Surgery_Schwartz

Surgery_Schwartz. more prone to failure. The endo-thelial lining is lost as part of the freezing process, making these grafts prone to early thrombosis. Cryopreserved grafts are also prone to aneurysmal degeneration. Despite the fact that these grafts have not performed as well as prosthetic bypasses and autogenous vein bypasses in clinical practice, they can still play a role when revascularization is required following removal of infected prosthetic bypass grafts, especially when the autog-enous vein is unavailable to create a new bypass through clean tissue planes.Human Umbilical Vein. Human umbilical vein (HUV) is less commonly used than PTFE because it is thicker and more cum-bersome to handle and because of concerns about aneurysmal degeneration. HUV allografts are stabilized with glutaralde-hyde and do not have viable cells or antigenic reactivity. These grafts have poor handling characteristics and require extra care when suturing because of an outer Dacron mesh wrapping that is used to


Surgery_Schwartz

Surgery_Schwartz. and do not have viable cells or antigenic reactivity. These grafts have poor handling characteristics and require extra care when suturing because of an outer Dacron mesh wrapping that is used to decrease aneurysmal degeneration. Dardik and col-leagues have reported favorable results after using HUV and an adjunctive distal arteriovenous fistula.188 One trial compar-ing HUV with PTFE and saphenous vein showed that HUV was better than PTFE but worse than saphenous vein in terms of 5-year patency in the above-knee location.189 In a system-atic review, HUV appears to perform better than cryopre-served veins in terms of 1-year graft patency in infrainguinal revascularization.190Prosthetic Conduits and Adjunctive Modifications. If a vein is truly unavailable, PTFE or Dacron is the best option for above-knee bypass. The addition of rings to PTFE did not con-fer benefit in a single prospective, randomized clinical trial.191 For infrageniculate prosthetic bypasses, use of a vein patch, cuff,


Surgery_Schwartz

Surgery_Schwartz. for above-knee bypass. The addition of rings to PTFE did not con-fer benefit in a single prospective, randomized clinical trial.191 For infrageniculate prosthetic bypasses, use of a vein patch, cuff, or other venous anastomotic modification can improve patency (52% patency at 2 years for PTFE with vein cuff vs. 29% for PTFE with no cuff) and also improve limb salvage (84% vs. 62%).192Although prosthetic grafts are quickly available, easy to handle, and do not require extensive dissection to harvest, their propensity to undergo thrombosis and develop neointimal hyperplasia makes them a less favorable alternative when com-pared to vein. In a recent review of vein and prosthetic above-knee femoropopliteal bypasses, the 5-year primary patency rates were reported to be 74% and 39%, respectively.193 Outcomes were even worse for below-knee prosthetic bypasses. Unfortu-nately, the use of autologous venous conduits is not possible in as many as 30% of patients. The great saphenous vein may be


Surgery_Schwartz

Surgery_Schwartz. Outcomes were even worse for below-knee prosthetic bypasses. Unfortu-nately, the use of autologous venous conduits is not possible in as many as 30% of patients. The great saphenous vein may be unsuitable because of small size and poor quality or unavailable due to prior harvest.Methods to improve prosthetic graft performance have consisted of altering the geometry at the distal anastomosis to get the benefit obtained with vein cuffs (Distaflo; Bard Peripheral Vascular, Tempe, AZ) and covalently bonding agents onto the luminal surface with anticoagulant, anti-inflammatory, and anti-proliferative characteristics (Propaten; Gore, Flagstaff, AZ). One randomized trial that compared precuffed PTFE versus PTFE with a vein cuff enrolled 104 patients at 10 centers. Of 89 patients, 47 were randomized to precuffed PTFE bypasses and 44 were randomized to bypasses with a vein cuff.194 At 1 and Brunicardi_Ch23_p0897-p0980.indd 96727/02/19 4:15 PM 968SPECIFIC CONSIDERATIONSPART II2 years,


Surgery_Schwartz

Surgery_Schwartz. to precuffed PTFE bypasses and 44 were randomized to bypasses with a vein cuff.194 At 1 and Brunicardi_Ch23_p0897-p0980.indd 96727/02/19 4:15 PM 968SPECIFIC CONSIDERATIONSPART II2 years, primary patency rates were 52% and 49% in the pre-cuffed group and 62% and 44% in the vein cuffed group, respec-tively. At 1 and 2 years, the limb salvage rates were 72% and 65% in the precuffed group and 75% and 62% in the vein cuffed group, respectively. Although numbers are small and follow-up short, the midterm analysis revealed that Distaflo precuffed grafts and PTFE grafts with vein cuff had similar results. The authors concluded that a precuffed graft was a reasonable alternative for infragenicular reconstruction in the absence of saphenous vein.194 Other authors have been less optimistic and question whether there is any benefit derived from geometri-cally altering prosthetic conduits.195Another approach for improving outcomes when using prosthetic for bypass grafts involves bonding


Surgery_Schwartz

Surgery_Schwartz. and question whether there is any benefit derived from geometri-cally altering prosthetic conduits.195Another approach for improving outcomes when using prosthetic for bypass grafts involves bonding anticoagulants to the conduit. The Gore Propaten graft has heparin bonded onto the luminal surface of the PTFE graft using Carmeda BioActive Surface (CBAS) technology, which immobilizes the heparin molecule with a single covalent bond that does not alter its anti-coagulant properties.196 The heparin binding does not alter the microstructure and handling characteristics of the PTFE. A pro-spective, randomized trial by Devine and colleagues suggested that heparin-bonded Dacron or PTFE was superior to plain PTFE for above-knee popliteal bypasses. The 3-year primary patency rate for the heparin-bonded grafts was 55% compared with 42% for PTFE (P <0.044). Both of these patency rates are inferior to great saphenous vein grafts; however, if the improved results with heparin bonding continue to be


Surgery_Schwartz

Surgery_Schwartz. grafts was 55% compared with 42% for PTFE (P <0.044). Both of these patency rates are inferior to great saphenous vein grafts; however, if the improved results with heparin bonding continue to be substantiated, then heparin-bonded prosthetic grafts will become the preferred con-duit for above-knee bypass in the absence of suitable vein.197 A recent review of available studies with this graft showed an 80% 1-year patency rate for below-knee bypasses.198 Randomized controlled clinical trials with more patients and longer follow-up are necessary to validate whether the Propaten vascular graft is superior to other prosthetics and whether it is comparable to autogenous vein for below-knee interventions.Clinical Results of Surgical and Endovascular Interventions for Femoropopliteal Occlusive DiseaseBalloon angioplasty of the femoropopliteal vessels has not enjoyed the degree of success seen with iliac angioplasty. Patency in this region is dependent on whether the patient pres-ents with


Surgery_Schwartz

Surgery_Schwartz. DiseaseBalloon angioplasty of the femoropopliteal vessels has not enjoyed the degree of success seen with iliac angioplasty. Patency in this region is dependent on whether the patient pres-ents with claudication versus limb-threatening ischemia, the sta-tus of the distal runoff vessels, and lesion morphology. Initial technical success for femoropopliteal angioplasty is seen in 80% to 90% of cases, with failure to cross a lesion occurring in 7% of stenoses and 18% of occlusive lesions. Studies have shown that PTA of the femoropopliteal segment achieved a greater than 90% technical success rate and had a 38% to 58% 5-year pri-mary patency rate.152,199 PTA of lesions longer than 7 to 10 cm results in compromised patency, whereas PTA of shorter lesions (<3 cm) gives fairly good results. Lofberg and colleagues per-formed 127 femoropopliteal PTA procedures and reported a primary patency rate at 5-year follow-up of 12% in limbs with occlusion longer than 5 cm versus 32% in limbs with


Surgery_Schwartz

Surgery_Schwartz. Lofberg and colleagues per-formed 127 femoropopliteal PTA procedures and reported a primary patency rate at 5-year follow-up of 12% in limbs with occlusion longer than 5 cm versus 32% in limbs with occlusion less than 5 cm in length.151 Occlusive lesions have much worse initial technical success rates than stenotic lesions. Concentric lesions respond better to PTA than eccentric lesions, and heavy calcifications have a negative impact on success rates. Distal runoff is another powerful predictor of long-term success.Johnston analyzed 254 consecutive patients who under-went femoropopliteal PTA and reported a 5-year patency rate of 53% for stenotic lesions and 36% for occlusive lesions in patients with good runoff versus a 5-year patency rate of 31% for stenotic lesions and 16% for occlusive lesions in patients with poor runoff.149 A meta-analysis by Hunink and colleagues showed that adjusted 5-year primary patencies after angioplasty of femoropopliteal lesions varied from 12% to 68%,


Surgery_Schwartz

Surgery_Schwartz. lesions in patients with poor runoff.149 A meta-analysis by Hunink and colleagues showed that adjusted 5-year primary patencies after angioplasty of femoropopliteal lesions varied from 12% to 68%, with the best results occurring in patients with claudication and stenotic lesions.152 Although the initial technical success is better for stenoses than occlusions, long-term patency rates for stenoses and short occlusions have been variable, and there have been conflicting results regarding the efficacy of stent use. Early pub-lished series that examined efficacy of femoropopliteal artery stents showed patency rates that were comparable to standalone PTA, with primary patency rates varying from 18% to 72% at 3 years.158 Patient selection and the anatomic character of the lesions may play important roles in the outcomes. Additionally, stent characteristics may contribute to the patency rate. Several recent clinical studies have demonstrated significant improve-ments in patency when the


Surgery_Schwartz

Surgery_Schwartz. roles in the outcomes. Additionally, stent characteristics may contribute to the patency rate. Several recent clinical studies have demonstrated significant improve-ments in patency when the newer generations of nitinol stents are used to treat SFA lesions.160,200Mewissen treated 137 lower limbs in 122 patients with CLI, secondary to TASC A (n = 12) or TASC B or C (n = 125) lesions in the SFA. Patients were treated with Cordis SMART self-expanding nitinol stents. Binary restenosis (>50%) was measured by standard duplex velocity criteria at various postint-ervention intervals. Primary stent patency, defined as absence of binary restenosis in this study, was calculated by life-table methods from the time of intervention. The mean lesion length was 12.2 cm (range, 4–28 cm). The technical success was 98%. Mean follow-up was 302 days. The primary stent patency rates were 92%, 76%, 66%, and 60% at 6, 12, 18, and 24 months, respectively.160 Ferreira and colleagues treated 59 patients who had


Surgery_Schwartz

Surgery_Schwartz. was 98%. Mean follow-up was 302 days. The primary stent patency rates were 92%, 76%, 66%, and 60% at 6, 12, 18, and 24 months, respectively.160 Ferreira and colleagues treated 59 patients who had 74 femoropopliteal lesions (60% TASC D) with Zilver nitinol self-expanding stents (Cook, Bloomington, IN). Mean recanalization length was 19 cm (range, 3–53 cm). Mean fol-low-up time was 2.4 years (range, 3 days–4.8 years). Kaplan-Meier estimates for primary patency rates were 90%, 78%, 74%, 69%, and 69% at 1, 2, 3, 4, and 4.8 years, respectively.201There is general agreement that for suboptimal PTA of an SFA lesion, stent placement is indicated, but a recent random-ized trial by Schillinger and associates suggests that primary stenting results in lower restenosis rates than PTA and selective stenting. Restenosis rates at 2 years were 45.7% versus 69.2% in favor of primary stenting compared with PTA and optional secondary stenting using an intent-to-treat analysis (P = 0.031). Consistently,


Surgery_Schwartz

Surgery_Schwartz. Restenosis rates at 2 years were 45.7% versus 69.2% in favor of primary stenting compared with PTA and optional secondary stenting using an intent-to-treat analysis (P = 0.031). Consistently, stenting, both primary and selective, was supe-rior to standalone PTA with respect to the occurrence of reste-nosis (49.2% vs. 74.3%; P = 0.028) by a treatment-received analysis.202Nitinol bare metal stents that are designed specifically for below-knee interventions are showing very encouraging results. Bosiers and colleagues reported their 12-month results using the commercially available non–drug-eluting Xpert (Abbott Vascular, Santa Clara, CA) nitinol stent system in below-knee arterial interventions.203 They had a 12-month primary patency rate of 76.3% and a limb salvage rate of 95.9%. They fol-lowed patients for 12 months and performed angiography with quantitative vessel analysis on the 73% of patients available. Angiography revealed a binary restenosis rate (>50%) of only 20.5%, which is


Surgery_Schwartz

Surgery_Schwartz. patients for 12 months and performed angiography with quantitative vessel analysis on the 73% of patients available. Angiography revealed a binary restenosis rate (>50%) of only 20.5%, which is comparable to well-accepted coronary drug-eluting stent study outcomes. The authors attributed this opti-mal performance to the maintenance of flow dynamics because Brunicardi_Ch23_p0897-p0980.indd 96827/02/19 4:15 PM 969ARTERIAL DISEASECHAPTER 23the stent was specifically designed for use in small vessels. Kickuth and colleagues also have obtained good results using the Xpert stent. After stent placement, the primary cumulative patency rate at 6 months for the study group of 35 patients was 82%. The sustained clinical improvement rate as evidenced by improved ABI was 80%, and freedom from major amputation was 100% at the 6-month follow-up. The rate of major compli-cations was 17%.204Wolf and colleagues published a multicenter, prospec-tive randomized trial comparing PTA with bypass in 263


Surgery_Schwartz

Surgery_Schwartz. amputation was 100% at the 6-month follow-up. The rate of major compli-cations was 17%.204Wolf and colleagues published a multicenter, prospec-tive randomized trial comparing PTA with bypass in 263 men who had iliac, femoral, or popliteal artery obstruction.205 In 56 patients, cumulative 1-year primary patency rate was 43% after PTA and 82% after bypass surgery, demonstrating that for long SFA stenoses or occlusions, surgery is better than PTA. Another recent randomized study (BASIL trial) of 452 patients with CLI demonstrated no difference in amputation-free survival at 6 months between surgery and PTA/stenting.206 The authors com-mented that surgery was somewhat more expensive and rec-ommended that endovascular intervention should be used as first-line therapy especially in medically unfit patients. They did conclude that at the 2-year follow-up, healthy patients with-out medical comorbidities derived greater benefit from surgery because it was associated with decreased need for


Surgery_Schwartz

Surgery_Schwartz. unfit patients. They did conclude that at the 2-year follow-up, healthy patients with-out medical comorbidities derived greater benefit from surgery because it was associated with decreased need for reintervention and had a decreased hazard ratio in terms of all-cause mortality. The recently published randomized prospective study compar-ing the treatment of SFA occlusive disease percutaneously with an ePTFE/nitinol self-expanding stent graft versus surgical fem-oral to above-knee popliteal artery bypass with synthetic graft material showed no difference between the two groups with respect to primary or secondary patency rate at four years.167 This finding suggests that ePTFE/nitinol self-expanding stent graft placement can be offered as an alternative to treatment of the SFA segment for revascularization when prosthetic bypass is being considered or when autologous conduit is unavailable. Using the 2000 TASC definitions and a Markov state transi-tion model decision analysis, Nolan and


Surgery_Schwartz

Surgery_Schwartz. when prosthetic bypass is being considered or when autologous conduit is unavailable. Using the 2000 TASC definitions and a Markov state transi-tion model decision analysis, Nolan and colleagues showed that PTA/stenting surpasses bypass efficacy for TASC C lesions if PTA/stenting primary patency is >32% at 5 years, patient age is >80 years, and/or greater saphenous vein bypass operative mortality is >6%.207NONATHEROSCLEROTIC DISORDERS OF BLOOD VESSELSThe majority of cases of peripheral vascular disease that are seen by vascular surgeons are attributable to underlying athero-sclerosis. Nonatherosclerotic disease states that result in arterial pathology are less commonly encountered, but are nonetheless important, as they are potentially treatable lesions that may mimic atherosclerotic lesions and result in vascular insuffi-ciency (see Table 23-18). A thorough knowledge of these rare disease states is important for the practicing vascular surgeon in order to make medical


Surgery_Schwartz

Surgery_Schwartz. lesions and result in vascular insuffi-ciency (see Table 23-18). A thorough knowledge of these rare disease states is important for the practicing vascular surgeon in order to make medical recommendations and provide appropri-ate surgical treatment.Giant Cell Arteritis (Temporal Arteritis)Giant cell arteritis is also known as temporal arteritis, which is a systemic chronic inflammatory vascular disease with many characteristics similar to those of Takayasu’s disease. The histo-logic and pathologic changes and laboratory findings are similar. Patients tend to be white women over the age of 50 years, with a high incidence in Scandinavia and women of Northern European descent. Genetic factors may play a role in disease pathogenesis, with a human leukocyte antigen (HLA) variant having been identified. Differences exist between Takayasu’s and giant cell arteritis in terms of presentation, disease location, and therapeutic efficacy. The inflammatory process typically involves the aorta and


Surgery_Schwartz

Surgery_Schwartz. Differences exist between Takayasu’s and giant cell arteritis in terms of presentation, disease location, and therapeutic efficacy. The inflammatory process typically involves the aorta and its extracranial branches, of which the superficial temporal artery is specifically affected.The clinical syndrome begins with a prodromal phase of constitutional symptoms, including headache, fever, malaise, and myalgias. The patients may be initially diagnosed with coexisting polymyalgia rheumatica; an HLA-related associa-tion may exist between the two diseases. As a result of vascular narrowing and end-organ ischemia, complications may occur such as visual alterations, including blindness and mural weak-ness, resulting in acute aortic dissection that may be devastating. Ischemic optic neuritis resulting in partial or complete blindness occurs in up to 40% of patients and is considered a medical emergency. Cerebral symptoms occur when the disease process extends to the carotid arteries. Jaw


Surgery_Schwartz

Surgery_Schwartz. resulting in partial or complete blindness occurs in up to 40% of patients and is considered a medical emergency. Cerebral symptoms occur when the disease process extends to the carotid arteries. Jaw claudication and temporal artery tenderness may be experienced. Aortic lesions are usually asymptomatic until later stages and consist of thoracic aneu-rysms and aortic dissections.The diagnostic gold standard is a temporal artery biopsy, which will show the classic histologic findings of multinucle-ated giant cells with a dense perivascular inflammatory infil-trate. Treatment regimens are centered on corticosteroids, and giant cell arteritis tends to rapidly respond. Remission rates are high, and treatment tends to have a beneficial and preventative effect on the development of subsequent vascular complications.Takayasu’s ArteritisTakayasu’s arteritis is a rare but well-recognized chronic inflam-matory arteritis affecting large vessels, predominantly the aorta and its main branches


Surgery_Schwartz

Surgery_Schwartz. vascular complications.Takayasu’s ArteritisTakayasu’s arteritis is a rare but well-recognized chronic inflam-matory arteritis affecting large vessels, predominantly the aorta and its main branches (Table 23-27). Chronic vessel inflamma-tion leads to wall thickening, fibrosis, stenosis, and thrombus formation. Symptoms are related to end-organ ischemia. The acute inflammation can destroy the arterial media and lead to aneurysm formation. This rare autoimmune disease occurs pre-dominantly in women between the ages of 10 and 40 years who are of Asian descent. Genetic studies have demonstrated a high frequency of HLA haplotypes in patients from Japan and Mexico, suggesting increased susceptibility to developing the disease in patients with certain alleles. However, these associations have not been seen in North America. Vascular inflammation leads Table 23-27Angiographic classification of Takayasu’s arteritisTYPEVESSEL INVOLVEMENTType IBranches from the aortic archType IIaAscending aorta,


Surgery_Schwartz

Surgery_Schwartz. been seen in North America. Vascular inflammation leads Table 23-27Angiographic classification of Takayasu’s arteritisTYPEVESSEL INVOLVEMENTType IBranches from the aortic archType IIaAscending aorta, aortic arch and its branchesType IIbAscending aorta, aortic arch and its branches, thoracic descending aortaType IIIThoracic descending aorta, abdominal aorta, and/or renal arteriesType IVAbdominal aorta and/or renal arteriesType VCombined features of types IIb and IVInvolvement of the coronary or pulmonary arteries is designated as C (+) or P (+), respectively.Brunicardi_Ch23_p0897-p0980.indd 96927/02/19 4:15 PM 970SPECIFIC CONSIDERATIONSPART IIto arterial wall thickening, stenosis, and eventually, fibrosis and thrombus formation. The pathologic changes produce stenosis, dilation, aneurysm formation, and/or occlusion.The clinical course of Takayasu’s arteritis begins with a “prepulseless” phase in which the patient demonstrates constitu-tional symptoms. These include fever, anorexia,


Surgery_Schwartz

Surgery_Schwartz. formation, and/or occlusion.The clinical course of Takayasu’s arteritis begins with a “prepulseless” phase in which the patient demonstrates constitu-tional symptoms. These include fever, anorexia, weight loss, gen-eral malaise, arthralgias, and malnutrition. As the inflammation progresses and stenoses develop, more characteristic features of the disease become evident. During the chronic phase, the dis-ease is inactive or “burned out.” It is during this latter stage that patients most frequently present with bruits and vascular insuf-ficiency according to the arterial bed involved. Laboratory data may show elevations in erythrocyte sedimentation rate, C-reactive protein, and white blood cell count, or conversely, anemia may predominate. Characteristic clinical features during the second phase vary according to the involved vascular bed and include hypertension reflecting renal artery stenosis, retinopathy, aortic regurgitation, cerebrovascular symptoms, angina and con-gestive heart


Surgery_Schwartz

Surgery_Schwartz. phase vary according to the involved vascular bed and include hypertension reflecting renal artery stenosis, retinopathy, aortic regurgitation, cerebrovascular symptoms, angina and con-gestive heart failure, abdominal pain or gastrointestinal bleeding, pulmonary hypertension, or extremity claudication.The gold standard for diagnosis remains angiography showing narrowing or occlusion of the entire aorta or its pri-mary branches, or focal or segmental changes in large arteries in the upper or lower extremities. Six types of Takayasu’s arteritis exist and are graded in terms of severity: type I, affecting the aorta and arch vessels; type IIa, affecting the ascending aorta, aortic arch, and branches; type IIb, affecting the ascending aorta, aortic arch and branches, and thoracic descending aorta; type III, affecting the thoracic descending aorta, abdominal aorta, and/or renal arteries; type IV, affecting the abdominal aorta and/or renal arteries; and type V, with combined features of


Surgery_Schwartz

Surgery_Schwartz. aorta; type III, affecting the thoracic descending aorta, abdominal aorta, and/or renal arteries; type IV, affecting the abdominal aorta and/or renal arteries; and type V, with combined features of types IIb and IV.208Treatment consists of steroid therapy initially, with cyto-toxic agents used in patients who do not achieve remission. Surgical treatment is performed only in advanced stages, and bypass needs to be delayed during active phases of inflam-mation. There is no role for endarterectomy, and synthetic or autogenous bypass grafts need to be placed onto disease-free segments of vessels. For focal lesions, there have been reports of success with angioplasty.Ehlers-Danlos SyndromeEhlers-Danlos syndrome is one of the more significant inheritable disorders affecting the connective tissue, along with Marfan’s syndrome. This syndrome represents a heterogenous group of connective tissue disorders (types I through IV) that were first described in 1682 by van Meekeren.238 It is an


Surgery_Schwartz

Surgery_Schwartz. tissue, along with Marfan’s syndrome. This syndrome represents a heterogenous group of connective tissue disorders (types I through IV) that were first described in 1682 by van Meekeren.238 It is an autosomal domi-nant disorder affecting approximately 1 in 5000 persons that is characterized by skin elasticity, joint hypermobility, tissue fragility, multiple ecchymoses, and subcutaneous pseudotu-mors. Ehlers-Danlos syndrome is a disorder of fibrillar collagen metabolism with identifiable, specific defects that have been found in the collagen biosynthetic pathway that produce clini-cally distinct forms of this disease. Ten different phenotypes have been described, each with variable modes of inheritance and biochemical defects. Of the four basic types of collagen found in the body, the predominant type in blood vessels is type III. Within the vessel wall, type III collagen contributes to structural integrity and tensile strength and plays a role in platelet aggregation and thrombus


Surgery_Schwartz

Surgery_Schwartz. predominant type in blood vessels is type III. Within the vessel wall, type III collagen contributes to structural integrity and tensile strength and plays a role in platelet aggregation and thrombus formation.Of the three types of Ehlers-Danlos syndrome that have arterial complications, type IV represents 5% of cases and is the one most likely to be seen by a vascular surgeon. These patients synthesize abnormal type III collagen (mutation COL3A1) and represent 5% of all cases.209 Affected individuals do not show the typical skin and joint manifestations, and thus typically pres-ent for diagnosis when a major vascular catastrophe occurs. In a review of 36 patients with this disorder, Cikrit and colleagues reported a 44% mortality rate from major hemorrhage prior to any surgical intervention.210 In the 20 patients who underwent 29 vascular procedures, there was a 29% mortality rate. Arterial rupture, aneurysm formation, and acute aortic dissection may occur in any major artery, with


Surgery_Schwartz

Surgery_Schwartz. In the 20 patients who underwent 29 vascular procedures, there was a 29% mortality rate. Arterial rupture, aneurysm formation, and acute aortic dissection may occur in any major artery, with the most frequent site of rupture being the abdominal cavity. Repair is problematic because the vessel wall is soft and sutures pull through the fragile tissue. Ligation may be the only option in many circumstances.Marfan’s SyndromeAnother heterogeneous heritable disorder of connective tissue, Marfan’s syndrome is characterized by abnormal musculo-skeletal, ocular, and cardiovascular features first described by Antoine Marfan in 1896.211 The inborn error of metabolism in this syndrome has been localized to the long arm of chromo-some 15 (15q21.3). Defects occur in fibrillin, a basic protein in the microfibrillar apparatus that serves as a backbone for elas-tin, which is one of the main extracellular structural proteins in blood vessels. This is an autosomal dominant gene with high penetrance;


Surgery_Schwartz

Surgery_Schwartz. microfibrillar apparatus that serves as a backbone for elas-tin, which is one of the main extracellular structural proteins in blood vessels. This is an autosomal dominant gene with high penetrance; however, approximately 15% to 20% of cases are secondary to new spontaneous mutations.Classic recognizable features of Marfan’s syndrome include tall stature, long limbs (dolichostenomelia), long fingers (arachnodactyly), joint hyperextensibility, chest wall deformi-ties, and scoliosis. Ocular manifestations are flattened corneas, lens subluxation, and myopia. Ninety-five percent of patients have cardiovascular involvement, which may include ascend-ing aortic dilatation, mitral valve prolapse, valvular regurgita-tion, and aortic dissection. Skin, central nervous system, and pulmonary features may be present as well. Aortic root dilata-tion will generally occur in all patients. This may not be evident on standard chest radiograph until dilatation has resulted in an ascending aortic


Surgery_Schwartz

Surgery_Schwartz. may be present as well. Aortic root dilata-tion will generally occur in all patients. This may not be evident on standard chest radiograph until dilatation has resulted in an ascending aortic aneurysm, aortic valve regurgitation, or dis-section. Left untreated, the cardiovascular complications are devastating and reduce the life expectancy to about 40 years for men and slightly higher for women. Death is usually attrib-utable to life-threatening complications of aortic regurgitation, dissection, and rupture after the ascending aorta has dilated to 6 cm or more.Aggressive medical management with β-adrenergic block-ing agents and other blood pressure–lowering regimens is cru-cial to treatment. Surgical intervention entails replacement of the aortic root with a composite valve graft (e.g., Bentall pro-cedure).212 Prophylactic operative repair is indicated for an aneurysm greater than 5.5 cm, with an acceptable perioperative mortality of less than 5%.Pseudoxanthoma ElasticumPseudoxanthoma


Surgery_Schwartz

Surgery_Schwartz. pro-cedure).212 Prophylactic operative repair is indicated for an aneurysm greater than 5.5 cm, with an acceptable perioperative mortality of less than 5%.Pseudoxanthoma ElasticumPseudoxanthoma elasticum is a rare inherited disorder of con-nective tissue that is characterized by an unbalanced elastic fiber metabolism and synthesis, resulting in fragmentation and calci-fication of the fibers. Clinical manifestations occur in the skin, ocular, gastrointestinal, and cardiovascular systems. Character-istic skin lesions are seen in the axilla, antecubital and popliteal fossae, and groin. The yellow, xanthoma-like papules occur in redundant folds of skin and are said to resemble plucked chicken skin. The inheritance pattern includes both autosomal dominant Brunicardi_Ch23_p0897-p0980.indd 97027/02/19 4:15 PM 971ARTERIAL DISEASECHAPTER 23and recessive types and has a prevalence of 1 in 160,000 indi-viduals.213 The ATP-binding cassette subfamily C member 6 (ABCC6) gene has been


Surgery_Schwartz

Surgery_Schwartz. 97027/02/19 4:15 PM 971ARTERIAL DISEASECHAPTER 23and recessive types and has a prevalence of 1 in 160,000 indi-viduals.213 The ATP-binding cassette subfamily C member 6 (ABCC6) gene has been demonstrated to be responsible, and 43 mutations have been identified, all of which lead to calcification of the internal elastic laminae of medium-sized vessel walls.214Cardiovascular features are common and include prema-ture coronary artery disease, cerebrovascular disease, renovas-cular hypertension, diminished peripheral pulses, and restrictive cardiomyopathy. Symptom onset typically occurs in the second decade of life, with onset at an average age of 13 years. Patients should be counseled to reduce potential contributing factors for atherosclerosis such as tobacco use and high cholesterol levels. Calcium intake should be restricted in adolescents, as a positive correlation has been found between disease severity and cal-cium intake. Surgical management involves standard vascular


Surgery_Schwartz

Surgery_Schwartz. levels. Calcium intake should be restricted in adolescents, as a positive correlation has been found between disease severity and cal-cium intake. Surgical management involves standard vascular techniques, with the exception that arterial conduits should not be employed in cardiac bypass.Kawasaki’s DiseaseKawasaki’s disease was first described in 1967, as a mucocu-taneous lymph node syndrome occurring in young children. In most studies, more than half the patients are younger than 2 years of age, with a higher prevalence in boys.215 Although originally described in Japan, the disease is found worldwide. An infec-tious agent may be causative; however, no specific agent has been identified. Immune activation with the contribution of cytokines, elastases, growth factors, and metalloproteinases is believed to be a mechanism for inflammation and aneurysm for-mation. Coronary artery aneurysms, the hallmark of the disease, histologically demonstrate a panarteritis with fibrinoid necro-sis.


Surgery_Schwartz

Surgery_Schwartz. is believed to be a mechanism for inflammation and aneurysm for-mation. Coronary artery aneurysms, the hallmark of the disease, histologically demonstrate a panarteritis with fibrinoid necro-sis. Coronary arteriography may show occlusions, recanaliza-tion, and localized stenosis, in addition to multiple aneurysms. A variety of constitutional symptoms and signs resulting from systemic vasculitis are present in the acute phase of the illness.Medical therapy for Kawasaki’s disease clearly decreases the manifestations of coronary artery involvement. Intravenous gamma globulin and aspirin therapy are most successful if begun within the first 10 days of illness. Up to 20% of untreated patients will develop coronary arterial lesions. A long-term, low-dose aspirin therapy regimen is usually recommended.Inflammatory Arteritis and VasculitisChronic inflammatory arteritis and vasculitis (i.e., inflamma-tory changes within veins as well as arteries) include a spec-trum of disease processes caused


Surgery_Schwartz

Surgery_Schwartz. Arteritis and VasculitisChronic inflammatory arteritis and vasculitis (i.e., inflamma-tory changes within veins as well as arteries) include a spec-trum of disease processes caused by immunologic mechanisms. These terms signify a necrotizing transmural inflammation of the vessel wall associated with antigen-antibody immune com-plex deposition within the endothelium. These conditions show pronounced cellular infiltration in the adventitia, thickened inti-mal fibrosis, and organized thrombus. These disease processes may clinically mimic atherosclerosis, and most are treated by corticosteroid therapy or chemotherapeutic agents. Even so, it is important to recognize distinguishing characteristics of each disease in order to establish the course of treatment and long-term prognosis. A classification system of systemic vasculitis by vessel size is shown in Table 23-28.Behçet’s DiseaseBehçet’s disease is a rare syndrome characterized by oral and genital ulcerations and ocular inflammation,


Surgery_Schwartz

Surgery_Schwartz. system of systemic vasculitis by vessel size is shown in Table 23-28.Behçet’s DiseaseBehçet’s disease is a rare syndrome characterized by oral and genital ulcerations and ocular inflammation, affecting males in Japan and the Mediterranean. An HLA linkage has been found, indicating a genetic component to the etiology.216 Vascular involvement is seen in 7% to 38% of patients and is localized Table 23-28Classification of vasculitis based on vessel involvementLarge-Vessel VasculitisTakayasu’s arteritisGiant cell arteritisBehçet’s diseaseMedium-Vessel VasculitisPolyarteritis nodosaKawasaki’s diseaseBuerger’s diseaseSmall-Vessel VasculitisHypersensitivity angiitisto the abdominal aorta, femoral artery, and pulmonary artery. Vascular lesions may also include venous complications such as deep venous thrombosis or superficial thrombophlebitis. Arterial aneurysmal degeneration can occur; however, this is an uncommon, albeit potentially devastating, complication. Mul-tiple true aneurysms and


Surgery_Schwartz

Surgery_Schwartz. venous thrombosis or superficial thrombophlebitis. Arterial aneurysmal degeneration can occur; however, this is an uncommon, albeit potentially devastating, complication. Mul-tiple true aneurysms and pseudoaneurysms may develop, and rupture of an aortic aneurysm is the major cause of death in patients with Behçet’s disease.217Histologically, degeneration of the vasa vasorum with surrounding perivascular lymphocyte infiltration is seen, along with thickening of the elastic laminae around the tunica media. Aneurysm formation is believed to be associated with a loss of the nutrient flow and elastic component of the vessels, lead-ing to progressive dilatation. Multiple aneurysms are relatively common, with a reported occurrence of 36% in affected Japanese patients.218 Furthermore, pseudoaneurysm formation after surgical bypass is common at anastomotic suture lines due to the vascular wall fragility and medial destruction. Systemic therapy with corticosteroids and immunosuppressive agents


Surgery_Schwartz

Surgery_Schwartz. formation after surgical bypass is common at anastomotic suture lines due to the vascular wall fragility and medial destruction. Systemic therapy with corticosteroids and immunosuppressive agents may diminish symptoms related to the inflammatory process; however, they have no effect on the rate of disease progression and arterial degeneration.Polyarteritis NodosaPolyarteritis nodosa (PAN) is another systemic inflammatory disease process, which is characterized by a necrotizing inflam-mation of medium-sized or small arteries that spares the small-est blood vessels (i.e., arterioles and capillaries). This disease predominantly affects men over women by a 2 to 1 ratio. PAN develops subacutely, with constitutional symptoms that last for weeks to months. Intermittent, low-grade fevers, malaise, weight loss, and myalgias are common presenting symptoms. As medium-sized vessels lie within the deep dermis, cutane-ous manifestations occur in the form of livedo reticularis, nod-ules,


Surgery_Schwartz

Surgery_Schwartz. malaise, weight loss, and myalgias are common presenting symptoms. As medium-sized vessels lie within the deep dermis, cutane-ous manifestations occur in the form of livedo reticularis, nod-ules, ulcerations, and digital ischemia.218 Skin biopsies of these lesions may be sufficient for diagnosis. Inflammation may be seen histologically, with pleomorphic cellular infiltrates and segmental transmural necrosis leading to aneurysm formation.Neuritis from nerve infarction occurs in 60% of patients, and gastrointestinal complications occur in up to 50%.219 Addi-tionally, renal involvement is found in 40% and manifests as microaneurysms within the kidney or segmental infarctions. Cardiac disease is a rare finding except at autopsy, where thickened, diseased coronary arteries may be seen, as well as patchy myocardial necrosis. Patients may succumb to renal fail-ure, intestinal hemorrhage, or perforation. End-organ ischemia from vascular occlusion or aneurysm rupture can be disastrous


Surgery_Schwartz

Surgery_Schwartz. as well as patchy myocardial necrosis. Patients may succumb to renal fail-ure, intestinal hemorrhage, or perforation. End-organ ischemia from vascular occlusion or aneurysm rupture can be disastrous Brunicardi_Ch23_p0897-p0980.indd 97127/02/19 4:15 PM 972SPECIFIC CONSIDERATIONSPART IIcomplications with high mortality rates. The mainstay of treat-ment is steroid and cytotoxic agent therapy. Up to 50% of patients with active PAN will experience remission with high dosing.Radiation-Induced ArteritisRadiation-induced arteritis results from progressive stenosis due to endothelial damage that leads to cellular proliferation and fibrosis. These are well-described complications of combined irradiation and chemotherapy for the treatment of head and neck malignancy. Arterial lesions are known complications of radia-tion and are similar to those found in atherosclerotic occlusive disease. A history of therapeutic irradiation to the neck can complicate the management of carotid artery


Surgery_Schwartz

Surgery_Schwartz. known complications of radia-tion and are similar to those found in atherosclerotic occlusive disease. A history of therapeutic irradiation to the neck can complicate the management of carotid artery occlusive disease. Radiation-induced damage to blood vessels has been well stud-ied. The small capillaries and sinusoids are most susceptible to radiation effects, as endothelial cells are the most radiosensi-tive cells. The radiation effects on the mediumand large-sized arteries include myointimal proliferation, with or without lipid deposits, and thrombosis. Characteristically, irregular spindle-shaped cells are seen replacing the normal endothelial cells in the healing phase. Occlusive lesions develop in the irradiated carotid arteries and are either the result of vessel wall fibrosis or, more commonly, due to accelerated atherosclerosis. Neuro-logic complications related to radiation-induced carotid artery disease are similar to those due to nonirradiated atherosclerotic occlusive


Surgery_Schwartz

Surgery_Schwartz. more commonly, due to accelerated atherosclerosis. Neuro-logic complications related to radiation-induced carotid artery disease are similar to those due to nonirradiated atherosclerotic occlusive disease.Rupture of the carotid artery has been reported following neck irradiation and is likely related to local wound compli-cation and superimposed infection. The diagnosis of radiation arteritis is based on the clinical history and confirmation of the occlusive lesion by duplex ultrasound, MRA, CTA, or sub-traction angiography. Irradiated lesions can be confined to the irradiated segment of the internal carotid artery with the remain-ing part of the vessel spared of disease. Characteristically, the radiation-induced atherosclerotic lesion does not involve the carotid bulb, unlike the nonradiated atherosclerotic lesions. The indications for intervention in radiation-induced carotid lesions are the same as previously discussed for atherosclerotic carotid occlusive lesions. However,


Surgery_Schwartz

Surgery_Schwartz. nonradiated atherosclerotic lesions. The indications for intervention in radiation-induced carotid lesions are the same as previously discussed for atherosclerotic carotid occlusive lesions. However, asymptomatic irradiated carotid artery lesions should be considered for intervention because they can be more prone to progression and develop-ment of neurologic complications. Endovascular treatment with carotid angioplasty/stenting has become the treatment of choice for radiation-induced lesions, although surgical endarterectomy and bypass have been shown to be safe. The rate of recurrent stenosis is higher in radiation-induced carotid lesions, whether stented or surgically treated.Raynaud’s SyndromeFirst described in 1862 by Maurice Reynaud, the term Raynaud’s syndrome applies to a heterogeneous symptom array associated with peripheral vasospasm, more commonly occurring in the upper extremities. The characteristically intermittent vasospasm classically follows exposure to various


Surgery_Schwartz

Surgery_Schwartz. symptom array associated with peripheral vasospasm, more commonly occurring in the upper extremities. The characteristically intermittent vasospasm classically follows exposure to various stimuli, including cold temperatures, tobacco, or emotional stress. Formerly, a distinc-tion was made between Raynaud’s “disease” and Raynaud’s “phenomenon” for describing a benign disease occurring in isolation or a more severe disease secondary to another under-lying disorder, respectively. However, many patients develop collagen vascular disorders at some point after the onset of vaso-spastic symptoms; progression to a connective tissue disorder ranges from 11% to 65% in reported series.220 Therefore, the term Raynaud’s syndrome is now used to encompass both the primary and secondary conditions.Characteristic color changes occur in response to the arterio-lar vasospasm, ranging from intense pallor to cyanosis to redness as the vasospasm occurs. The digital vessels then relax, even-tually leading


Surgery_Schwartz

Surgery_Schwartz. color changes occur in response to the arterio-lar vasospasm, ranging from intense pallor to cyanosis to redness as the vasospasm occurs. The digital vessels then relax, even-tually leading to reactive hyperemia. The majority of patients are young women less than 40 years of age. Up to 70% to 90% of reported patients are women, although many patients with only mild symptoms may never present for treatment.220 Geo-graphic regions with cooler, damp climates such as the Pacific Northwest and Scandinavian countries have a higher reported prevalence of the syndrome. Certain occupational groups, such as those who use vibrating tools, may be more predisposed to Raynaud’s syndrome or digital ischemia. The exact patho-physiologic mechanism behind the development of such severe vasospasm remains elusive, and much attention has focused on increased levels of α2-adrenergic receptors and their hypersen-sitivity in patients with Raynaud’s syndrome, as well as abnor-malities in the thermoregulatory


Surgery_Schwartz

Surgery_Schwartz. and much attention has focused on increased levels of α2-adrenergic receptors and their hypersen-sitivity in patients with Raynaud’s syndrome, as well as abnor-malities in the thermoregulatory response, which is governed by the sympathetic nervous system.The diagnosis of severe vasospasm may be made using noninvasive measurements in the vascular laboratory. Angiog-raphy is usually reserved for those who have digital ulceration and in whom an embolic or obstructive cause is believed to be present and potentially surgically correctable. Different changes in digital blood pressure will occur in patients with Raynaud’s syndrome. Normal individuals will show only a slight decrease in digital blood pressure in response to external cold stimuli, whereas those with Raynaud’s syndrome will show a similar curve until a critical temperature is reached. It is at this point that arterial closure acutely occurs.There is no cure for Raynaud’s syndrome; thus, all treat-ments mainly palliate symptoms


Surgery_Schwartz

Surgery_Schwartz. similar curve until a critical temperature is reached. It is at this point that arterial closure acutely occurs.There is no cure for Raynaud’s syndrome; thus, all treat-ments mainly palliate symptoms and decrease the severity and perhaps frequency of attacks. Conservative measures predomi-nate, including the wearing of gloves, use of electric or chemi-cally activated hand warmers, avoiding occupational exposure to vibratory tools, abstinence from tobacco, and relocating to a warmer, dryer climate. The majority (90%) of patients will respond to avoidance of cold and other stimuli. The remaining 10% of patients with more persistent or severe syndromes can be treated with a variety of vasodilatory drugs, albeit with only a 30% to 60% response rate. Calcium channel–blocking agents such as diltiazem and nifedipine are the drugs of choice. The selective serotonin reuptake inhibitor fluoxetine has been shown to reduce the frequency and duration of vasospastic episodes. Intravenous infusions


Surgery_Schwartz

Surgery_Schwartz. and nifedipine are the drugs of choice. The selective serotonin reuptake inhibitor fluoxetine has been shown to reduce the frequency and duration of vasospastic episodes. Intravenous infusions of prostaglandins have been reserved for nonresponders with severe symptoms.Surgical therapy is limited to debridement of digital ulcer-ations and amputation of gangrenous digits, which are rare complications. Upper extremity sympathectomy may provide relief in 60% to 70% of patients; however, the results are short-lived with a gradual recurrence of symptoms in 60% of patients within 10 years.221Fibromuscular DysplasiaFMD is a vasculopathy of uncertain etiology that is character-ized by segmental arterial involvement. Histologically, fibrous tissue proliferation, smooth muscle cell hyperplasia, and elastic fiber destruction alternate with mural thinning. The characteris-tic beaded appearance of FMD is due to areas of medial thinning alternating with areas of stenosis. The most commonly affected


Surgery_Schwartz

Surgery_Schwartz. elastic fiber destruction alternate with mural thinning. The characteris-tic beaded appearance of FMD is due to areas of medial thinning alternating with areas of stenosis. The most commonly affected Brunicardi_Ch23_p0897-p0980.indd 97227/02/19 4:15 PM 973ARTERIAL DISEASECHAPTER 23are medium-sized arteries, including the internal carotid, renal, vertebral, subclavian, mesenteric, and iliac arteries. The inter-nal carotid artery is the second most common site of involve-ment after the renal arteries. FMD occurs most frequently in women (90%) and is recognized at approximately 55 years of age.222 Only 10% of patients with FMD will have complications attributable to the disease. Pathologically, FMD is a heterog-enous group of four distinct types of lesions that are subgrouped based on the predominant site of involvement within the vessel wall. Of the four types (medial fibroplasia, intimal fibroplasia, medial hyperplasia, and perimedial dysplasia), medial fibropla-sia is the most


Surgery_Schwartz

Surgery_Schwartz. the predominant site of involvement within the vessel wall. Of the four types (medial fibroplasia, intimal fibroplasia, medial hyperplasia, and perimedial dysplasia), medial fibropla-sia is the most common pathologic type, affecting the internal carotid artery (ICA) and the renal artery, and occurring in 85% of reported cases.223The two main clinical syndromes associated with FMD are TIAs from disease in the internal carotid artery and hyper-tension from renal artery involvement. Symptoms produced by FMD are generally secondary to associated arterial stenosis and are clinically indistinguishable from those caused by atheroscle-rotic disease. Often, asymptomatic disease is found incidentally on conventional angiographic studies being performed for other reasons. Within the internal carotid artery, FMD lesions tend to be located higher in the extracranial segment than with athero-sclerotic lesions and may not be readily demonstrated by duplex scan.Clinically, symptoms are due to


Surgery_Schwartz

Surgery_Schwartz. carotid artery, FMD lesions tend to be located higher in the extracranial segment than with athero-sclerotic lesions and may not be readily demonstrated by duplex scan.Clinically, symptoms are due to encroachment on the ves-sel lumen and a reduction in flow. Additionally, thrombi may form in areas of mural dilatation from a stagnation of flow, lead-ing to distal embolization. Surgical treatment has been favored for symptomatic patients with angiographically proven disease. Due to the distal location of FMD lesions in the extracranial carotid artery, resection and repair are not usually feasible. Instead, graduated luminal dilatation under direct vision has been used successfully in patients, with antiplatelet therapy continued postoperatively. PTA has been used effectively in patients with FMD-induced hypertension. Several series have documented a high technical success rate, with recurrence rates of 8% to 23% at more than 1 year.223 However, the therapeutic effect of blood pressure


Surgery_Schwartz

Surgery_Schwartz. FMD-induced hypertension. Several series have documented a high technical success rate, with recurrence rates of 8% to 23% at more than 1 year.223 However, the therapeutic effect of blood pressure control may continue to be observed despite restenosis. Surgical reconstruction of the renal arteries for FMD has good long-term results and is recommended for recurrent lesions after angioplasty. Open balloon angioplasty of the ICA has been described, which allows for precise fluo-roscopic guidance, rather than blind dilatation with calibrated metal probes, and back-bleeding after dilatation to eliminate cerebral embolization. Distal neuroprotective devices may allow this procedure to be performed completely percutane-ously, thereby lessening the threat of cerebral emboli.Nonatherosclerotic Disease Affecting the Popliteal Artery DiseaseThere are three distinct nonatherosclerotic disease entities that may result in lower extremity claudication that predominantly occur in 40to 50-year-old


Surgery_Schwartz

Surgery_Schwartz. Affecting the Popliteal Artery DiseaseThere are three distinct nonatherosclerotic disease entities that may result in lower extremity claudication that predominantly occur in 40to 50-year-old men. Adventitial cystic disease, pop-liteal artery entrapment syndrome, and Buerger’s disease should be considered in any young patients presenting with intermittent claudication.Adventitial Cystic Disease of the Popliteal Artery. The first successful operative repair of popliteal artery occlusion caused by a cyst arising from the adventitia was reported in 1954 by Ejrup and Hierton.224 Adventitial cystic disease is a rare arterial condition occurring at an incidence of 0.1%, usually in the popliteal artery. This disease affects men in a ratio of approximately 5:1 and appears predominantly in the fourth and fifth decades. The incidence is approximately 1 in 1200 cases of claudication or 1 in 1000 peripheral arteriograms. The predominance of reported cases is found in Japan and Europe. However,


Surgery_Schwartz

Surgery_Schwartz. and fifth decades. The incidence is approximately 1 in 1200 cases of claudication or 1 in 1000 peripheral arteriograms. The predominance of reported cases is found in Japan and Europe. However, this disease may affect other vascular sites, such as the femoral, external iliac, radial, ulnar, and brachial arteries. Besides claudication as a symptom, this diagnosis should be considered in young patients who have a mass in a nonaxial ves-sel in proximity to a related joint. These synovial-like, mucin-filled cysts reside in the subadventitial layer of the vessel wall and have a similar macroscopic appearance to ganglion cysts. Despite this similarity and suggestion of a joint origin for these lesions, histochemical markers have failed to link the cystic lin-ing to synovium.Patients presenting at a young age with bilateral lower extremity claudication and minimal risk factors for atheroma formation should be evaluated for adventitial cystic disease, as well as the other two


Surgery_Schwartz

Surgery_Schwartz. presenting at a young age with bilateral lower extremity claudication and minimal risk factors for atheroma formation should be evaluated for adventitial cystic disease, as well as the other two nonatherosclerotic vascular lesions described here. Because of luminal encroachment and com-pression, peripheral pulses may be present in the limb when extended, but then can disappear during knee joint flexion. Noninvasive studies may suggest arterial stenosis with ele-vated velocities. Color-flow duplex scanning followed by T2-weighted MRI now appears to be the best diagnostic choice. Angiography will demonstrate a smooth, well-defined, crescent-shaped filling defect, the classic “scimitar” sign.224 There may be associated calcification in the cyst wall and no other evidence of atherosclerotic occlusive disease.Various therapeutic methods have been described for the treatment of adventitial cystic disease. The recommended treat-ments are excision of the cyst with the cystic wall,


Surgery_Schwartz

Surgery_Schwartz. occlusive disease.Various therapeutic methods have been described for the treatment of adventitial cystic disease. The recommended treat-ments are excision of the cyst with the cystic wall, enucleation, or simple aspiration when the artery is stenotic. Retention of the cystic lining leads to continued secretion of the cystic fluid and recurrent lesions. In 30% of patients who have an occluded artery, resection of the affected artery, followed by an interposi-tion graft using autogenous saphenous vein, is recommended.Popliteal Artery Entrapment Syndrome. Love and col-leagues first coined the term popliteal artery entrapment in 1965 to describe a syndrome combining muscular involvement with arterial ischemia occurring behind the knee, with the suc-cessful surgical repair having taken place 6 years earlier.225 This is a rare disorder with an estimated prevalence of 0.16% that occurs with a male-to-female ratio of 15:1. Five types of anatomic entrapment have been defined, according to the


Surgery_Schwartz

Surgery_Schwartz. years earlier.225 This is a rare disorder with an estimated prevalence of 0.16% that occurs with a male-to-female ratio of 15:1. Five types of anatomic entrapment have been defined, according to the posi-tion of the medial head of the gastrocnemius muscle, abnormal muscle slips or tendinous bands, or the course of the popliteal artery itself (Table 23-29). Concomitant popliteal vein impinge-ment occurs in up to 30% of cases. Twenty-five percent of cases are bilateral.The typical patient presents with swelling and claudica-tion of isolated calf muscle groups following vigorous physi-cal activity. Various differential diagnoses must be considered when encountering patients with symptoms and signs sugges-tive of popliteal artery entrapment syndrome (Table 23-30). In a large series of 240 patients, the median age for surgical treat-ment was 28.5 years.226 Noninvasive studies with ABIs should be performed with the knee extended and the foot in a neutral, forced plantar, and dorsiflexed


Surgery_Schwartz

Surgery_Schwartz. patients, the median age for surgical treat-ment was 28.5 years.226 Noninvasive studies with ABIs should be performed with the knee extended and the foot in a neutral, forced plantar, and dorsiflexed position. A drop in pressure of 50% or greater or dampening of the plethysmographic wave-forms in plantar or dorsiflexion is a classic finding. Contraction Brunicardi_Ch23_p0897-p0980.indd 97327/02/19 4:15 PM 974SPECIFIC CONSIDERATIONSPART IITable 23-29Classification of popliteal entrapment syndromeTYPEDESCRIPTIONIPopliteal artery is displaced medially around a normal medial head of the gastrocnemiusIIMedial head of gastrocnemius, which arises lateral to popliteal arteryIIIPopliteal artery is compressed by an accessory slip of muscle from medial head of gastrocnemiusIVEntrapment by a deeper popliteus muscleVAny of the above plus popliteal vein entrapmentVIFunctional entrapmentTable 23-30Differential diagnosis for popliteal entrapment syndromeVascular EtiologiesAtherosclerosisBuerger’s


Surgery_Schwartz

Surgery_Schwartz. popliteus muscleVAny of the above plus popliteal vein entrapmentVIFunctional entrapmentTable 23-30Differential diagnosis for popliteal entrapment syndromeVascular EtiologiesAtherosclerosisBuerger’s diseaseTraumaPopliteal aneurysmAdventitial cystic diseaseExtrinsic compressionCardiac embolismDeep vein thrombosisVenous entrapmentMusculoskeletal EtiologiesGastrocnemius or soleus strainPeriostitisCompartment syndromeStress fracturesTibialis posterior tendonitisMuscular anomaliesGeneral Neurologic EtiologiesSpinal stenosisof the gastrocnemius should compress the entrapped popliteal artery. The sudden onset of signs and symptoms of acute isch-emia with absent distal pulses is consistent with popliteal artery occlusion secondary to entrapment. Other conditions resulting from entrapment are thrombus formation with distal emboli or popliteal aneurysmal degeneration. Although CT and MRI have been employed, angiography remains the most widely used test. Angiography performed with the foot in a


Surgery_Schwartz

Surgery_Schwartz. formation with distal emboli or popliteal aneurysmal degeneration. Although CT and MRI have been employed, angiography remains the most widely used test. Angiography performed with the foot in a neutral position may demonstrate classical medial deviation of the popliteal artery or normal anatomic positioning. Coexisting abnormalities may include stenosis, luminal irregularity, delayed flow, aneurysm, or complete occlusion. Diagnostic accuracy is increased with the use of ankle stress view-active plantar flexion and passive dorsiflexion.The treatment of popliteal artery entrapment consists of surgical decompression of the impinged artery with possible arterial reconstruction. Division of the anomalous musculoten-dinous insertion site with or without saphenous vein interposi-tion grafting to bypass the damaged arterial segment has been described to be the procedure of choice. The natural history of entrapment is progressive arterial degeneration leading to com-plete arterial thrombosis.


Surgery_Schwartz

Surgery_Schwartz. bypass the damaged arterial segment has been described to be the procedure of choice. The natural history of entrapment is progressive arterial degeneration leading to com-plete arterial thrombosis. In such instances, thrombolytic ther-apy is needed with subsequent release of the functional arterial impairment. Lysis will improve distal runoff and may improve limb-salvage and bypass patency rates.Buerger’s Disease (Thromboangiitis Obliterans)Buerger’s disease, also known as thromboangiitis obliterans, is a progressive nonatherosclerotic segmental inflammatory disease that most often affects smalland medium-sized arteries, veins, and nerves of the upper and lower extremities. The clinical and pathologic findings of this disease entity were published in 1908 by Leo Buerger in a description of 11 amputated limbs.227 The typical age range for occurrence is 20 to 50 years, and the dis-order is more frequently found in males who smoke. The upper extremities may be involved, and a migratory


Surgery_Schwartz

Surgery_Schwartz. of 11 amputated limbs.227 The typical age range for occurrence is 20 to 50 years, and the dis-order is more frequently found in males who smoke. The upper extremities may be involved, and a migratory superficial phlebi-tis may be present in up to 16% of patients, thus indicating a sys-temic inflammatory response. In young adults presenting to the Mayo Clinic (1953–1981) with lower limb ischemia, Buerger’s disease was diagnosed in 24%.228 Conversely, the diagnosis was made in 9% of patients with ischemic finger ulcerations. The cause of thromboangiitis obliterans is unknown; however, use of or exposure to tobacco is essential to both the diagnosis and progression of the disease.Pathologically, thrombosis occurs in smallto medium-sized arteries and veins with associated dense polymorphonu-clear leukocyte aggregation, microabscesses, and multinucleated giant cells. The chronic phase of the disease shows a decrease in the hypercellularity and frequent recanalization of the vessel lumen.


Surgery_Schwartz

Surgery_Schwartz. leukocyte aggregation, microabscesses, and multinucleated giant cells. The chronic phase of the disease shows a decrease in the hypercellularity and frequent recanalization of the vessel lumen. End-stage lesions demonstrate organized thrombus and blood vessel fibrosis. Although the disease is common in Asia, North American males do not appear to have any particular pre-disposition, as the diagnosis is made in less than 1% of patients with severe limb ischemia.Buerger’s disease typically presents in young male smok-ers, with symptoms beginning prior to age 40. Patients initially present with foot, leg, arm, or hand claudication, which may be mistaken for joint or neuromuscular problems. Progression of the disease leads to calf claudication and eventually ischemic rest pain and ulcerations on the toes, feet, or fingers. A complete history should exclude diabetes, hyperlipidemia, or autoimmune disease as possible etiologies for the occlusive lesions. Because it is likely that multiple


Surgery_Schwartz

Surgery_Schwartz. on the toes, feet, or fingers. A complete history should exclude diabetes, hyperlipidemia, or autoimmune disease as possible etiologies for the occlusive lesions. Because it is likely that multiple limbs are involved, angiography should be performed of all four limbs. Even if symptoms are not yet present in a limb, angiographic findings may be demonstrated. Characteristic angiographic findings show disease confinement to the distal circulation, usually infrapopliteal and distal to the brachial artery. The occlusions are segmental and show “skip” lesions with extensive collateralization, the so-called corkscrew collaterals.The treatment of thromboangiitis obliterans revolves around strict smoking cessation. In patients who are able to abstain, disease remission is impressive, and amputation avoid-ance is increased. In the experience reported from the Oregon Health Sciences Center, no disease progression with associated tissue loss occurred after discontinuation of tobacco. The role of


Surgery_Schwartz

Surgery_Schwartz. avoid-ance is increased. In the experience reported from the Oregon Health Sciences Center, no disease progression with associated tissue loss occurred after discontinuation of tobacco. The role of surgical intervention is minimal in Buerger’s disease, as there is often no acceptable target vessel for bypass. Furthermore, autog-enous vein conduits are limited secondary to coexisting migra-tory thrombophlebitis. Mills and associates reported their results Brunicardi_Ch23_p0897-p0980.indd 97427/02/19 4:15 PM 975ARTERIAL DISEASECHAPTER 23of 31% limb loss in 26 patients over 15 years, thus authenti-cating the virulence of Buerger’s disease involving the lower extremities.229 In addition, others have described a significant discrepancy in limb loss in patients who continued to smoke versus those who discontinued tobacco use (67% vs. 35%).REFERENCESEntries highlighted in bright blue are key references. 1. Norgren L, Hiatt WR, Dormandy JA, et al. Inter-society consensus for the


Surgery_Schwartz

Surgery_Schwartz. versus those who discontinued tobacco use (67% vs. 35%).REFERENCESEntries highlighted in bright blue are key references. 1. Norgren L, Hiatt WR, Dormandy JA, et al. Inter-society consensus for the management of peripheral arterial disease (TASC II). Eur J Vasc Endovasc Surg. 2007;33(suppl 1): S1-S75. 2. Jones DN, Rutherford RB. Peripheral vascular assessment and its role in predicting wound healing potential. Clin Podiatr Med Surg. 1991;8(4):909-921. 3. Favaretto E, Pili C, Amato A, et al. Analysis of agreement between Duplex ultrasound scanning and arteriography in patients with lower limb artery disease. J Cardiovasc Med (Hagerstown). 2007;8(5):337-341. 4. Jakobs TF, Wintersperger BJ, Becker CR. MDCT-imaging of peripheral arterial disease. Semin Ultrasound CT MR. 2004; 25(2):145-155. 5. Hertzer NR, Beven EG, Young JR, et al. Coronary artery dis-ease in peripheral vascular patients. A classification of 1000 coronary angiograms and results of surgical management. Ann Surg.


Surgery_Schwartz

Surgery_Schwartz. NR, Beven EG, Young JR, et al. Coronary artery dis-ease in peripheral vascular patients. A classification of 1000 coronary angiograms and results of surgical management. Ann Surg. 1984;199(2):223-233. 6. Eagle KA, Coley CM, Newell JB, et al. Combining clini-cal and thallium data optimizes preoperative assessment of cardiac risk before major vascular surgery. Ann Intern Med. 1989;110(11):859-866. 7. McFalls EO, Ward HB, Moritz TE, et al. Predictors and out-comes of a perioperative myocardial infarction following elective vascular surgery in patients with documented coro-nary artery disease: results of the CARP trial. Eur Heart J. 2008;29(3):394-401. 8. Landoni G, Pisano A, Lomivorotov V, et al. Randomized evi-dence for reduction of perioperative mortality: an updated consensus process. J Cardiothorac Vasc Anesth. 2017;31(2): 719-730. 9. Ali WE, Vaidya SR, Ejeh SU, Okoroafor KU. Meta-analysis study comparing percutaneous coronary intervention/drug eluting stent versus coronary artery


Surgery_Schwartz

Surgery_Schwartz. Cardiothorac Vasc Anesth. 2017;31(2): 719-730. 9. Ali WE, Vaidya SR, Ejeh SU, Okoroafor KU. Meta-analysis study comparing percutaneous coronary intervention/drug eluting stent versus coronary artery bypass surgery of unpro-tected left main coronary artery disease: Clinical outcomes during short-term versus long-term (>1 year) follow-up. Medi-cine (Baltimore). 2018;97(7):e9909. 10. Altit R, Gray WA. New innovations in drug-eluting stents for peripheral arterial disease. Curr Cardiol Rep. 2017;19(11):117. 11. Parodi JC, Marin ML, Veith FJ. Transfemoral, endovascular stented graft repair of an abdominal aortic aneurysm. Arch Surg. 1995;130(5):549-552. 12. Brinster CJ, Milner R. Fenestrated endovascular aortic repair and clinical trial devices for complex abdominal aortic aneu-rysms. J Cardiovasc Surg (Torino). 2018;59(3):342-359. 13. Ergun O, Canyigit M, Hidiroglu M, et al. Endovascular treat-ment for acute traumatic thoracic aortic transection. Ulus Travma Acil Cerrahi Derg.


Surgery_Schwartz

Surgery_Schwartz. J Cardiovasc Surg (Torino). 2018;59(3):342-359. 13. Ergun O, Canyigit M, Hidiroglu M, et al. Endovascular treat-ment for acute traumatic thoracic aortic transection. Ulus Travma Acil Cerrahi Derg. 2015;21(4):285-290. 14. Donnan GA, Fisher M, Macleod M, Davis SM. Stroke. Lancet. 2008;371(9624):1612-1623. 15. Chaer RA, DeRubertis B, Patel S, Lin SC, Kent CK, Faries PL. Current management of extracranial carotid artery disease. Rev Recent Clin Trials. 2006;1(3):293-301. 16. Grant EG, Benson CB, Moneta GL, et al. Carotid artery stenosis: grayscale and Doppler ultrasound diagnosis--Society of Radi-ologists in Ultrasound consensus conference. Ultrasound Q. 2003;19(4):190-198. 17. Brinjikji W, Huston J 3rd, Rabinstein AA, Kim GM, Lerman A, Lanzino G. Contemporary carotid imaging: from degree of stenosis to plaque vulnerability. J Neurosurg. 2016; 124(1):27-42. 18. Zhao DL, Wan Y, Wang GK, et al. Evaluation of image quality in carotid and cerebrovascular disease: a comparative study between


Surgery_Schwartz

Surgery_Schwartz. stenosis to plaque vulnerability. J Neurosurg. 2016; 124(1):27-42. 18. Zhao DL, Wan Y, Wang GK, et al. Evaluation of image quality in carotid and cerebrovascular disease: a comparative study between subtraction and routine computed tomography angi-ography. Echocardiography. 2016;33(11):1735-1740. 19. Cheng SF, Brown MM. Contemporary medical therapies of atherosclerotic carotid artery disease. Semin Vasc Surg. 2017; 30(1):8-16. 20. Kita MW. Carotid endarterectomy in symptomatic carotid stenosis: NASCET comparative results at 30 months of follow-up. J Insur Med. 1992;24(1):42-46. 21. Warlow CP. Symptomatic patients: the European Carotid Surgery Trial (ECST). J Mal Vasc. 1993;18(3):198-201. 22. Rothwell PM, Eliasziw M, Gutnikov SA, et al. Analysis of pooled data from the randomised controlled trials of endar-terectomy for symptomatic carotid stenosis. Lancet. 2003; 361(9352):107-116. 23. Topakian R, Strasak AM, Sonnberger M, et al. Timing of stent-ing of symptomatic carotid stenosis is


Surgery_Schwartz

Surgery_Schwartz. trials of endar-terectomy for symptomatic carotid stenosis. Lancet. 2003; 361(9352):107-116. 23. Topakian R, Strasak AM, Sonnberger M, et al. Timing of stent-ing of symptomatic carotid stenosis is predictive of 30-day outcome. Eur J Neurol. 2007;14(6):672-678. 24. Roederer GO, Langlois YE, Jager KA, et al. The natural his-tory of carotid arterial disease in asymptomatic patients with cervical bruits. Stroke. 1984;15(4):605-613. 25. Fisher M, Martin A, Cosgrove M, Norris JW. The NASCET-ACAS plaque project. North American Symptomatic Carotid Endarterectomy Trial. Asymptomatic Carotid Atherosclerosis Study. Stroke. 1993;24(12 suppl):I24-25; discussion I31-2. 26. Halliday A, Mansfield A, Marro J, et al. Prevention of dis-abling and fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomised controlled trial. Lancet. 2004;363(9420):1491-1502. 27. Coward LJ, Featherstone RL, Brown MM. Safety and efficacy of endovascular treatment of


Surgery_Schwartz

Surgery_Schwartz. without recent neurological symptoms: randomised controlled trial. Lancet. 2004;363(9420):1491-1502. 27. Coward LJ, Featherstone RL, Brown MM. Safety and efficacy of endovascular treatment of carotid artery stenosis compared with carotid endarterectomy: a Cochrane systematic review of the randomized evidence. Stroke. 2005;36(4):905-911. 28. Lin PH, Barshes NR, Annambhotla S, Huynh TT. Prospec-tive randomized trials of carotid artery stenting versus carotid endarterectomy: an appraisal of the current literature. Vasc Endovascular Surg. 2008;42(1):5-11. 29. Berkefeld J, Chaturvedi S. The International Carotid Stent-ing Study and the North American Carotid Revascularization Endarterectomy versus Stenting Trial: fueling the debate about carotid artery stenting. Stroke. 2010;41(11):2714-2715. 30. Brott TG, Hobson RW 2nd, Howard G, et al. Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med. 2010;363(1):11-23. 31. Bonati LH, Jongen LM, Haller S, et al. New


Surgery_Schwartz

Surgery_Schwartz. TG, Hobson RW 2nd, Howard G, et al. Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med. 2010;363(1):11-23. 31. Bonati LH, Jongen LM, Haller S, et al. New ischaemic brain lesions on MRI after stenting or endarterectomy for symptom-atic carotid stenosis: a substudy of the International Carotid Stenting Study (ICSS). Lancet Neurol. 2010;9(4):353-362. 32. Ricotta JJ, Aburahma A, Ascher E, et al. Updated Society for Vas-cular Surgery guidelines for management of extracranial carotid disease: executive summary. J Vasc Surg. 2011;54(3)832-836. 33. Crawford RS, Chung TK, Hodgman T, Pedraza JD, Corey M, Cambria RP. Restenosis after eversion vs patch closure carotid endarterectomy. J Vasc Surg. 2007;46(1):41-48. 34. Organ N, Walker PJ, Jenkins J, Foster W, Jenkins J. 15 year experience of carotid endarterectomy at the Royal Brisbane and Women’s Hospital: outcomes and changing trends in man-agement. Eur J Vasc Endovasc Surg. 2008;35(3):273-279. 35. Zhou W,


Surgery_Schwartz

Surgery_Schwartz. J. 15 year experience of carotid endarterectomy at the Royal Brisbane and Women’s Hospital: outcomes and changing trends in man-agement. Eur J Vasc Endovasc Surg. 2008;35(3):273-279. 35. Zhou W, Felkai DD, Evans M, et al. Ultrasound criteria for severe in-stent restenosis following carotid artery stenting. J Vasc Surg. 2008;47(1):74-80. 36. Lin PH, Zhou W, Kougias P, El Sayed HF, Barshes NR, Huynh TT. Factors associated with hypotension and bradycardia after Brunicardi_Ch23_p0897-p0980.indd 97527/02/19 4:15 PM 976SPECIFIC CONSIDERATIONSPART IIcarotid angioplasty and stenting. J Vasc Surg. 2007;46(5): 846-853; discussion 853-844. 37. Plouin PF, Perdu J, La Batide-Alanore A, Boutouyrie P, Gimenez-Roqueplo AP, Jeunemaitre X. Fibromuscular dys-plasia. Orphanet J Rare Dis. 2007;2:28. 38. Zhou W, Lin PH, Bush RL, et al. Carotid artery aneurysm: evolution of management over two decades. J Vasc Surg. 2006;43(3):493-496; discussion 497. 39. Woolen S, Gemmete JJ. Paragangliomas of the head


Surgery_Schwartz

Surgery_Schwartz. W, Lin PH, Bush RL, et al. Carotid artery aneurysm: evolution of management over two decades. J Vasc Surg. 2006;43(3):493-496; discussion 497. 39. Woolen S, Gemmete JJ. Paragangliomas of the head and neck. Neuroimaging Clin N Am. 2016;26(2):259-278. 40. Khan MM, Khan MI, Ali H, Kazmi T, Iqbal H. Diagnostic, surgical, and postoperative challenges of neuroendocrine tumors of the neck: clinical experience and literature review. Ann Vasc Surg. 2017;45:92-97. 41. Chandra V, Trang K, Virgin-Downey W, Dalman RL, Mell MW. Long-term outcomes after repair of symptom-atic abdominal aortic aneurysms. J Vasc Surg. 2018. pii: S0741-5214(18)30435-X. 42. Dotter CT, Judkins MP, Rosch J. Transluminal angioplasty in arteriosclerotic obstruction of the lower extremities. Med Times. 1969;97(7):95-108. 43. Lin CJ, Lin CY, Stitziel NO. Genetics of the extracellular matrix in aortic aneurysmal diseases. Matrix Biol. 2018. pii: S0945-053X(17)30468-7. 44. Matthews EO, Rowbotham SE, Moxon JV, Jones RE, Vega de


Surgery_Schwartz

Surgery_Schwartz. CJ, Lin CY, Stitziel NO. Genetics of the extracellular matrix in aortic aneurysmal diseases. Matrix Biol. 2018. pii: S0945-053X(17)30468-7. 44. Matthews EO, Rowbotham SE, Moxon JV, Jones RE, Vega de Ceniga M, Golledge J. Meta-analysis of the association between peripheral artery disease and growth of abdominal aortic aneurysms. Br J Surg. 2017;104(13):1765-1774. 45. Boese A, Chang L, Yin KJ, Chen YE, Lee JP, Hamblin MH. Sex Differences in Abdominal Aortic Aneurysms. Am J Physiol Heart Circ Physiol. 2018. 46. Fleming C, Whitlock EP, Beil TL, Lederle FA. Screening for abdominal aortic aneurysm: a best-evidence systematic review for the U.S. Preventive Services Task Force. Ann Intern Med. 2005;142(3):203-211. 47. Lederle FA, Johnson GR, Wilson SE, et al. Yield of repeated screening for abdominal aortic aneurysm after a 4-year inter-val. Aneurysm Detection and Management Veterans Affairs Cooperative Study Investigators. Arch Intern Med. 2000; 160(8):1117-1121. 48. Patel MS, Brown DA,


Surgery_Schwartz

Surgery_Schwartz. aortic aneurysm after a 4-year inter-val. Aneurysm Detection and Management Veterans Affairs Cooperative Study Investigators. Arch Intern Med. 2000; 160(8):1117-1121. 48. Patel MS, Brown DA, Wilson SE. Relevance of the ADAM and UK Small Aneurysm trial data in the age of endovascular aneurysm repair. Arch Surg. 2009;144(9):806-810. 49. Soares Ferreira R, Gomes Oliveira N, Oliveira-Pinto J, et al. Review on management and outcomes of ruptured abdomi-nal aortic aneurysm in women. J Cardiovasc Surg (Torino). 2018;59(2):195-200. 50. Marques-Rios G, Oliveira-Pinto J, Mansilha A. Predictors of long-term mortality following elective endovascular repair of abdominal aortic aneurysms. Int Angiol. 2018;37(4):277-285. 51. Yang JH, Kim JW, Choi HC, et al. Comparison of clinical outcomes between surgical repair and endovascular stent for the treatment of abdominal aortic aneurysm. Vasc Specialist Int. 2017;33(4):140-145. 52. Williams CR, Brooke BS. Effectiveness of open versus endo-vascular


Surgery_Schwartz

Surgery_Schwartz. surgical repair and endovascular stent for the treatment of abdominal aortic aneurysm. Vasc Specialist Int. 2017;33(4):140-145. 52. Williams CR, Brooke BS. Effectiveness of open versus endo-vascular abdominal aortic aneurysm repair in population set-tings: a systematic review of statewide databases. Surgery. 2017;162(4):707-720. 53. Joo HC, Lee SH, Chang BC, Lee S, Yoo KJ, Youn YN. Late open conversion after endovascular abdominal aortic repair: a 20 year experience. J Cardiovasc Surg (Torino). 2018. 54. Spanos K, Antoniou G, Giannoukas AD, et al. Durability of fenestrated endovascular aortic repair for juxta-renal abdomi-nal aortic aneurysm repair. J Cardiovasc Surg (Torino). 2018; 59(2):213-224. 55. Georgiadis GS, van Herwaarden JA, Saengprakai W, et al. Endovascular treatment of complex abdominal and thoracoabdominal type IV aortic aneurysms with fenestrated technology. J Cardiovasc Surg (Torino). 2017;58(4):574-590. 56. Cochennec F, Kobeiter H, Gohel M, et al. Early results of


Surgery_Schwartz

Surgery_Schwartz. abdominal and thoracoabdominal type IV aortic aneurysms with fenestrated technology. J Cardiovasc Surg (Torino). 2017;58(4):574-590. 56. Cochennec F, Kobeiter H, Gohel M, et al. Early results of physician modified fenestrated stent grafts for the treatment of thoraco-abdominal aortic aneurysms. Eur J Vasc Endovasc Surg. 2015;50(5):583-592. 57. Mendes BC, Greiten LE, Oderich GS. Endovascular repair of a thoracoabdominal aortic aneurysm with a patient-specific fenestrated-branched stent-graft. J Endovasc Ther. 2017;24(5):665-669. 58. Sala-Almonacil VA, Zaragoza-Garcia JM, Ramirez-Montoya M, Molina-Nacher V, Martinez-Perello I, Gomez-Palones FJ. Fenestrated and chimney endovascular aneurysm repair versus open surgery for complex abdominal aortic aneurysms. J Car-diovasc Surg (Torino). 2017;58(6):801-813. 59. Oderich GS, Ribeiro M, Hofer J, et al. Prospective, nonran-domized study to evaluate endovascular repair of pararenal and thoracoabdominal aortic aneurysms using fenestrated-branched


Surgery_Schwartz

Surgery_Schwartz. GS, Ribeiro M, Hofer J, et al. Prospective, nonran-domized study to evaluate endovascular repair of pararenal and thoracoabdominal aortic aneurysms using fenestrated-branched endografts based on supraceliac sealing zones. J Vasc Surg. 2017;65(5):1249-1259 e1210. 60. Schurink GW, Aarts NJ, van Bockel JH. Endoleak after stent-graft treatment of abdominal aortic aneurysm: a meta-analysis of clinical studies. Br J Surg. 1999;86(5):581-587. 61. Kuziez MS, Sanchez LA, Zayed MA. Abdominal aortic aneu-rysm type II endoleaks. J Cardiovasc Dis Diagn. 2016;4(5). pii: 255. 62. Zaiem F, Almasri J, Tello M, Prokop LJ, Chaikof EL, Murad MH. A systematic review of surveillance after endovascular aortic repair. J Vasc Surg. 2018;67(1):320-331 e337. 63. Lin PH, Bush RL, Chaikof EL, et al. A prospective evaluation of hypogastric artery embolization in endovascular aortoiliac aneurysm repair. J Vasc Surg. 2002;36(3):500-506. 64. Elisha S, Nagelhout J, Heiner J, Gabot M. Anesthesia case management for


Surgery_Schwartz

Surgery_Schwartz. evaluation of hypogastric artery embolization in endovascular aortoiliac aneurysm repair. J Vasc Surg. 2002;36(3):500-506. 64. Elisha S, Nagelhout J, Heiner J, Gabot M. Anesthesia case management for endovascular aortic aneurysm repair. AANA J. 2014;82(2):145-152. 65. Nelson PR, Kracjer Z, Kansal N, et al. A multicenter, ran-domized, controlled trial of totally percutaneous access ver-sus open femoral exposure for endovascular aortic aneurysm repair (the PEVAR trial). J Vasc Surg. 2014;59(5):1181-1193. 66. Prinssen M, Verhoeven EL, Buth J, et al. A randomized trial comparing conventional and endovascular repair of abdominal aortic aneurysms. N Engl J Med. 2004;351(16): 1607-1618. 67. Greenhalgh RM, Brown LC, Kwong GP, Powell JT, Thomp-son SG. Comparison of endovascular aneurysm repair with open repair in patients with abdominal aortic aneurysm (EVAR trial 1), 30-day operative mortality results: ran-domised controlled trial. Lancet. 2004;364(9437):843-848. 68. Lederle FA, Freischlag


Surgery_Schwartz

Surgery_Schwartz. open repair in patients with abdominal aortic aneurysm (EVAR trial 1), 30-day operative mortality results: ran-domised controlled trial. Lancet. 2004;364(9437):843-848. 68. Lederle FA, Freischlag JA, Kyriakides TC, et al. Long-term comparison of endovascular and open repair of abdominal aor-tic aneurysm. N Engl J Med. 2012;367(21):1988-1997. 69. Matsumura JS, Brewster DC, Makaroun MS, Naftel DC. A multicenter controlled clinical trial of open versus endovas-cular treatment of abdominal aortic aneurysm. J Vasc Surg. 2003;37(2):262-271. 70. Greenberg RK, Chuter TA, Sternbergh WC 3rd, Fearnot NE. Zenith AAA endovascular graft: intermediate-term results of the US multicenter trial. J Vasc Surg. 2004;39(6):1209-1218. 71. Zarins CK. The US AneuRx Clinical Trial: 6-year clinical update 2002. J Vasc Surg. 2003;37(4):904-908. 72. Criado FJ, Clark NS, McKendrick C, Longway J, Domer GS. Update on the talent LPS AAA stent graft: results with “enhanced talent.” Semin Vasc Surg.


Surgery_Schwartz

Surgery_Schwartz. update 2002. J Vasc Surg. 2003;37(4):904-908. 72. Criado FJ, Clark NS, McKendrick C, Longway J, Domer GS. Update on the talent LPS AAA stent graft: results with “enhanced talent.” Semin Vasc Surg. 2003;16(2): 158-165. 73. Bertges DJ, Zwolak RM, Deaton DH, et al. Current hospital costs and medicare reimbursement for endovascular abdomi-nal aortic aneurysm repair. J Vasc Surg. 2003;37(2):272-279.Brunicardi_Ch23_p0897-p0980.indd 97627/02/19 4:15 PM 977ARTERIAL DISEASECHAPTER 23 74. Seiwert AJ, Wolfe J, Whalen RC, Pigott JP, Kritpracha B, Beebe HG. Cost comparison of aortic aneurysm endograft exclusion versus open surgical repair. Am J Surg. 1999;178(2):117-120. 75. Angle N, Dorafshar AH, Moore WS, et al. Open versus endo-vascular repair of abdominal aortic aneurysms: what does each really cost? Ann Vasc Surg. 2004;18(5):612-618. 76. Lederle FA, Stroupe KT, Kyriakides TC, Ge L, Freischlag JA, Open vs endovascular repair Veterans Affairs cooperative study G. Long-term


Surgery_Schwartz

Surgery_Schwartz. does each really cost? Ann Vasc Surg. 2004;18(5):612-618. 76. Lederle FA, Stroupe KT, Kyriakides TC, Ge L, Freischlag JA, Open vs endovascular repair Veterans Affairs cooperative study G. Long-term cost-effectiveness in the Veterans Affairs open vs endovascular repair study of aortic abdominal aneu-rysm: a randomized clinical trial. JAMA Surg. 2016;151(12): 1139-1144. 77. Abraha I, Luchetta ML, De Florio R, et al. Ultrasonography for endoleak detection after endoluminal abdominal aortic aneu-rysm repair. Cochrane Database Syst Rev. 2017;6:CD010296. 78. Baum RA, Stavropoulos SW, Fairman RM, Carpenter JP. Endoleaks after endovascular repair of abdominal aortic aneu-rysms. J Vasc Interv Radiol. 2003;14(9 pt 1):1111-1117. 79. Dubenec SR, White GH, Pasenau J, Tzilalis V, Choy E, Erdelez L. Endotension. A review of current views on pathophysiol-ogy and treatment. J Cardiovasc Surg (Torino). 2003;44(4): 553-557. 80. Kougias P, Lin PH, Dardik A, Lee WA, El Sayed HF, Zhou W. Successful


Surgery_Schwartz

Surgery_Schwartz. L. Endotension. A review of current views on pathophysiol-ogy and treatment. J Cardiovasc Surg (Torino). 2003;44(4): 553-557. 80. Kougias P, Lin PH, Dardik A, Lee WA, El Sayed HF, Zhou W. Successful treatment of endotension and aneurysm sac enlargement with endovascular stent graft reinforcement. J Vasc Surg. 2007;46(1):124-127. 81. Lin PH, Bush RL, Katzman JB, et al. Delayed aortic aneurysm enlargement due to endotension after endovascular abdominal aortic aneurysm repair. J Vasc Surg. 2003;38(4):840-842. 82. Buth J, Harris PL, Van Marrewijk C, Fransen G. Endoleaks during follow-up after endovascular repair of abdominal aortic aneurysm. Are they all dangerous? J Cardiovasc Surg (Torino). 2003;44(4):559-566. 83. Harris PL, Vallabhaneni SR, Desgranges P, Becquemin JP, van Marrewijk C, Laheij RJ. Incidence and risk factors of late rup-ture, conversion, and death after endovascular repair of infra-renal aortic aneurysms: the EUROSTAR experience. European Collaborators on Stent/graft


Surgery_Schwartz

Surgery_Schwartz. Laheij RJ. Incidence and risk factors of late rup-ture, conversion, and death after endovascular repair of infra-renal aortic aneurysms: the EUROSTAR experience. European Collaborators on Stent/graft techniques for aortic aneurysm repair. J Vasc Surg. 2000;32(4):739-749. 84. Mehta M, Paty PS, Roddy SP, et al. Treatment options for delayed AAA rupture following endovascular repair. J Vasc Surg. 2011;53(1):14-20. 85. May J, White GH, Yu W, et al. Endoluminal repair of abdomi-nal aortic aneurysms: strengths and weaknesses of various prostheses observed in a 4.5-year experience. J Endovasc Surg. 1997;4(2):147-151. 86. Teufelsbauer H, Prusa AM, Prager M, et al. Endovascular treatment of a multimorbid patient with late AAA rupture after stent-graft placement: 1-year follow-up. J Endovasc Ther. 2002;9(6):896-900. 87. Yasuhara H. Acute mesenteric ischemia: the challenge of gas-troenterology. Surg Today. 2005;35(3):185-195. 88. Zelenock GB, Graham LM, Whitehouse WM Jr, et al. Splanch-nic


Surgery_Schwartz

Surgery_Schwartz. 2002;9(6):896-900. 87. Yasuhara H. Acute mesenteric ischemia: the challenge of gas-troenterology. Surg Today. 2005;35(3):185-195. 88. Zelenock GB, Graham LM, Whitehouse WM Jr, et al. Splanch-nic arteriosclerotic disease and intestinal angina. Arch Surg. 1980;115(4):497-501. 89. Karwowski J, Arko F. Surgical management of mesenteric ischemia. Tech Vasc Interv Radiol. 2004;7(3):151-154. 90. Mitchell EL, Moneta GL. Mesenteric duplex scanning. Per-spect Vasc Surg Endovasc Ther. 2006;18(2):175-183. 91. Moneta GL, Lee RW, Yeager RA, Taylor LM Jr, Porter JM. Mesenteric duplex scanning: a blinded prospective study. J Vasc Surg. 1993;17(1):79-84; discussion 85-76. 92. Kougias P, El Sayed HF, Zhou W, Lin PH. Management of chronic mesenteric ischemia. The role of endovascular ther-apy. J Endovasc Ther. 2007;14(3):395-405. 93. Kougias P, Lau D, El Sayed HF, Zhou W, Huynh TT, Lin PH. Determinants of mortality and treatment outcome following surgical interventions for acute mesenteric ischemia. J


Surgery_Schwartz

Surgery_Schwartz. 2007;14(3):395-405. 93. Kougias P, Lau D, El Sayed HF, Zhou W, Huynh TT, Lin PH. Determinants of mortality and treatment outcome following surgical interventions for acute mesenteric ischemia. J Vasc Surg. 2007;46(3):467-474. 94. Jimenez JC, Harlander-Locke M, Dutson EP. Open and laparo-scopic treatment of median arcuate ligament syndrome. J Vasc Surg. 2012;56(3):869-873. 95. Park WM, Cherry KJ Jr, Chua HK, et al. Current results of open revascularization for chronic mesenteric ischemia: a standard for comparison. J Vasc Surg. 2002;35(5):853-859. 96. Silva JA, White CJ, Collins TJ, et al. Endovascular therapy for chronic mesenteric ischemia. J Am Coll Cardiol. 2006;47(5): 944-950. 97. Furrer J, Gruntzig A, Kugelmeier J, Goebel N. Treatment of abdominal angina with percutaneous dilatation of an arteria mesenterica superior stenosis. Preliminary communication. Cardiovasc Intervent Radiol. 1980;3(1):43-44. 98. AbuRahma AF, Stone PA, Bates MC, Welch CA. Angioplasty/stenting of the


Surgery_Schwartz

Surgery_Schwartz. of an arteria mesenterica superior stenosis. Preliminary communication. Cardiovasc Intervent Radiol. 1980;3(1):43-44. 98. AbuRahma AF, Stone PA, Bates MC, Welch CA. Angioplasty/stenting of the superior mesenteric artery and celiac trunk: early and late outcomes. J Endovasc Ther. 2003;10(6):1046-1053. 99. Kasirajan K, O’Hara PJ, Gray BH, et al. Chronic mesenteric ischemia: open surgery versus percutaneous angioplasty and stenting. J Vasc Surg. 2001;33(1):63-71. 100. Atkins MD, Kwolek CJ, LaMuraglia GM, Brewster DC, Chung TK, Cambria RP. Surgical revascularization versus endovascular therapy for chronic mesenteric ischemia: a com-parative experience. J Vasc Surg. 2007;45(6):1162-1171. 101. Oderich GS, Erdoes LS, Lesar C, et al. Comparison of covered stents versus bare metal stents for treatment of chronic athero-sclerotic mesenteric arterial disease. J Vasc Surg. 2013;58(5): 1316-1323. 102. Textor SC. Atherosclerotic renal artery stenosis: overtreated but underrated? J Am Soc Nephrol.


Surgery_Schwartz

Surgery_Schwartz. of chronic athero-sclerotic mesenteric arterial disease. J Vasc Surg. 2013;58(5): 1316-1323. 102. Textor SC. Atherosclerotic renal artery stenosis: overtreated but underrated? J Am Soc Nephrol. 2008;19(4):656-659. 103. Tafur JD, White CJ. Renal artery stenosis: when to revascular-ize in 2017. Curr Probl Cardiol. 2017;42(4):110-135. 104. Cherr GS, Hansen KJ, Craven TE, et al. Surgical manage-ment of atherosclerotic renovascular disease. J Vasc Surg. 2002;35(2):236-245. 105. Hansen KJ, Cherr GS, Craven TE, et al. Management of ischemic nephropathy: dialysis-free survival after surgical repair. J Vasc Surg. 2000;32(3):472-481; discussion 481-482. 106. Guzman RP, Zierler RE, Isaacson JA, Bergelin RO, Strand-ness DE Jr. Renal atrophy and arterial stenosis. A prospec-tive study with duplex ultrasound. Hypertension. 1994;23(3): 346-350. 107. van de Ven PJ, Kaatee R, Beutler JJ, et al. Arterial stenting and balloon angioplasty in ostial atherosclerotic renovas-cular disease: a randomised


Surgery_Schwartz

Surgery_Schwartz. ultrasound. Hypertension. 1994;23(3): 346-350. 107. van de Ven PJ, Kaatee R, Beutler JJ, et al. Arterial stenting and balloon angioplasty in ostial atherosclerotic renovas-cular disease: a randomised trial. Lancet. 1999;353(9149): 282-286. 108. Surowiec SM, Sivamurthy N, Rhodes JM, et al. Percutane-ous therapy for renal artery fibromuscular dysplasia. Ann Vasc Surg. 2003;17(6):650-655. 109. van Jaarsveld BC, Krijnen P. Prospective studies of diagno-sis and intervention: the Dutch experience. Semin Nephrol. 2000;20(5):463-473. 110. White CJ, Ramee SR, Collins TJ, Jenkins JS, Escobar A, Shaw D. Renal artery stent placement: utility in lesions dif-ficult to treat with balloon angioplasty. J Am Coll Cardiol. 1997;30(6):1445-1450. 111. Blum U, Krumme B, Flugel P, et al. Treatment of ostial renal-artery stenoses with vascular endoprostheses after unsuccess-ful balloon angioplasty. N Engl J Med. 1997;336(7):459-465. 112. Watson PS, Hadjipetrou P, Cox SV, Piemonte TC, Eisenhauer AC. Effect of


Surgery_Schwartz

Surgery_Schwartz. stenoses with vascular endoprostheses after unsuccess-ful balloon angioplasty. N Engl J Med. 1997;336(7):459-465. 112. Watson PS, Hadjipetrou P, Cox SV, Piemonte TC, Eisenhauer AC. Effect of renal artery stenting on renal function and size in patients with atherosclerotic renovascular disease. Circulation. 2000;102(14):1671-1677. 113. Harden PN, MacLeod MJ, Rodger RS, et al. Effect of renal-artery stenting on progression of renovascular renal failure. Lancet. 1997;349(9059):1133-1136.Brunicardi_Ch23_p0897-p0980.indd 97727/02/19 4:15 PM 978SPECIFIC CONSIDERATIONSPART II 114. Leertouwer TC, Gussenhoven EJ, Bosch JL, et al. Stent place-ment for renal arterial stenosis: where do we stand? A meta-analysis. Radiology. 2000;216(1):78-85. 115. Lyden SP, Smouse HB. TASC II and the endovascular man-agement of infrainguinal disease. J Endovasc Ther. 2009; 16(2 suppl 2):II5-II18. 116. Martin D, Katz SG. Axillofemoral bypass for aortoiliac occlu-sive disease. Am J Surg.


Surgery_Schwartz

Surgery_Schwartz. II and the endovascular man-agement of infrainguinal disease. J Endovasc Ther. 2009; 16(2 suppl 2):II5-II18. 116. Martin D, Katz SG. Axillofemoral bypass for aortoiliac occlu-sive disease. Am J Surg. 2000;180(2):100-103. 117. Criado E, Burnham SJ, Tinsley EA Jr, Johnson G Jr, Keagy BA. Femorofemoral bypass graft: analysis of patency and fac-tors influencing long-term outcome. J Vasc Surg. 1993;18(3): 495-504; discussion 504-495. 118. Patel A, Taylor SM, Langan EM 3rd, et al. Obturator bypass: a classic approach for the treatment of contemporary groin infection. Am Surg. 2002;68(8):653-658; discussion 658-659. 119. Sautner T, Niederle B, Herbst F, et al. The value of obturator canal bypass. A review. Arch Surg. 1994;129(7):718-722. 120. Brewster DC, Cambria RP, Darling RC, et al. Long-term results of combined iliac balloon angioplasty and distal surgi-cal revascularization. Ann Surg. 1989;210(3):324-330; discus-sion 331. 121. van den Akker PJ, van Schilfgaarde R, Brand R, van Bockel


Surgery_Schwartz

Surgery_Schwartz. results of combined iliac balloon angioplasty and distal surgi-cal revascularization. Ann Surg. 1989;210(3):324-330; discus-sion 331. 121. van den Akker PJ, van Schilfgaarde R, Brand R, van Bockel JH, Terpstra JL. Long term success of aortoiliac operation for arteriosclerotic obstructive disease. Surg Gynecol Obstet. 1992;174(6):485-496. 122. Insall RL, Loose HW, Chamberlain J. Long-term results of double-balloon percutaneous transluminal angioplasty of the aorta and iliac arteries. Eur J Vasc Surg. 1993;7(1):31-36. 123. Mendelsohn FO, Santos RM, Crowley JJ, et al. Kissing stents in the aortic bifurcation. Am Heart J. 1998;136(4 pt 1): 600-605. 124. Haulon S, Mounier-Vehier C, Gaxotte V, et al. Percutaneous reconstruction of the aortoiliac bifurcation with the “kiss-ing stents” technique: long-term follow-up in 106 patients. J Endovasc Ther. 2002;9(3):363-368. 125. Sapoval MR, Long AL, Pagny JY, et al. Outcome of per-cutaneous intervention in iliac artery stents. Radiology.


Surgery_Schwartz

Surgery_Schwartz. long-term follow-up in 106 patients. J Endovasc Ther. 2002;9(3):363-368. 125. Sapoval MR, Long AL, Pagny JY, et al. Outcome of per-cutaneous intervention in iliac artery stents. Radiology. 1996;198(2):481-486. 126. Mousa AY, Beauford RB, Flores L, Faries PL, Patel P, Fogler R. Endovascular treatment of iliac occlusive disease: review and update. Vascular. 2007;15(1):5-11. 127. Psacharopulo D, Ferrero E, Ferri M, et al. Increasing efficacy of endovascular recanalization with covered stent graft for TransAtlantic Inter-Society Consensus II D aortoiliac complex occlusion. J Vasc Surg. 2015;62(5):1219-1226. 128. Bosiers M, Iyer V, Deloose K, Verbist J, Peeters P. Flemish experience using the Advanta V12 stent-graft for the treatment of iliac artery occlusive disease. J Cardiovasc Surg (Torino). 2007;48(1):7-12. 129. Szilagyi DE, Elliott JP Jr, Smith RF, Reddy DJ, McPharlin M. A thirty-year survey of the reconstructive surgical treatment of aortoiliac occlusive disease. J Vasc Surg.


Surgery_Schwartz

Surgery_Schwartz. 2007;48(1):7-12. 129. Szilagyi DE, Elliott JP Jr, Smith RF, Reddy DJ, McPharlin M. A thirty-year survey of the reconstructive surgical treatment of aortoiliac occlusive disease. J Vasc Surg. 1986;3(3):421-436. 130. Indes JE, Pfaff MJ, Farrokhyar F, et al. Clinical outcomes of 5358 patients undergoing direct open bypass or endovascular treatment for aortoiliac occlusive disease: a systematic review and meta-analysis. J Endovasc Ther. 2013;20(4):443-455. 131. Becker GJ, Cikrit DF, Lalka SG, et al. Early experience with the Palmaz stent in human iliac angioplasty. Indiana Med. 1989;82(4):286-292. 132. Tsetis D, Uberoi R. Quality improvement guidelines for endo-vascular treatment of iliac artery occlusive disease. Cardiovasc Intervent Radiol. 2008;31(2):238-245. 133. Powell RJ, Fillinger M, Bettmann M, et al. The durability of endovascular treatment of multisegment iliac occlusive dis-ease. J Vasc Surg. 2000;31(6):1178-1184. 134. Timaran CH, Stevens SL, Grandas OH, Freeman MB, Gold-man