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Anesthesia for conventional abdominal aortic reconstruction requires an understanding of the pathophysiology, an extensive knowledge of the surgical procedure, the ability to interpret sophisticated hemodynamic data, and skillful pharmacologic control and manipulation of hemodynamics. Preoperative and intraoperative communication with the surgical team is essential. All open operative procedures on the abdominal aorta and its major branches require large incisions and extensive dissection, clamping and unclamping of the aorta or its major branches, various durations of organ ischemia-reperfusion, significant fluid shifts and temperature fluctuations, and activation of neurohumoral and inflammatory responses.
Over the past decade, the growth and development of catheter-based technology for the treatment of peripheral arterial disease have generated tremendous interest for less invasive methods to treat aortic disease. Endovascular aortic surgery has emerged as a less invasive alternative to conventional surgical repair. The endovascular field is evolving rapidly, with new devices, technical innovations, and indications for aortic disease. The major objectives of surgical treatment of the aorta are to relieve symptoms, reduce the frequency of associated complications, and in the case of aortic aneurysm, prevent rupture.
Prevalence of abdominal aortic aneurysms is high among elderly men, approaching 8%.[168] [169] Age, smoking, family history of abdominal aortic aneurysm, and atherosclerotic
Abdominal aortic aneurysm is a multifactorial disease associated with aortic aging and atherosclerosis.[175] Although no unified concept of pathogenesis exists, there are genetic, biochemical, metabolic, infectious, mechanical, and hemodynamic factors that may contribute to the development of abdominal aortic aneurysmal disease.[176] [177] Adventitial elastin degradation (elastolysis), a hallmark of abdominal aortic aneurysm formation, may be the primary event.[178] Chronic inflammation is a prominent feature of abdominal aortic aneurysms and likely plays a fundamental role in the destruction of connective tissue in the aortic wall.[179] Concomitant aortoiliac occlusive disease is present in approximately 20% to 25% of patients with abdominal aortic aneurysms.[180] Approximately 5% of patients undergoing abdominal aortic resection have inflammatory aneurysms.[180] Rare causes of abdominal aortic aneurysm disease include trauma, mycotic infection, syphilis, and Marfan syndrome.
The natural history of abdominal aortic aneurysmal disease is one of progressive enlargement and ultimate rupture and death. In 1950, Estes[181] published a classic study of the natural history of abdominal aortic aneurysms in 102 patients. Only 19% of these patients survived 5 years, and rupture was the cause of death in 63%. The first successful abdominal aortic aneurysm resection and graft replacement (homograft implantation) was accomplished by Dubost and colleagues[182] in 1951. In 1966, Szilagyi and colleagues[183] confirmed the principle of elective graft replacement to prevent the eventual rupture of abdominal aortic aneurysm and to prolong life. Perioperative mortality from elective infrarenal aortic aneurysm resection has progressively declined from 18% to 20% during the 1950s, to 6% to 8% in the mid-1960s, to 5 to 6% in the early 1970s, to 2% to 4% in the 1980s, when it plateaued.[184] A publication of 1000 consecutive elective infrarenal aneurysms over a 15-year period reported a perioperative mortality rate of 2.4%.[185] Hertzer and coworkers[186] reported a mortality rate of 1.2% for 1135 consecutive elective abdominal aortic repairs at the Cleveland Clinic. These single-center mortality rates are considerably lower than the mortality rates of 5.6% to 8.4% reported from large national data sets.[172] [187] The higher mortality rates on the national level have prompted some to suggest that all of the technologic and treatment advances over the past 2 decades have not had an impact on outcomes of patients with abdominal aortic aneurysms.[187] Regionalization of care and endovascular treatments currently hold the most promise for improvement in operative mortality.
For ruptured abdominal aortic aneurysms, the perioperative mortality rate has not changed significantly over the past 4 decades and remains nearly 50%, [187] [188] [189] [190] with few exceptions. Taking into consideration patients with rupture who die before reaching a hospital, the overall mortality rate after rupture may very well exceed 90%.[190] In most patients with ruptured abdominal aortic aneurysm, the presence of an aneurysm is previously unknown.[191] To decrease the incidence of rupture, selective screening has been recommended and is under investigation. Screening once for abdominal aortic aneurysm at age 65 has been reported to identify most aneurysms that are of clinical significance.[169] Although screening for abdominal aortic aneurysm may not be a cost-effective strategy, studies have reported up to a 55% reduction in the incidence of aneurysm rupture with screening.[168] [192]
The diameter and rate of expansion of abdominal aortic aneurysms are the best predictors of the risk of rupture.[193] [194] The Joint Council of the American Association for Vascular Surgery and Society for Vascular Surgery published revised guidelines for the treatment of abdominal aortic aneurysms.[195] These guidelines emphasize that it is not possible or appropriate to recommend a single threshold diameter for operative intervention that can be generalized to all patients. There is near-uniform agreement that elective repair should be undertaken in all abdominal aortic aneurysms with a diameter of 6 cm or greater.[183] Although some controversy exists regarding elective abdominal aortic aneurysm repair when diameter is in the 5.5- to 5.9-cm range,[196] it is currently accepted that the risk of rupture for a 5.5-cm aneurysm (per year) is equal to or greater than perioperative mortality, and surgical repair is indicated. The 1-year incidence of probable rupture in patients refusing or unfit for elective repair has been reported as 9.4%, 10.2%, and 32.5% for aneurysms 5.5 to 5.9 cm, 6.0 to 6.9 cm, and 7.0 cm or larger, respectively.[197] The risk of rupture may be higher in women.[198] [199]
The natural history of abdominal aortic aneurysms 4.0 to 5.5 cm in diameter is not well defined, and significant controversy exists regarding surgical repair.[200] [201] [202] Two prospective randomized clinical trials conducted in the United Kingdom[203] (United Kingdom Small Aneurysm Trial) and the United States[204] (Aneurysm Detection and Management Study) concluded that surveillance of abdominal aortic aneurysms of 4.0 to 5.5 cm is a safe management option and that early surgical repair did not result in any long-term survival advantage. However, surgical repair is often recommended if such aneurysms become symptomatic or expand more than 0.5 cm in a 6-month period. Aneurysms less than 4 cm in diameter are thought to be relatively benign in terms of rupture and expansion.[205] [206]
The long-term durability of open infrarenal abdominal aortic aneurysm repair is excellent and well established. The incidence of late graft complications is very low (0.4% to 2.3%).[186] [207] The rate for late survival after repair of nonruptured abdominal aortic aneurysms is 92% at 1 year and 67% at 5 years.[190]
The infrarenal aorta and the iliac arteries are two of the most common sites of chronic atherosclerosis.[208]
Therapeutic options for managing aortoiliac occlusive disease include anatomic or direct reconstruction (i.e., aortobifemoral bypass), extra-anatomic or indirect bypass grafts (i.e., axillofemoral bypass), and catheter-based endoluminal techniques (i.e., percutaneous transluminal angioplasty with or without stent insertion). Aortobifemoral bypass is viewed as the gold standard in treating aortoiliac occlusive disease.[212] Extra-anatomic bypass grafts are usually reserved for specific indications, usually involving infection, failure of previous reconstruction, or prohibitive risk patients. Reduced long-term patency and inferior functional results are frequently the tradeoff for lower perioperative morbidity and mortality.[213] [214] Catheter-based endoluminal techniques, such as percutaneous transluminal angioplasty, are used for relatively localized disease and may be reasonable alternatives to aortobifemoral bypass in 10% to 15% of patients with aortoiliac occlusive disease.[212]
Atherosclerosis is the most common cause of renal artery stenosis. Occlusive lesions are located almost exclusively in the proximal segment and orifice of the renal artery and are usually an extension of aortic atherosclerosis. Fibromuscular dysplasia involving the renal arteries occurs primarily in the distal two thirds. Hemodynamically significant renal artery stenosis may cause hypertension through activation of the reninangiotensin system, and bilateral involvement may result in renal failure. Indications for intervention include control of hypertension and salvage of renal function. Operative interventions include aortorenal bypass, extra-anatomic bypass (i.e., hepatorenal or splenorenal bypass), or transaortic endarterectomy. Percutaneous transluminal angioplasty of the renal artery is used as the first-line treatment in selected patients. Suprarenal or supraceliac aortic cross-clamping is frequently required for operative interventions. Patients with renovascular hypertension frequently have poorly controlled hypertension despite maximal medical therapy.
Stenosis at the origin of the celiac and mesenteric arteries occurs from extension of aortic atherosclerosis. The inferior mesenteric artery is by far the most commonly involved, followed by the superior mesenteric artery and the celiac artery. Occlusion of a single vessel rarely causes ischemic symptoms because of the extensive nature of visceral collateralization. However, occlusion or significant stenosis of any two vessels may sufficiently compromise collateral flow and give rise to chronic visceral ischemia. Operative repair of visceral artery stenosis is reserved for symptomatic patients. Operative interventions include transaortic endarterectomy and bypass grafts, which frequently require supraceliac aortic cross-clamping. For reasons that are unclear, this condition affects women about four times as often as men.[189] Mortality rates for such procedures range from 7% to 18%. Acute mesenteric artery occlusion can be caused by embolus or, less commonly, thrombosis. To avoid the extremely high mortality associated with this condition, diagnosis and surgical intervention must occur before gangrene of the bowel develops.
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