosis of the aorta and renal artery (two thirds of cases) and fibromuscular dysplasia are the two primary causes of renovascular hypertension. Less common causes of hypertension include renal artery emboli, renal artery aneurysms, renal artery dissection, hypoplasia of the renal arteries, and stenosis of the suprarenal aorta.
Atherosclerosis characteristically produces stenosis at the orifice of the main renal artery. The lesion usually consists of aortic atheroma that protrudes over the renal artery orifice. Less commonly, the atheroma arises in the renal artery itself. Renal artery stenosis is more common in men over age 45 years and is bilateral in about 95% of cases.
Fibromuscular dysplasia usually involves the middle and distal thirds of the main renal artery and may extend into the branches. Medial fibroplasia is the most common variety of fibromuscular dysplasia, accounting for 85% of these lesions. It is bilateral in 50% of cases. Concentric rings of hyperplasia that project into the arterial lumen cause the arterial stenoses. Renal artery aneurysms frequently coexist. Fibromuscular dysplasia occurs mainly in young women, with onset of hypertension usually occurring before age 45 years. It is the causative disorder in 10% of children with hypertension. Developmental renal artery hypoplasia, coarctation of the aorta, and Takayasu aortitis are other vascular causes of hypertension in childhood.
Hypertension due to renal artery stenosis results from the kidney’s response to reduced blood flow. Cells of the juxtaglomerular complex secrete renin, which acts on circulating angiotensinogen to form angiotensin I, which is rapidly converted to angiotensin II by ACE. This octapeptide constricts arterioles, increases aldosterone secretion, and promotes sodium retention. Due to the excess aldosterone, hypertension becomes volume-dependent. Over time, pathologic changes occur in the uninvolved kidney, and the hypertension may not be sensitive to ACE inhibition. With sodium restriction and volume reduction (diuretics), the hypertension may once again become sensitive to ACE inhibition. If both kidneys have renal artery stenoses, or if the disease exists in a solitary kidney, renal insufficiency may occur with ACE inhibitor administration with a loss of pressure in the glomerulus due to a reduction of angiotensin II constriction of the efferent arteriole.
Clinical Findings
Most patients are asymptomatic, but irritability, headache, and emotional depression are seen in a few. Persistent elevation of the diastolic pressure is usually the only abnormal physical finding. A bruit is frequently audible to one or both sides of the midline in the flank or upper abdomen. Other signs of atherosclerosis may be present when this is the cause of the renal artery disease.
Other clues to the presence of renovascular hypertension include absence of a family history of hypertension, early onset of hypertension (particularly during childhood or during early adulthood), marked acceleration of the degree of hypertension, resistance to control with antihypertensive drugs, and rapid deterioration of renal function. One should suspect renovascular hypertension if initial diastolic pressure is greater than 115 mm Hg or if renal function deteriorates while a patient is being given ACE inhibitors. Sudden onset of pulmonary edema with severe hypertension also is highly suggestive of renovascular hypertension.
In the past, several diagnostic tests were devised to diagnose renovascular hypertension. Divided urinary excretion studies, selective renin determinations from renal vein samples, and captopril renal scintigraphy are now rarely used.
Noninvasive or minimally invasive imaging of the renal arteries is justified when the patient has a precipitous drop in blood pressure, decreased renal function with an ACE inhibitor, difficult-to-control hypertension, or unexplained deteriorating renal function.
In experienced hands, duplex ultrasound scanning has an overall agreement with angiography of over 90%. Renal artery stenosis is characterized by peak systolic velocities in the range of 180-200 cm/s, and the ratio of these velocities to those in the aorta approaches 3.5. CTA or MRA may provide high-resolution images of diseased renal arteries, although must be used with caution in patients with renal insufficiency. The contrast required with CTA is nephrotoxic and gadolinium has been associated with systemic nephrogenic fibrosis in patients with reduced renal clearance.
Renal arteriography is the most accepted method for delineating the obstructive lesion. Since atherosclerotic disease most often involves the origins of the renal arteries, a midstream aortogram should be obtained in addition to selective renal artery catheterization. The presence of collateral vessels circumventing a renal artery stenosis suggests a hemodynamically significant renal artery lesion.
Nonionic contrast agents should be used and the patient should be prepared with overnight hydration. Administration of N-acetylcysteine and periprocedural sodium bicarbonate infusion may give added protections but aggressive hydration remains the primary treatment to reduce the incidence of acute tubular necrosis with angiography and should be used routinely.
Treatment
Patients with renovascular hypertension require aggressive management of modifiable risk factors. If hypertension responds well to medical therapy and the renal function is stable, no intervention on the renal artery stenosis is needed.
Percutaneous transluminal angioplasty (PTA) and stenting is the preferred procedure for most patients (Figure 34–13). Although clearly valuable for some patients, the overall results of percutaneous interventions for renal artery stenosis have been mixed, and large randomized clinical trials suggest that medical treatment with angiotensin receptor blockers may be as effective as stenting in most cases. Patients with fibromuscular dysplasia typically respond to angioplasty alone.
Figure 34–13. Renal artery occlusive disease. A: Aortogram demonstrating ostial lesion in left renal artery. B: Renal stent constrained on delivery catheter over wire positioned across lesion. C:Arteriogram demonstrating widely patent renal artery following balloon angioplasty and stent placement.
In the very young, surgery is still the primary mode of treatment due to concern regarding the long-term durability of angioplasty and stenting. Surgical repair also is required for failed angioplasty and stenting, renal revascularization during a procedure on the aorta, and lesions that are in branch vessels. As with any operation, the indications for arterial reconstruction are influenced by the extent of disease, the patient’s life expectancy, and the anticipated morbidity associated with operation. Nephrectomy may be considered when arterial repair is impossible or especially hazardous and the disease is unilateral.
Options include endarterectomy, which is most easily accomplished through an incision into the adjacent aorta, or bypass using prosthetic or autogenous conduits. An alternative is “nonanatomic” bypass such as a hepatorenal or splenorenal procedure. The celiac and splenic arteries often have coexistent occlusive atherosclerotic disease that mandates preoperative arteriographic assessment of these vessels.
Extracorporeal techniques have been developed for distal branch aneurysms or extensive fibromuscular dysplasia. These require removal of the kidney from the abdomen (ex vivo arterial reconstruction), continuous cold perfusion of its vascular tree, and microvascular techniques for arterial replacement. The kidney is then either returned to a site near its original position or transplanted to the ipsilateral iliac fossa.
Prognosis
Procedures for revascularization of the renal artery are successful in lowering blood pressure in over 90% of patients with fibromuscular hyperplasia. Operation for atherosclerotic stenosis results in improvement or cure of hypertension in about 60%. The results for angioplasty and stenting are not as good, perhaps because of atheroembolization to the kidney during angioplasty.
The results of intervention for salvage of renal function are better than those for treatment of hypertension. The procedural mortality rate of operative renovascular surgery in children is almost nil, whereas it increases to 2%–8% in adults with diffuse atherosclerosis. Stenting of the renal arteries is also very well tolerated.
Herrmann SM, Textor SC: Diagnostic criteria for renovascular disease: where are we now? Nephrol Dial Transplant 2012;27:2657.
Mousa AY, Campbell JE, Stone PA, Broce M, Bates MC, et al: Short- and long-term outcomes of percutaneous transluminal angioplasty/stenting of renal fibromuscular dysplasia over a ten-year period. J Vasc Surg 2012;55:421.
Wheatley K, Ives N, Gray R, Kalra PA, Moss JG, et al: Revascularization versus medical therapy for renal-artery stenosis. N Engl J Med 2009;361:1953.
MESENTERIC ISCHEMIA SYNDROMES
General Considerations
The celiac axis and the superior and inferior mesenteric arteries are the principal sources of blood supply to the stomach and intestines, with the inferior mesenteric artery and internal iliac arteries supplying flow to the distal colon (Figure 34–14). The anatomic collateral interconnections between these arteries are numerous. Single or even multiple visceral artery lesions are generally well tolerated, because collateral flow is readily available (Figure 34–15).
Figure 34–14. Visceral arterial circulation and interconnections.
Figure 34–15. Three-dimensional CT angiogram demonstrating a critical superior mesenteric artery stenosis (arrow) and collateral vessel enlargement originating at the inferior mesenteric artery (arrowhead).
Atherosclerosis is the cause of obstructive lesions in the visceral arteries in the vast majority of cases. Vasculitis (eg, lupus erythematosus, Takayasu disease) is much less common. When atherosclerosis is the cause, the usual lesion is a collar of plaque spilling over from the aorta that creates a proximal stenosis or occlusion. Associated atherosclerosis in the aorta and its other branches is common.
CHRONIC MESENTERIC ISCHEMIA
Clinical Findings
The principal complaint is postprandial abdominal pain, which has been labeled abdominal or visceral angina. Pain characteristically appears 15–30 minutes after the beginning of a meal and lasts for an hour or longer. Pain is occasionally so severe and prolonged that opiates are required for relief. Pain occurs as a deep-seated, steady ache in the epigastrium, occasionally radiating to the right or left upper quadrant. Weight loss results from reluctance to eat. Although mild degrees of malabsorption can occur, gastrointestinal absorption studies are not helpful. Diarrhea and vomiting have been described. An upper abdominal bruit may be heard.
Ultrasound can be diagnostic in experienced hands but CTA or arteriography in the anteroposterior and especially the lateral projections demonstrate both the arterial lesion and the patterns of collateral blood flow. Patients should be well hydrated before these procedures because they can precipitate hypercoagulability and osmotic diuresis with dehydration, vascular occlusion, and bowel infarction.
Treatment
Percutaneous transluminal angioplasty (PTA) and stenting has gained acceptance as a first line of therapy for mesenteric ischemia. Results are best for focal, nonorificial stenoses. Embolization to the gut is a rare but potentially fatal complication of instrumentation of these lesions.
Surgical revascularization of the superior mesenteric and celiac axes may be performed by either endarterectomy or graft replacement. During endarterectomy, a sleeve of aortic intima and the orifice lesions in the celiac or superior mesenteric arteries are removed. The operation is performed by a retroperitoneal approach to the aorta through a left thoracoabdominal incision. Alternatively, Dacron grafts may be brought antegrade from the lower thoracic aorta or retrograde from the iliac arteries to the celiac axis or superior mesenteric artery—operations that are performed from within the abdomen.
Operation should be avoided in patients with acute vasculitis as the underlying cause of mesenteric ischemia; high-dose steroids and immunosuppressive agents are indicated instead.
Prognosis
Opening flow to the mesenteric vascular bed almost always results in relief of symptoms. The limited durability of endovascular therapy necessitates close follow-up and reintervention if symptoms recur.
ACUTE MESENTERIC ISCHEMIA
Acute mesenteric ischemia is a highly morbid disorder. Patients classically present with excruciating diffuse abdominal pain with a surprising absence of physical findings such as abdominal tenderness or distention—unless actual bowel perforation produces a surgical abdomen. Symptoms of chronic mesenteric ischemia may precede this catastrophic event, or the onset may be sudden if the cause is embolic occlusion of the superior mesenteric artery. The diagnosis can be difficult, and its recognition is often delayed, resulting in irreversible bowel ischemia. The mortality rate from acute mesenteric ischemia remains high. Patients who require massive bowel resection rarely survive or, if they survive, can develop incapacitating short-gut syndrome. The prognosis improves dramatically if revascularization can be achieved prior to intestinal infarction. This obviously requires early diagnosis, which will only occur if the practitioner has a high index of suspicion.
CELIAC ARTERY COMPRESSION
External compression of the celiac artery, or median arcuate ligament syndrome, is an unusual cause of visceral ischemia. It generally affects young adults, with women more often affected than men, and is commonly associated with rapid weight loss. The classic sign is a loud epigastric bruit with exhalation as the crus of the diaphragm descends to compress the artery. The artery is scarred and must be repaired in conjunction with release of the compressing ligament. The diagnosis is difficult to make with certainty because some compression of the celiac artery by the arcuate ligament is common. Surgery should be advised only after an unsuccessful search for other causes of postprandial pain.
Patients with median arcuate ligament compression respond favorably to operation in most cases; however, some of these patients are not improved even though a technically adequate operation is performed.
Aburahma AF, Campbell JE, Stone PA, Hass SM, Mousa AY, et al: Perioperative and late clinical outcomes of percutaneous transluminal stentings of the celiac and superior mesenteric arteries over the past decade. J Vasc Surg 2013;57:1052.
Tallarita T, Oderich GS, Gloviczki P, Duncan A, Kalra M, et al: Patient survival after open and endovascular mesenteric revascularization for chronic mesenteric ischemia. J Vasc Surg 2013;57:747.
ARTERIAL ANEURYSMS
General Considerations
An aneurysm is defined as a localized dilation of an artery to at least 1.5 times its normal diameter. The expanding vessel elongates as well as dilates. A true aneurysm involves primary dilation of the artery, including all vessel wall layers (intima, media, and adventitia). A false aneurysm, also called pseudoaneurysm, is characterized by a disruption of the artery wall, does not include all layers of the wall, and may actually be a pulsatile hematoma not contained by the artery wall but by a fibrous capsule. A false aneurysm caused by infection is called a mycotic aneurysm.
False aneurysms of the femoral artery secondary to catheterization are the most numerous of all aneurysms. Infrarenal abdominal aortic aneurysms (AAA) are the most common of the true aneurysms. In descending order, other arteries affected are the iliac arteries, the popliteal artery, the arch and descending portions of the thoracic aorta (including dilation after aortic dissection), the common femoral artery, the carotid arteries, and other peripheral arteries. Other rare causes of true aneurysms include Marfan syndrome, Ehlers–Danlos syndrome, Behçet disease, and cystic medial necrosis.
ABDOMINAL AORTIC ANEURYSMS
AAA are found in 2% of the elderly male population, and the incidence may be increasing. In selected groups, the incidence is higher—5% of patients with coronary artery disease and as many as 50% of patients with femoral or popliteal aneurysms have aortic aneurysms. Men are four times as likely to be affected as women. Ruptured aortic aneurysms are a cause of death of men age greater than 65 years in the United States, resulting in 15,000 deaths per year.
Numerous mechanisms have been proposed for the cause of AAA. Structural issues may contribute; reductions in the number of elastic lamellae and virtual absence of vasa vasorum in the media of the distal abdominal aorta compared with the thoracic aorta may favor aneurysmal degeneration. Excessive protease activity or local reductions in the concentration of protease inhibitors have been implicated in aneurysm formation, allowing for the enzymatic destruction of the two principal structural elements of the aorta, elastin, and collagen. There may be hemodynamic factors as well, owing to large pulsatile stresses because of tapering geometry, increased stiffness, and reflected pressure waves from branch vessels in the infrarenal aorta. Genetic factors influencing connective tissue metabolism and structure also have been associated with AAA development. Indeed, a positive family history of aortic aneurysms infers a 20% chance that a first-degree family member will have an aneurysm.
In terms of risk factors, cigarette smoking has a powerful influence on developing an aortic aneurysm, with an 8:1 preponderance of AAA in smokers compared with nonsmokers. The excess prevalence associated with smoking accounted for 78% of all AAA that were 4 cm or larger in the Veterans Administration ADAM study sample. Hypertension is present in 40% of patients with AAA but did not correlate with enlargement in the ADAM study. Surprisingly, diabetics appear to have a lower incidence of aortic aneurysm formation.
Ninety percent of aneurysms of the abdominal aorta occur between the takeoff of the renal arteries and the aortic bifurcation but may include variable portions of the common iliac arteries. Rupture with exsanguination is the major complication of AAA. Unfortunately, neither the expansion rate nor the rupture risk is predictable. Tension on the aneurysm wall is governed by the law of Laplace. Thus, rupture risk is related to diameter. While relating this to an individual’s risk is not possible, population-wide risks have been established. Because most aneurysms cause no symptoms prior to rupture, the number of deaths due to ruptured AAA has not changed significantly in the past 20 years. This has prompted a recommendation for ultrasound screening of smoking males over the age of 65 years.
Clinical Findings
The vast majority of unruptured aneurysms are asymptomatic. Rarely, intact AAAs produce back pain due to pressure on nerves or erosion into vertebral bodies. Severe pain in the absence of rupture characterizes the rare inflammatory aneurysm that is surrounded by 2-4 cm of perianeurysmal retroperitoneal inflammatory reaction.
Eighty percent of 5 cm AAAs are palpable as a pulsatile abdominal mass in the mid-abdomen just above and to the left side of the umbilicus. Physical examination for an AAA is less reliable in obese patients. The aneurysm may be slightly tender to palpation. Extreme tenderness suggests a “symptomatic aneurysm” and is found in inflammatory aneurysms or if the aneurysm has recently expanded. A truly noninflammatory, symptomatic (tender) aneurysm demands urgent surgery.
Plain films of the abdomen reveal calcification in the outer layers of only 20% of abdominal aneurysms.
Ultrasound is the least expensive method for measuring the size of infrarenal aortic aneurysms. Repeated ultrasound examinations are cost effective for observing small AAAs and may be used to follow resolution of the aneurysm after endovascular repair. However, ultrasound examinations do not delineate adjacent structures as well as CT or MR and are less reliable in obese patients.
CT scan or MRI with 3D reconstructions are both accurate methods for assessing aneurysm diameter, although the ADAM trail showed that there can be substantial interreader variability in size determinations (Figure 34–16). An important source of error occurs when the course of the aneurysmal aorta is diagonal to the cross-sectional image. This creates an elliptical image of the AAA and a falsely elevated diameter in the larger dimension. CT scans provide valuable information about aneurysm location and size as well as important adjacent structures that affect AAA repair, such as horseshoe kidneys or other renal abnormalities, and venous anomalies, including retroaortic renal veins, circumaortic renal veins, and left-sided or duplicated vena cavae, which may have important surgical implications. If the patient has a multiplanar CT scan, aortograms, once routine studies in planning operative management of AAAs, are not needed.
Figure 34–16. CT showing the typical position of a 5.5-cm abdominal aortic aneurysm and its proximity to the abdominal wall.
Most aneurysms continue to enlarge and will eventually rupture if left untreated. The average expansion rate for an AAA is 0.4 cm per year. The rate of expansion correlates with continued smoking, initial aneurysm diameter, and the degree of obstructive pulmonary disease. An expansion of 0.5 cm in 6 months or 1 cm over 12 months qualifies as rapid enlargement and suggests the aneurysm is unstable and should be repaired.
Aneurysm size is currently the best determinant of rupture risk. About 40% of aneurysms 5.5-6 cm or larger in diameter will rupture within 5 years if untreated, and the average survival of an untreated patient is 17 months. In contrast, the ADAM study found a 0.5% per year rupture rate in AAAs 4-5.4 cm, an overall rate remarkably similar to a comparable trial in the United Kingdom. Thus, surgery is recommended for aneurysms 5.5 cm or more in size, but small aortic aneurysms can be safely followed. Regardless of size, repair is mandatory for an aneurysm that is symptomatic or enlarging rapidly.
Figure 34–17. A: Three-dimensional CT angiogram reconstruction of abdominal aortic aneurysm. White arrow points to aortic flow lumen at same level as that in panel B. B: Axial CT view. White arrow points to flow lumen, black arrow points to thrombus within aneurysm sac. Notice only aortic flow lumen visualized on CT angiogram, just as in conventional angiography. Total diameter of the aorta, including area containing thrombus, is used in predicting rupture risk and determining need for intervention. C: Three-dimensional CT angiogram following aortic stent graft repair.
The most important intermediate or long-term adverse outcome of endovascular repair is persistent perfusion of the aneurysm (“endoleak”). These are divided into types denoting clinical importance. A type 1 endoleak denotes ineffective proximal or distal sealing with pressurization of the aneurysm sac and should be fixed immediately. A type 2 endoleak results in persistent flow through the aneurysm between small aortic branches, usually from the inferior mesenteric artery to a patent lumbar artery. These have relatively low pressures and, unless the aneurysm is enlarging, are not treated. Pressurization of the aneurysm through the graft itself is a type 3 endoleak. The graft should be repaired or replaced if the aneurysm continues to enlarge over time due to a type 2 or type 3 leak.
Rupture has occurred after endovascular aortic aneurysm repair. The rate of late ruptures is low but underscores that patients need extended follow-up to ensure the durability of endovascular aneurysm repair. Endograft repair is more expensive than open repair in spite of the lower periprocedural morbidity and shorter hospital stays. The devices are expensive ($10,000-15,000), and there is further cost due to the extended follow-up with imaging studies to identify graft movement or endoleak.
Figure 34–18. Replacement of an aortic aneurysm with a synthetic bifurcation graft. The laminated clot within the aneurysm has been removed, and the outer wall is closed over the graft.
Elective infrarenal abdominal aneurysmectomy has a 2%–4% operative death rate and a 5%–10% rate of complications, such as bleeding, renal failure, myocardial infarction, graft infection, limb loss, bowel ischemia, and erectile dysfunction. Paraplegia is a very rare complication due to involvement of an abnormally low artery of Adamkiewicz, a major collateral of the anterior spinal artery. Malignant tumors are encountered unexpectedly in about 4% of cases, although that rate is now dwindling with the routine use of multiplanar CT scans. If gastrointestinal malignancy is encountered during an aneurysm resection, the aneurysm repair should be done first unless there is impending bowel obstruction.
Long-term results of open aneurysmectomy are excellent: graft failure rate is low and false aneurysm formation at the anastomoses is rare. The long-term survival of these patients is determined principally by their extent of coronary artery disease.
ILIAC ANEURYSMS
Iliac artery aneurysms generally occur in conjunction with AAAs. Isolated iliac aneurysms are unusual, but in some cases, the iliac segment of the aneurysmal artery may enlarge at a greater rate than the aortic segment and is the primary reason for repair. As with aortic aneurysms, most iliac aneurysms are asymptomatic. However, they may present with symptoms related to compression or erosion of surrounding structures, such as obstructive uropathy with ureteral obstruction, neuropathy from compression of local nerves, and unilateral leg swelling from compression of the adjacent iliac vein.
Physical examination can suggest the diagnosis of large (> 4 cm) iliac artery aneurysms if the physician is alert to that possibility. Most symptomatic iliac aneurysms can be palpated as pulsatile masses on abdominal or rectal examinations. However, iliac aneurysms are usually found incidentally on ultrasound or CT.
Similar to aortic aneurysms, iliac aneurysms tend to enlarge and rupture unpredictably, but size is the most important determinant of rupture risk. Iliac aneurysms that are less than 3.5 cm in size should be followed up with serial imaging. Those that enlarge to 4 cm should be repaired in patients without serious operative risk factors.
The challenge of iliac aneurysm repair is in preserving flow to the pelvis through at least one internal iliac artery to prevent pelvic ischemia that can present as buttock claudication, impotence, or ischemia of the distal colon. Open repair of isolated iliac arteries is well tolerated and can be done through a retroperitoneal approach. If the ipsilateral hypogastric artery is also aneurysmal, repair will require opening the sac and ligating the branches from within the aneurysm, taking care not to injure the iliac veins surrounding the aneurysm.
SUPRARENAL AORTIC ANEURYSMS
Aneurysms of the segment of aorta between the diaphragm and the renal arteries account for only 10% of AAAs, with 6% being pararenal and 4% involving the visceral vessels. Resection and graft replacement of the upper abdominal aorta is an operation of far greater magnitude and risk than operations on the infrarenal aorta. Involvement of the renal arteries doubles operative mortality with substantial additional risk for involvement of the visceral vessels. Renal failure and bowel ischemia are much more common after repair of these aneurysms than after repair of infrarenal aortic aneurysms. There is also a risk of paraplegia if flow is interrupted to the artery of Adamkiewicz. An extended incision is usually necessary, and provisions must be made for revascularization of the celiac axis and the superior mesenteric and renal arteries. The use of perfusion catheters for the visceral and renal arteries has improved results, and left heart bypass is used in true thoracoabdominal aneurysms.
Because of the mortality and morbidity of repair of suprarenal aneurysms, there has been considerable interest in endovascular repair of these aneurysms using branched systems. Initial experience from selected centers, including our own, has shown dramatic reduction in morbidity and mortality from these technically demanding endovascular procedures. In patients judged to be high risk for open repair, branched graft repair has equaled the best reported results for open repair.
RUPTURED AORTIC ANEURYSMS
General Considerations
With increasing aneurysm size, lateral pressure within the aneurysm will eventually lead to spontaneous rupture of the aneurysm wall. Although immediate exsanguination may ensue, there is often an interval of several hours between the first episode of bleeding and death from exsanguination when the initial bleed is contained in the retroperitoneal tissues, a “contained rupture.” When the periaortic tissue can no longer contain the expanding hematoma, “free rupture” occurs with exsanguination into the free peritoneal cavity.
Clinical Findings
The patient presents with sudden, severe abdominal pain that usually radiates into the back and occasionally into the inguinal region. Lightheadedness or syncope results from blood loss. Pain may lessen and lightheadedness may disappear after the first hemorrhage, only to reappear and progress to shock if bleeding continues. When bleeding remains contained in the periaortic tissue, a discrete, pulsatile abdominal mass may be felt. In contrast with an intact aneurysm, the ruptured aneurysm at this stage is painful to palpation. Signs of an acute abdomen may be present. As bleeding continues, usually into the retroperitoneum, the discrete mass is replaced by a poorly defined mid-abdominal fullness, often extending toward the left flank.
Shock can be profound, manifested by peripheral vasoconstriction, hypotension, and anuria. Unfortunately, the classic triad of pain, a pulsatile abdominal mass, and hypotension is not always present, and precious time may be lost while confirming the diagnosis. An abdominal ultrasound performed in the emergency room will confirm the presence of an aortic aneurysm but may not disclose hemorrhage. CT scans reliably confirm hemorrhage from an aneurysm, but in unstable patients, the delay in progressing to the operating room precludes their use. It is best to follow the adage that a patient with an AAA, signs of an acute abdomen, and hypotension belongs in the operating room.
Treatment & Prognosis
Repair should be performed as soon as intravenous fluids have been started, the airway has been secured, and blood has been sent for cross-matching. Surgical control of the aorta proximal and distal to the aneurysm must be obtained immediately and should be attempted from the abdomen. Attempts to control the proximal aorta through the chest have been associated with poor outcomes. A successfuloutcome of the operation is related to the patient’s condition on arrival, the promptness of diagnosis, and the speed of operative control of bleeding and blood replacement. The operative death rate is between 30% and 80%, with an average of approximately 50%. Because many patients with ruptured aneurysms die before reaching the hospital, the overall death rate approaches 80%. Without operation, the outcome is uniformly fatal. Many centers are now treating ruptured AAA using endovascular stent grafts; morbidity and mortality remain high and abdominal compartment syndrome has been a complication requiring evacuation of the retroperitoneal hematoma.
INFLAMMATORY ANEURYSMS
Inflammatory aneurysms are degenerative aneurysms that elicit a unique inflammatory response adjacent to the external calcified layer of the aneurysm wall. Although similar to retroperitoneal fibrosis, the inflammation is usually confined to the anterior aorta and iliac arteries. The aneurysm may be responsible to chronic abdominal pain and is tender to palpation. One fourth of patients have some degree of ureteral obstruction. CT scanning reliably demonstrates the characteristic thickened wall and confirms the diagnosis. Characteristic pathologic changes include infiltration of the aortic wall by lymphocytes, plasma cells, occasional multinucleated giant cells, and lymphoid follicles with germinal centers. Inflammation resolves in most cases after successful repair. Inflammatory aneurysms are easily recognized at operation by the dense, shiny, white, fibrotic material that envelops the adjacent viscera, especially the duodenum, left renal vein, and inferior vena cava. Those structures are therefore especially vulnerable to operative injury. Endovascular repair is ideal and is the procedure of choice for inflammatory aneurysms. After repair, the inflammatory tissue usually regresses.
INFECTED (MYCOTIC) ANEURYSMS
The confusing term “mycotic aneurysm” is commonly used to denote infected aneurysms in general, which are rarely fungal. The aneurysm is secondary to a microbial aortitis in which virulent bacteria infect the aorta and destroy the aortic wall. Historically, salmonella infection was the most common cause. In the current era, staphylococcus is the more common infection due to intravenous drug use. These organisms may involve every major artery, but aortic involvement predominates.
The typical patient presents with a rapidly enlarging, tender pulsatile mass that may feel warm, if palpable. Fever is present, and half the patients have positive blood cultures. Alternatively, the aneurysm may be discovered late, after successful treatment of the infection. Angiography of these patients may show a saccular false aneurysm. Treatment consists of excision and remote bypass grafting if possible. Liberal application of muscle flap coverage techniques facilitates healing. Direct repair has been successful when done after a course of antibiotics. A prolonged course of antibiotics should be given to guard against recurrence.
PERIPHERAL ARTERIAL ANEURYSMS
General Considerations
Popliteal artery aneurysms account for 70% of peripheral arterial aneurysms. Like aortic aneurysms, they are silent until critically symptomatic. However, unlike aortic aneurysms, they rarely rupture. The presenting manifestations are due to peripheral embolization and thrombosis, possibly due to movement of the artery with knee flexion. Popliteal aneurysms may embolize repetitively over time and occlude distal arteries. Due to the redundant parallel arterial supply to the foot, ischemia does not occur until a final embolus occludes flow to the remaining tibial/peroneal artery. Acute ischemia caused by popliteal aneurysms has a poor prognosis because of the chronicity of the process. The results of both chemical and mechanical thrombolysis may be disappointing because of clot age and adherence to the artery wall. After presentation with acute ischemia, approximately one third of patients will require an amputation. To prevent embolization and thrombosis, popliteal artery aneurysms should be repaired electively if greater than 2 cm in diameter or at any size if lined with thrombus.
Primary aneurysms of the femoral artery are much less common than aneurysms of the popliteal artery. However, pseudoaneurysms of the femoral artery following arterial punctures for arteriography and cardiac catheterization occur with an incidence ranging from 0.05% to 6%. Thrombosis and embolization are the main risks of femoral true or false aneurysms and, like popliteal aneurysms, should be repaired when greater than 2 cm in diameter.
Clinical Findings
Until progressive embolization or thrombosis occurs, peripheral artery aneurysms are usually asymptomatic. The patient may be aware of a pulsatile mass when the aneurysm is in the groin, but popliteal aneurysms are often undetected by the patient and physician. Peripheral aneurysms may produce symptoms by compressing the local vein or nerve, but this is unusual. In most patients, the first symptom is due to ischemia of acute arterial occlusion. The pathologic findings range from rapidly developing gangrene to moderate ischemia that slowly lessens as collateral circulation develops. Symptoms from recurrent embolization to the leg are often transient if they occur at all. Sudden ischemia may appear in a toe or part of the foot, followed by slow resolution, and the true diagnosis may be elusive. The onset of recurrent episodes of pain in the foot, particularly if accompanied by cyanosis, suggests embolization and requires investigation of the heart and proximal arterial tree.
Because popliteal pulses are somewhat difficult to palpate even in normal individuals, a particularly prominent or easily felt pulse is suggestive of aneurysmal dilation and should be investigated by ultrasound. Since popliteal aneurysms are bilateral in 60% of cases, the diagnosis of thrombosis of a popliteal aneurysm is often aided by the palpation of a pulsatile aneurysm in the contralateral popliteal space. Approximately 50% of patients with popliteal aneurysms have an aneurysmal abdominal aorta.
Duplex color ultrasound is the most efficient investigation to confirm the diagnosis of peripheral aneurysm, to measure its size and configuration, and to demonstrate mural thrombus.
Arteriography may not demonstrate aneurysms accurately, because mural thrombus reduces the apparent diameter of the lumen. Three-dimensional imaging by CTA or MRA is required—especially when operation is considered—to define the anatomy and plan intervention.
Early operation is indicated for an aneurysm that is greater than 2 cm in size associated with any peripheral embolization or an aneurysm with mural thrombus. Urgent operation is indicated when acute embolization or thrombosis has caused acute ischemia. Intra-arterial thrombolysis may be done in the setting of acute ischemia if examination (light touch) suggests that immediate surgery is not imperative to prevent tissue loss. Bypass with saphenous vein may include either excision or exclusion, depending on location. If exclusion rather than resection is performed, the geniculate “feeder” arteries within the aneurysm should be ligated or progressive enlargement can still occur.
Endovascular repair with covered stents can be used but are less durable than open repair and should be reserved for patients at high operative risk.
Acute pseudoaneurysms of the femoral artery due to arterial punctures can be successfully treated using ultrasound-guided compression and thrombin injections if the aneurysm is not large.
The long-term patency of bypass for femoral and popliteal aneurysms is generally excellent but depends on the adequacy of the outflow tract. Late graft occlusion is less common than in similar operations for occlusive disease.
UPPER EXTREMITY ANEURYSMS
Subclavian Artery Aneurysms
Subclavian artery aneurysms are less common than aneurysms of the lower extremity, and most supraclavicular pulsatile masses represent tortuous vessels, not aneurysms. Pseudoaneurysms due to injections by drug addicts are becoming increasingly frequent. An anomaly, the aberrant right subclavian artery (incidence 0.5%), arises from the aorta distal to the left subclavian and courses behind the esophagus. As found in other aberrant arteries, enlargement is common and may compress the esophagus against the trachea, causing difficulty swallowing (termed dysphagia lusoria). This anomaly also is the most common cause of a nonrecurrent laryngeal nerve.
A true subclavian artery aneurysm is usually due to poststenotic dilation in a patient with thoracic outlet syndrome or a large callous from a fractured clavicle. As with popliteal aneurysms, the most common manifestation is embolization with episodic hand ischemia and Raynaud’s phenomenon. The diagnosis is often missed. Sudden onset Raynaud’s, particularly with a history of waxing and waning digital ischemia, is indication for arterial imaging. Treatment consists of resection of the restricting structures at the time of arterial replacement.
Radial Artery False Aneurysms
The incidence of radial artery false aneurysms has increased as a result of increasing use of radial artery catheters. Occasionally, the aneurysm is infected. If the Allen test is normal and adequate collateralization is confirmed with imaging, treatment consists of excision and ligation. If the ulnar collaterals are insufficient to preserve viability of the hand, excision and replacement with vein should be performed.
Small aneurysms of the palmer arch may be due to repetitive trauma. These aneurysms can be responsible for emboli to the digital arteries. The adage that hand ischemia requires angiography should be applied to ensure that all potentially reversible causes of hand ischemia, including these unusual aneurysms, be identified.
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VISCERAL ARTERY ANEURYSMS
General Considerations
The etiology of this interesting group of aneurysms is generally unknown. Most often they occur as single lesions in a younger age group than those at risk for aortic aneurysms. Rupture is the primary danger and is one cause of “abdominal apoplexy.”
Splenic Artery Aneurysms
Aneurysms of the splenic artery account for more than 60% of splanchnic artery aneurysms. Women are affected four times more commonly than men and often during childbearing years. Arterial fibrodysplasia and portal hypertension predispose to formation of splenic artery aneurysms. Rupture, the major complication, has been reported in less than 2% of splenic aneurysms; it rarely occurs with lesions smaller than 2-3 cm in diameter. Rupture during pregnancy tends to occur in the third trimester and is associated with a 75% maternal death rate and 90% fetal death rate. Diagnosis is most often made from plain x-ray films of the abdomen, showing concentric calcification in the upper left quadrant.
Intervention is indicated for patients with symptomatic aneurysms, aneurysms in pregnant women, and patients who have a low operative risk profile with aneurysms greater than 3 cm in diameter. Endovascular repair with covered stent grafts is ideal with the use of microcatheters developed for intracranial work, improving the ability to negotiate the often tortuous splenic artery. Laparoscopic ligation of the artery is also feasible.
Hepatic Artery Aneurysms
Hepatic artery aneurysms account for 20% of splanchnic artery aneurysms. There is a 2:1 male-to-female ratio, and the frequency of reported rupture is about 20%. Aneurysm rupture is associated with a 35% mortality rate. Rupture into the biliary tree producing hemobilia is as frequent as intraperitoneal rupture. The symptom triad of intermittent abdominal pain, gastrointestinal bleeding, and jaundice strongly suggests the diagnosis and is present in about one third of patients. Surgery is usually required to control bleeding. If the common hepatic artery is involved, the artery may be safely ligated if collateral flow through the gastroduodenal artery has been demonstrated. Aneurysms in other portions of the artery usually require vascular reconstruction. Endovascular placement with a covered stent is preferred if the anatomy is suitable.
Superior Mesenteric Artery Aneurysms
Aneurysms of the proximal superior mesenteric artery account for 5% of all splanchnic artery aneurysms. Unlike splenic or hepatic aneurysms, 60% of superior mesenteric artery aneurysms are mycotic. The aneurysm may involve the origin or branches of the artery. Symptoms include nonspecific abdominal pain. The diagnosis can be made on CT scan.
Operative therapy for mycotic superior mesenteric artery aneurysms includes ligation if there are adequate collaterals or replacement with a segment of autogenous vessel. Endovascular stent graft placement is not advisable in an acute infection. However, it is valuable for true aneurysms as long as critical branches can be avoided. For distal branch aneurysms, bowel resection may be necessary.
RENAL ARTERY ANEURYSMS
This uncommon aneurysm occurs in less than 0.1% of the population and is often associated with hypertension. The aneurysm is usually saccular and located at a primary or secondary bifurcation of the renal arteries. Women are affected slightly more frequently than men. There are three principal categories: (1) idiopathic, (2) aneurysms associated with medial fibrodysplastic disease, and (3) arteritis-related microaneurysms.
Renovascular hypertension may occur because of distortion of the involved or nearby vessels by the aneurysm. Spontaneous rupture of renal artery aneurysms is rare except during pregnancy. CT scans or digital subtraction angiography should be performed to monitor enlargement. Operation is indicated in women of childbearing age or in patients with associated renal artery disease, uncontrolled hypertension, or large aneurysms. Most renal artery aneurysms can be repaired in situ, but ex vivo repair is occasionally required. Endovascular options are usually limited due to the involved vessel size and the aneurysm’s proximity to artery branch points.
VASOCONSTRICTIVE DISORDERS
General Considerations
Vasoconstrictive disorders are characterized by abnormal activity of the sympathetic nervous system that reduces peripheral blood flow, causing tissue ischemia.
Raynaud’s Disease/Phenomenon
Raynaud’s disease/phenomenon consists of sequential pallor, cyanosis, and rubor of fingers or toes after exposure to cold. Excessive vasoconstriction, sluggish flow, and reflex vasodilation produce the characteristic white-blue-red color changes. In Raynaud’s disease, this response, due to spasm alone without underlying arterial lesions, is quite common and benign.
Sudden onset or progression of symptoms suggests underlying arterial lesions that exaggerate the normal reduction in blood flow caused by vasoconstriction. This is termed Raynaud’s phenomenon, a more virulent entity associated primarily with immunologic and connective tissue disorders (eg, scleroderma, systemic lupus erythematosus, polymyositis, or drug-induced vasculitis). However, repeated embolization, occupational trauma (vibration injury, cold injury), and other disorders (cold agglutinins, chronic renal failure, and neoplasia) also have been reported.
Hyperreactivity to cold stimuli may be the initial presentation of arterial pathology. In new onset or severe cases of Raynaud’s-type symptoms, a search for underlying pathology is required. All patients with Raynaud syndrome should avoid cold exposure, tobacco, oral contraceptives, β-adrenergic blocking agents, and ergotamine preparations. Calcium-channel blockers are generally prescribed but may cause hypotension. Transdermal prostaglandins, ketanserin, and cilostazol also have been used, with relief of symptoms in some patients. In rare cases, symptoms progress to tissue loss. Finger amputation is necessary once gangrene has developed.
Acrocyanosis
Acrocyanosis is a common, chronic, benign vasoconstrictive disorder related to Raynaud syndrome that is largely restricted to young women. It is characterized by persistent cyanosis of the hands and feet. The changes disappear with exposure to a warm environment. Examination in a cool room shows diffuse symmetric cyanosis, coldness, and occasionally hyperhidrosis of the hands and feet. Cyanosis of the skin of the calf, thigh, or forearm usually displays a reticulated pattern and has been called livedo reticularis and cutis marmorata. The peripheral pulses may diminish in the cold but return to normal with rewarming.
THORACIC OUTLET SYNDROME
General Considerations
Thoracic outlet syndrome refers to the variety of disorders caused by abnormal compression of arterial, venous, or neural structures in the base of the neck. Numerous mechanisms for compression have been described, including cervical rib, anomalous ligaments, hypertrophy of the anterior scalene muscle, and positional changes that alter the normal relation of the first rib to the structures that pass over it. Patients may describe a history of cervical trauma.
Symptoms rarely develop until adulthood. For this reason, it has been assumed that an alteration of normal structural relationships that occurs with advancing years is the primary factor. Even anomalous cervical ribs seem well tolerated during childhood and adolescence.
Transient circulatory changes may occur, but the primary cause of symptoms in most patients is intermittent compression of one or more trunks of the brachial plexus. Thus, neurologic symptoms predominate over those of ischemia or venous compression. When present, compression of the subclavian artery and vein in the thoracic outlet also can produce severe sequelae. Compression of the subclavian artery can produce stenosis and poststenotic dilation of the artery, leading to arterial occlusion or emboli, as discussed earlier. Compression of the vein between the anterior scalene, clavicle, and first rib can produce thrombosis, which can result in severe upper extremity pain and swelling. Compression may be exaggerated with exercise precipitating an occlusion. This syndrome is termed effort thrombosis or Paget–Schroetter syndrome.
Clinical Findings
Neural symptoms consist of pain, paresthesias, or numbness in the distribution of one or more trunks of the brachial plexus (usually in the ulnar distribution). Most patients associate their symptoms with certain positions of the shoulder girdle. These may occur from prolonged hyperabduction, as in house painters, hairdressers, and truck drivers. Others may relate their symptoms to the downward traction of the shoulder girdle produced by carrying heavy objects. Numbness of the hands often wakes the patient from sleep. On physical examination, motor deficits are rare and usually indicate severe compression of long duration. Muscular atrophy may be present in the hand. Pulses can be weakened by abduction of the arm with the head rotated to the opposite side (Adson test), though pulse reduction by this maneuver often occurs in completely asymptomatic persons. Light percussion over the brachial plexus in the supraclavicular fossa may reproduce the symptoms in patients with chronic neurologic impingement.
Arterial symptoms are less common and often the result of emboli. A bruit may be heard over the subclavian artery with abduction of the arm, but this is not a specific finding. Venous occlusion results in unilateral arm swelling. There are good collaterals around the shoulder girdle, but symptoms may be debilitating in young active patients, the very patient in whom this is most likely to occur.
Neurogenic thoracic outlet compression must be differentiated from other disorders that mimic this condition (eg, carpal tunnel syndrome and cervical disk disease). Cervical x-rays and peripheral nerve conduction studies are not diagnostic but are valuable to eliminate other possibilities. Unfortunately, there is no recognized objective study to unequivocally confirm the diagnosis of neurogenic thoracic outlet syndrome. Arteriograms may demonstrate subclavian or axillary artery stenosis when the arm is in abduction. This finding is not diagnostic, but poststenotic dilation of the artery is distinctly abnormal and indicates a definite lesion.
Treatment
Most patients with neurogenic TOS benefit from postural correction and a physical therapy program directed toward restoring the normal relation and strength of the structures in the shoulder girdle. Surgical techniques for decompression of the thoracic outlet are reserved for patients who have not responded after 3-6 months of conservative treatment. Some surgeons prefer transaxillary first rib resection, while others prefer a supraclavicular approach. With either operation, the anterior scalene muscle and any associated fibrous bands should be excised. Up to 90% of patients report cure or significant improvement.
Symptomatic arterial stenoses require decompression of the thoracic outlet in combination with arterial reconstruction. Effort thrombosis of the subclavian vein is usually best treated by catheter-directed thrombolysis of the venous occlusion followed by thoracic outlet decompression with or without operative venous reconstruction or angioplasty. Outcomes for these patients with vascular TOS symptoms are excellent with 80%–90% asymptomatic at 6 months.
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Schneider DB, Dimuzio PJ, Martin ND, et al: Combination treatment of venous thoracic outlet syndrome: open surgical decompression and intraoperative angioplasty. J Vasc Surg 2004;40:599.
ARTERIOVENOUS FISTULAS
Arteriovenous fistulas may be congenital, often called “malformations,” or acquired. Abnormal communications between arteries and veins occur in many diseases and affect vessels of all sizes and in many locations. In congenital fistulas, the systemic effect is often not great, because although the communications may be multiple, they are small. When a limb is involved, extensive arteriovenous communications may exist with increased flow and increased muscle mass and bone length. Surgical correction is rarely successful because of the numerous A-V connections. Massive swelling can be treated with ablation therapy but it also is rarely curative.
Acquired fistulas are usually the result of trauma, violent, or iatrogenic. These communications can have considerable flow, and high-output heart failure can occur. The third class of fistulas is surgically created fistulas for hemodialysis access.
Arteriovenous malformations in the gastrointestinal tract may cause hemorrhage. Osler–Weber–Rendu disease or syndrome (also termed hereditary hemorrhagic telangiectasia) is an autosomal dominant disorder characterized by gastrointestinal bleeding and epistaxis due to large arteriovenous anomalies in the gastrointestinal tract and lungs. Pulmonary lesions cause recirculation with lower Po2, polycythemia, clubbing, and cyanosis.
Penetrating injuries either from trauma or iatrogenic ones from arterial punctures are the most common causes of acquired fistulas. Blunt trauma, erosion of an atherosclerotic or mycotic arterial aneurysm into adjacent veins, communication with an arterial prosthetic graft, or neoplastic invasion can all cause arteriovenous fistulas as well. When large vessels are involved, the presentation may be dramatic. For example, if an aortic aneurysm ruptures into the inferior vena cava, the fistula enlarges rapidly and can result in cardiac dilation and failure.
ARTERIOVENOUS FISTULA FOR HEMODIALYSIS
General Considerations
A successful arteriovenous fistula for hemodialysis access requires a large vein (> 5 mm) that lies close to the skin for at least 20 cm. The cephalic vein is ideal for this purpose. A 3-mm vein will usually be able to dilate to 5-6 mm after arterializations. The radial artery to cephalic vein arteriovenous fistula (Cimino fistula) is the classic hemodialysis access fistula. If no suitable vein is available for an autogenous fistula, prosthetic grafts are used, most commonly PTFE. These are most commonly placed in a loop configuration. The poor patency rates of these grafts, 40% at 2 years, and potential for infection have driven national guidelines to encourage a higher rate of autogenous fistula formation. To maximize autogenous vein utilization, current practice includes transposing deep veins such as the basilic vein in the upper arm to the subcutaneous tissue. All veins used for access require dilation and “arterialization” of the wall, which takes at least 6 weeks prior to cannulization for dialysis. Transposed veins may take even longer to mature.
Flow rates of at least 300 cc/min are necessary for efficient dialysis. Patients with a newly created arteriovenous access should be watched carefully for arterial steal and distal extremity ischemia. Diabetics are the most vulnerable to this complication because of calcified proximal arteries or intrinsic arterial lesions of the arm. High-output cardiac failure occurs only rarely.
Clinical Findings
A typical continuous machinery murmur can be heard over the arteriovenous fistulas and is often associated with a palpable thrill and locally increased skin temperature. Proximally, the arteries and veins dilate, and the pulse distal to the lesion diminishes. There may be signs of venous insufficiency, coolness, and hypertrophy distal to the communication on the involved extremity. Tachycardia occurs in some patients as a feature of increased cardiac output. The pulse rate slows (Branham sign) when the fistula is occluded by compression.
In contrast, venous malformations rarely produce hemodynamic effects. In this disorder, the presence of a mass, which may or may not be tender, is the principal finding. Because flow rates are low, bruits and thrills are absent.
MRI has become the imaging study of choice for the evaluation and follow-up of peripheral arteriovenous malformations, but CTA also gives excellent anatomic information. Precise delineation of arteriovenous fistulas can be done with selective angiography.
Treatment
Not all arteriovenous connections require treatment. Most venous malformations should be treated conservatively. In addition, small peripheral fistulas may be observed and will often remain asymptomatic. Some are surgically inaccessible.
The indications for intervention include hemorrhage, local expansion, severe venous or arterial insufficiency, cosmetic deformity, and, rarely, heart failure. Most fistulas are now managed by embolization under radiographic control. The embolic material used includes blood clot, glass beads, and Gelfoam. Arteriovenous malformations of the head and neck and of the pelvis appear particularly well suited for this form of therapy. Direct injection of sclerosant compounds into venous malformations under fluoroscopic control also has been successful in at least temporarily reducing flow and swelling.
Surgical options are generally reserved for large acquired fistulas. When the fistulous connections involve substantial portions of an extremity, local ligation is invariably followed by recurrence, and only temporary palliation can be expected. Covered stent grafts are now being used for a variety of traumatic fistulas.
Prognosis
The results of therapy vary according to the extent, location, and type of fistula. In general, traumatic fistulas have the most favorable prognosis. Congenital fistulas are more difficult to eradicate because of the numerous arteriovenous connections present.
Sidawy AN, Spergel LM, Besarab A, Allon M, Jennings WC, et al: The Society for Vascular Surgery: clinical practice guidelines for the surgical placement and maintenance of arteriovenous hemodialysis access. J Vasc Surg 2008;48:2S.
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