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Surgery_Schwartz_6502 | 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. 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_6503 | 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. 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_6504 | 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. 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_6505 | 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. 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_6506 | 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. 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_6507 | 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. 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_6508 | 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. 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_6509 | 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. 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_6510 | 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. 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_6511 | 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. 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_6512 | 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. 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_6513 | 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. 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_6514 | 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. 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_6515 | 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. 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_6516 | 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. 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_6517 | 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. 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_6518 | 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. 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_6519 | 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. 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_6520 | 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. 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_6521 | 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. 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_6522 | 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. 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_6523 | 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. 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_6524 | 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. 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_6525 | 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. 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_6526 | 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. 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_6527 | 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. 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_6528 | 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. 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_6529 | 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. 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_6530 | 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. 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_6531 | 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. 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_6532 | 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. 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_6533 | 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. 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_6534 | 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. 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_6535 | 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. 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_6536 | 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. 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_6537 | 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. 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_6538 | 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. 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_6539 | 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. 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_6540 | 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. 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_6541 | 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. 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_6542 | 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. 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_6543 | 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. 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_6544 | 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. 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_6545 | 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. 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_6546 | 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. 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_6547 | 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. 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_6548 | 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. 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_6549 | 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. 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_6550 | 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. 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 |
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Surgery_Schwartz_6563 | 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. 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_6564 | 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. 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_6565 | 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. 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 |
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Surgery_Schwartz_6583 | Surgery_Schwartz | EC, Ohki T, Veith FJ, et al. Does subintimal angio-plasty have a role in the treatment of severe lower extremity ischemia? J Vasc Surg. 2003;37(2):386-391. 156. Treiman GS, Whiting JH, Treiman RL, McNamara RM, Ashrafi A. Treatment of limb-threatening ischemia with percu-taneous intentional extraluminal recanalization: a preliminary evaluation. J Vasc Surg. 2003;38(1):29-35. 157. Ingle H, Nasim A, Bolia A, et al. Subintimal angioplasty of isolated infragenicular vessels in lower limb ischemia: long-term results. J Endovasc Ther. 2002;9(4):411-416. 158. Becquemin JP, Favre JP, Marzelle J, Nemoz C, Corsin C, Leizorovicz A. Systematic versus selective stent placement after superficial femoral artery balloon angioplasty: a mul-ticenter prospective randomized study. J Vasc Surg. 2003; 37(3):487-494. 159. Gray BH, Sullivan TM, Childs MB, Young JR, Olin JW. High incidence of restenosis/reocclusion of stents in the percutaneous treatment of long-segment superficial femo-ral artery disease | Surgery_Schwartz. EC, Ohki T, Veith FJ, et al. Does subintimal angio-plasty have a role in the treatment of severe lower extremity ischemia? J Vasc Surg. 2003;37(2):386-391. 156. Treiman GS, Whiting JH, Treiman RL, McNamara RM, Ashrafi A. Treatment of limb-threatening ischemia with percu-taneous intentional extraluminal recanalization: a preliminary evaluation. J Vasc Surg. 2003;38(1):29-35. 157. Ingle H, Nasim A, Bolia A, et al. Subintimal angioplasty of isolated infragenicular vessels in lower limb ischemia: long-term results. J Endovasc Ther. 2002;9(4):411-416. 158. Becquemin JP, Favre JP, Marzelle J, Nemoz C, Corsin C, Leizorovicz A. Systematic versus selective stent placement after superficial femoral artery balloon angioplasty: a mul-ticenter prospective randomized study. J Vasc Surg. 2003; 37(3):487-494. 159. Gray BH, Sullivan TM, Childs MB, Young JR, Olin JW. High incidence of restenosis/reocclusion of stents in the percutaneous treatment of long-segment superficial femo-ral artery disease |
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Surgery_Schwartz_6586 | Surgery_Schwartz | 16. 167. McQuade K, Gable D, Pearl G, Theune B, Black S. Four-year randomized prospective comparison of percutaneous ePTFE/nitinol self-expanding stent graft versus prosthetic femoral-popliteal bypass in the treatment of superficial femoral artery occlusive disease. J Vasc Surg. 2010;52(3):584-590; discus-sion 590-581, 591 e581-591 e587. 168. Ramaiah V, Gammon R, Kiesz S, et al. Midterm outcomes from the TALON Registry: treating peripherals with SilverHawk: outcomes collection. J Endovasc Ther. 2006;13(5):592-602. 169. Franzone A, Ferrone M, Carotenuto G, et al. The role of ather-ectomy in the treatment of lower extremity peripheral artery disease. BMC Surg. 2012;12(suppl 1):S13. 170. Scheinert D, Laird JR Jr, Schroder M, Steinkamp H, Balzer JO, Biamino G. Excimer laser-assisted recanalization of long, chronic superficial femoral artery occlusions. J Endovasc Ther. 2001;8(2):156-166. 171. Steinkamp HJ, Rademaker J, Wissgott C, et al. Percutane-ous transluminal laser angioplasty versus | Surgery_Schwartz. 16. 167. McQuade K, Gable D, Pearl G, Theune B, Black S. Four-year randomized prospective comparison of percutaneous ePTFE/nitinol self-expanding stent graft versus prosthetic femoral-popliteal bypass in the treatment of superficial femoral artery occlusive disease. J Vasc Surg. 2010;52(3):584-590; discus-sion 590-581, 591 e581-591 e587. 168. Ramaiah V, Gammon R, Kiesz S, et al. Midterm outcomes from the TALON Registry: treating peripherals with SilverHawk: outcomes collection. J Endovasc Ther. 2006;13(5):592-602. 169. Franzone A, Ferrone M, Carotenuto G, et al. The role of ather-ectomy in the treatment of lower extremity peripheral artery disease. BMC Surg. 2012;12(suppl 1):S13. 170. Scheinert D, Laird JR Jr, Schroder M, Steinkamp H, Balzer JO, Biamino G. Excimer laser-assisted recanalization of long, chronic superficial femoral artery occlusions. J Endovasc Ther. 2001;8(2):156-166. 171. Steinkamp HJ, Rademaker J, Wissgott C, et al. Percutane-ous transluminal laser angioplasty versus |
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Surgery_Schwartz_6590 | Surgery_Schwartz | fistula as an adjunct to femoro-infrap-opliteal PTFE bypass. Eur J Vasc Endovasc Surg. 1999;17(3): 197-201. 184. Davies AH, Hawdon AJ, Sydes MR, Thompson SG. Is duplex surveillance of value after leg vein bypass grafting? Princi-pal results of the Vein Graft Surveillance Randomised Trial (VGST). Circulation. 2005;112(13):1985-1991. 185. Baldwin ZK, Pearce BJ, Curi MA, et al. Limb salvage after infrainguinal bypass graft failure. J Vasc Surg. 2004;39(5): 951-957. 186. Stone PA, Flaherty SK, Aburahma AF, et al. Factors affect-ing perioperative mortality and wound-related complications following major lower extremity amputations. Ann Vasc Surg. 2006;20(2):209-216. 187. Holzenbein TJ, Pomposelli FB Jr, Miller A, et al. The upper arm basilic-cephalic loop for distal bypass grafting: techni-cal considerations and follow-up. J Vasc Surg. 1995;21(4): 586-592; discussion 592-594. 188. Dardik H, Wengerter K, Qin F, et al. Comparative decades of experience with glutaraldehyde-tanned human | Surgery_Schwartz. fistula as an adjunct to femoro-infrap-opliteal PTFE bypass. Eur J Vasc Endovasc Surg. 1999;17(3): 197-201. 184. Davies AH, Hawdon AJ, Sydes MR, Thompson SG. Is duplex surveillance of value after leg vein bypass grafting? Princi-pal results of the Vein Graft Surveillance Randomised Trial (VGST). Circulation. 2005;112(13):1985-1991. 185. Baldwin ZK, Pearce BJ, Curi MA, et al. Limb salvage after infrainguinal bypass graft failure. J Vasc Surg. 2004;39(5): 951-957. 186. Stone PA, Flaherty SK, Aburahma AF, et al. Factors affect-ing perioperative mortality and wound-related complications following major lower extremity amputations. Ann Vasc Surg. 2006;20(2):209-216. 187. Holzenbein TJ, Pomposelli FB Jr, Miller A, et al. The upper arm basilic-cephalic loop for distal bypass grafting: techni-cal considerations and follow-up. J Vasc Surg. 1995;21(4): 586-592; discussion 592-594. 188. Dardik H, Wengerter K, Qin F, et al. Comparative decades of experience with glutaraldehyde-tanned human |
Surgery_Schwartz_6591 | Surgery_Schwartz | considerations and follow-up. J Vasc Surg. 1995;21(4): 586-592; discussion 592-594. 188. Dardik H, Wengerter K, Qin F, et al. Comparative decades of experience with glutaraldehyde-tanned human umbilical cord vein graft for lower limb revascularization: an analysis of 1275 cases. J Vasc Surg. 2002;35(1):64-71. 189. Johnson WC, Lee KK. A comparative evaluation of polytet-rafluoroethylene, umbilical vein, and saphenous vein bypass grafts for femoral-popliteal above-knee revascularization: a prospective randomized Department of Veterans Affairs coop-erative study. J Vasc Surg. 2000;32(2):268-277. 190. Fahner PJ, Idu MM, van Gulik TM, Legemate DA. Sys-tematic review of preservation methods and clinical Brunicardi_Ch23_p0897-p0980.indd 97927/02/19 4:15 PM 980SPECIFIC CONSIDERATIONSPART IIoutcome of infrainguinal vascular allografts. J Vasc Surg. 2006;44(3):518-524. 191. Gupta SK, Veith FJ, Kram HB, Wengerter KR. Prospective, randomized comparison of ringed and nonringed | Surgery_Schwartz. considerations and follow-up. J Vasc Surg. 1995;21(4): 586-592; discussion 592-594. 188. Dardik H, Wengerter K, Qin F, et al. Comparative decades of experience with glutaraldehyde-tanned human umbilical cord vein graft for lower limb revascularization: an analysis of 1275 cases. J Vasc Surg. 2002;35(1):64-71. 189. Johnson WC, Lee KK. A comparative evaluation of polytet-rafluoroethylene, umbilical vein, and saphenous vein bypass grafts for femoral-popliteal above-knee revascularization: a prospective randomized Department of Veterans Affairs coop-erative study. J Vasc Surg. 2000;32(2):268-277. 190. Fahner PJ, Idu MM, van Gulik TM, Legemate DA. Sys-tematic review of preservation methods and clinical Brunicardi_Ch23_p0897-p0980.indd 97927/02/19 4:15 PM 980SPECIFIC CONSIDERATIONSPART IIoutcome of infrainguinal vascular allografts. J Vasc Surg. 2006;44(3):518-524. 191. Gupta SK, Veith FJ, Kram HB, Wengerter KR. Prospective, randomized comparison of ringed and nonringed |
Surgery_Schwartz_6592 | Surgery_Schwartz | of infrainguinal vascular allografts. J Vasc Surg. 2006;44(3):518-524. 191. Gupta SK, Veith FJ, Kram HB, Wengerter KR. Prospective, randomized comparison of ringed and nonringed polytetra-fluoroethylene femoropopliteal bypass grafts: a preliminary report. J Vasc Surg. 1991;13(1):163-172. 192. Stonebridge PA, Prescott RJ, Ruckley CV. Randomized trial comparing infrainguinal polytetrafluoroethylene bypass graft-ing with and without vein interposition cuff at the distal anas-tomosis. The Joint Vascular Research Group. J Vasc Surg. 1997;26(4):543-550. 193. Klinkert P, van Dijk PJ, Breslau PJ. Polytetrafluoroethylene femorotibial bypass grafting: 5-year patency and limb salvage. Ann Vasc Surg. 2003;17(5):486-491. 194. Panneton JM, Hollier LH, Hofer JM. Multicenter randomized prospective trial comparing a pre-cuffed polytetrafluoroethyl-ene graft to a vein cuffed polytetrafluoroethylene graft for infra-genicular arterial bypass. Ann Vasc Surg. 2004;18(2):199-206. 195. Bellosta R, Luzzani L, | Surgery_Schwartz. of infrainguinal vascular allografts. J Vasc Surg. 2006;44(3):518-524. 191. Gupta SK, Veith FJ, Kram HB, Wengerter KR. Prospective, randomized comparison of ringed and nonringed polytetra-fluoroethylene femoropopliteal bypass grafts: a preliminary report. J Vasc Surg. 1991;13(1):163-172. 192. Stonebridge PA, Prescott RJ, Ruckley CV. Randomized trial comparing infrainguinal polytetrafluoroethylene bypass graft-ing with and without vein interposition cuff at the distal anas-tomosis. The Joint Vascular Research Group. J Vasc Surg. 1997;26(4):543-550. 193. Klinkert P, van Dijk PJ, Breslau PJ. Polytetrafluoroethylene femorotibial bypass grafting: 5-year patency and limb salvage. Ann Vasc Surg. 2003;17(5):486-491. 194. Panneton JM, Hollier LH, Hofer JM. Multicenter randomized prospective trial comparing a pre-cuffed polytetrafluoroethyl-ene graft to a vein cuffed polytetrafluoroethylene graft for infra-genicular arterial bypass. Ann Vasc Surg. 2004;18(2):199-206. 195. Bellosta R, Luzzani L, |
Surgery_Schwartz_6593 | Surgery_Schwartz | a pre-cuffed polytetrafluoroethyl-ene graft to a vein cuffed polytetrafluoroethylene graft for infra-genicular arterial bypass. Ann Vasc Surg. 2004;18(2):199-206. 195. Bellosta R, Luzzani L, Carugati C, Melloni C, Sarcina A. Which distal anastomosis should be used in PTFE femoro-tibial bypass? J Cardiovasc Surg (Torino). 2005;46(5):499-503. 196. Begovac PC, Thomson RC, Fisher JL, Hughson A, Gallhagen A. Improvements in GORE-TEX vascular graft performance by Carmeda BioActive surface heparin immobilization. Eur J Vasc Endovasc Surg. 2003;25(5):432-437. 197. Devine C, Hons B, McCollum C. Heparin-bonded Dacron or polytetrafluoroethylene for femoropopliteal bypass grafting: a multicenter trial. J Vasc Surg. 2001;33(3):533-539. 198. Walluscheck KP, Bierkandt S, Brandt M, Cremer J. Infrain-guinal ePTFE vascular graft with bioactive surface heparin bonding. First clinical results. J Cardiovasc Surg (Torino). 2005;46(4):425-430. 199. Hunink MG, Donaldson MC, Meyerovitz MF, et al. Risks and | Surgery_Schwartz. a pre-cuffed polytetrafluoroethyl-ene graft to a vein cuffed polytetrafluoroethylene graft for infra-genicular arterial bypass. Ann Vasc Surg. 2004;18(2):199-206. 195. Bellosta R, Luzzani L, Carugati C, Melloni C, Sarcina A. Which distal anastomosis should be used in PTFE femoro-tibial bypass? J Cardiovasc Surg (Torino). 2005;46(5):499-503. 196. Begovac PC, Thomson RC, Fisher JL, Hughson A, Gallhagen A. Improvements in GORE-TEX vascular graft performance by Carmeda BioActive surface heparin immobilization. Eur J Vasc Endovasc Surg. 2003;25(5):432-437. 197. Devine C, Hons B, McCollum C. Heparin-bonded Dacron or polytetrafluoroethylene for femoropopliteal bypass grafting: a multicenter trial. J Vasc Surg. 2001;33(3):533-539. 198. Walluscheck KP, Bierkandt S, Brandt M, Cremer J. Infrain-guinal ePTFE vascular graft with bioactive surface heparin bonding. First clinical results. J Cardiovasc Surg (Torino). 2005;46(4):425-430. 199. Hunink MG, Donaldson MC, Meyerovitz MF, et al. Risks and |
Surgery_Schwartz_6594 | Surgery_Schwartz | ePTFE vascular graft with bioactive surface heparin bonding. First clinical results. J Cardiovasc Surg (Torino). 2005;46(4):425-430. 199. Hunink MG, Donaldson MC, Meyerovitz MF, et al. Risks and benefits of femoropopliteal percutaneous balloon angioplasty. J Vasc Surg. 1993;17(1):183-192; discussion 192-194. 200. Dua A, Koprowski S, Upchurch G, Lee CJ, Desai SS. Pro-gressive shortfall in open aneurysm experience for vascular surgery trainees with the impact of fenestrated and branched endovascular technology. J Vasc Surg. 2017;65(1):257-261. 201. Ferreira M, Lanziotti L, Monteiro M, et al. Superficial femo-ral artery recanalization with self-expanding nitinol stents: long-term follow-up results. Eur J Vasc Endovasc Surg. 2007; 34(6):702-708. 202. Schillinger M, Sabeti S, Dick P, et al. Sustained benefit at 2 years of primary femoropopliteal stenting compared with balloon angioplasty with optional stenting. Circulation. 2007;115(21):2745-2749. 203. Bosiers M, Deloose K, Verbist J, | Surgery_Schwartz. ePTFE vascular graft with bioactive surface heparin bonding. First clinical results. J Cardiovasc Surg (Torino). 2005;46(4):425-430. 199. Hunink MG, Donaldson MC, Meyerovitz MF, et al. Risks and benefits of femoropopliteal percutaneous balloon angioplasty. J Vasc Surg. 1993;17(1):183-192; discussion 192-194. 200. Dua A, Koprowski S, Upchurch G, Lee CJ, Desai SS. Pro-gressive shortfall in open aneurysm experience for vascular surgery trainees with the impact of fenestrated and branched endovascular technology. J Vasc Surg. 2017;65(1):257-261. 201. Ferreira M, Lanziotti L, Monteiro M, et al. Superficial femo-ral artery recanalization with self-expanding nitinol stents: long-term follow-up results. Eur J Vasc Endovasc Surg. 2007; 34(6):702-708. 202. Schillinger M, Sabeti S, Dick P, et al. Sustained benefit at 2 years of primary femoropopliteal stenting compared with balloon angioplasty with optional stenting. Circulation. 2007;115(21):2745-2749. 203. Bosiers M, Deloose K, Verbist J, |
Surgery_Schwartz_6595 | Surgery_Schwartz | Sustained benefit at 2 years of primary femoropopliteal stenting compared with balloon angioplasty with optional stenting. Circulation. 2007;115(21):2745-2749. 203. Bosiers M, Deloose K, Verbist J, Peeters P. Nitinol stenting for treatment of “below-the-knee” critical limb ischemia: 1-year angiographic outcome after Xpert stent implantation. J Car-diovasc Surg (Torino). 2007;48(4):455-461. 204. Kickuth R, Keo HH, Triller J, Ludwig K, Do DD. Initial clinical experience with the 4-F self-expanding XPERT stent system for infrapopliteal treatment of patients with severe claudication and critical limb ischemia. J Vasc Interv Radiol. 2007;18(6):703-708. 205. Wolf GL, Wilson SE, Cross AP, Deupree RH, Stason WB. Sur-gery or balloon angioplasty for peripheral vascular disease: a randomized clinical trial. Principal investigators and their Associates of Veterans Administration Cooperative Study Number 199. J Vasc Interv Radiol. 1993;4(5):639-648. 206. Adam DJ, Beard JD, Cleveland T, et al. | Surgery_Schwartz. Sustained benefit at 2 years of primary femoropopliteal stenting compared with balloon angioplasty with optional stenting. Circulation. 2007;115(21):2745-2749. 203. Bosiers M, Deloose K, Verbist J, Peeters P. Nitinol stenting for treatment of “below-the-knee” critical limb ischemia: 1-year angiographic outcome after Xpert stent implantation. J Car-diovasc Surg (Torino). 2007;48(4):455-461. 204. Kickuth R, Keo HH, Triller J, Ludwig K, Do DD. Initial clinical experience with the 4-F self-expanding XPERT stent system for infrapopliteal treatment of patients with severe claudication and critical limb ischemia. J Vasc Interv Radiol. 2007;18(6):703-708. 205. Wolf GL, Wilson SE, Cross AP, Deupree RH, Stason WB. Sur-gery or balloon angioplasty for peripheral vascular disease: a randomized clinical trial. Principal investigators and their Associates of Veterans Administration Cooperative Study Number 199. J Vasc Interv Radiol. 1993;4(5):639-648. 206. Adam DJ, Beard JD, Cleveland T, et al. |
Surgery_Schwartz_6596 | Surgery_Schwartz | trial. Principal investigators and their Associates of Veterans Administration Cooperative Study Number 199. J Vasc Interv Radiol. 1993;4(5):639-648. 206. Adam DJ, Beard JD, Cleveland T, et al. Bypass versus angio-plasty in severe ischaemia of the leg (BASIL): multicentre, ran-domised controlled trial. Lancet. 2005;366(9501):1925-1934. 207. Nolan B, Finlayson S, Tosteson A, Powell R, Cronenwett J. The treatment of disabling intermittent claudication in patients with superficial femoral artery occlusive disease--decision analysis. J Vasc Surg. 2007;45(6):1179-1184. 208. Maffei S, Di Renzo M, Bova G, Auteri A, Pasqui AL. Takayasu’s arteritis: a review of the literature. Intern Emerg Med. 2006;1(2):105-112. 209. Baxter BT. Heritable diseases of the blood vessels. Cardiovasc Pathol. 2005;14(4):185-188. 210. Cikrit DF, Glover JR, Dalsing MC, Silver D. The Ehlers-Danlos specter revisited. Vasc Endovascular Surg. 2002; 36(3):213-217. 211. Ho NC, Tran JR, Bektas A. Marfan’s syndrome. Lancet. | Surgery_Schwartz. trial. Principal investigators and their Associates of Veterans Administration Cooperative Study Number 199. J Vasc Interv Radiol. 1993;4(5):639-648. 206. Adam DJ, Beard JD, Cleveland T, et al. Bypass versus angio-plasty in severe ischaemia of the leg (BASIL): multicentre, ran-domised controlled trial. Lancet. 2005;366(9501):1925-1934. 207. Nolan B, Finlayson S, Tosteson A, Powell R, Cronenwett J. The treatment of disabling intermittent claudication in patients with superficial femoral artery occlusive disease--decision analysis. J Vasc Surg. 2007;45(6):1179-1184. 208. Maffei S, Di Renzo M, Bova G, Auteri A, Pasqui AL. Takayasu’s arteritis: a review of the literature. Intern Emerg Med. 2006;1(2):105-112. 209. Baxter BT. Heritable diseases of the blood vessels. Cardiovasc Pathol. 2005;14(4):185-188. 210. Cikrit DF, Glover JR, Dalsing MC, Silver D. The Ehlers-Danlos specter revisited. Vasc Endovascular Surg. 2002; 36(3):213-217. 211. Ho NC, Tran JR, Bektas A. Marfan’s syndrome. Lancet. |
Surgery_Schwartz_6597 | Surgery_Schwartz | DF, Glover JR, Dalsing MC, Silver D. The Ehlers-Danlos specter revisited. Vasc Endovascular Surg. 2002; 36(3):213-217. 211. Ho NC, Tran JR, Bektas A. Marfan’s syndrome. Lancet. 2005;366(9501):1978-1981. 212. Davies JE, Sundt TM. Surgery insight: the dilated ascending aorta—indications for surgical intervention. Nat Clin Pract Cardiovasc Med. 2007;4(6):330-339. 213. London NJ, Srinivasan R, Naylor AR, et al. Subintimal angio-plasty of femoropopliteal artery occlusions: the long-term results. Eur J Vasc Surg. 1994;8(2):148-155. 214. Chassaing N, Martin L, Calvas P, Le Bert M, Hovnanian A. Pseudoxanthoma elasticum: a clinical, pathophysiological and genetic update including 11 novel ABCC6 mutations. J Med Genet. 2005;42(12):881-892. 215. Yeung RS. Pathogenesis and treatment of Kawasaki’s disease. Curr Opin Rheumatol. 2005;17(5):617-623. 216. Greco A, De Virgilio A, Ralli M, et al. Behcet’s disease: new insights into pathophysiology, clinical features and treatment options. Autoimmun Rev. | Surgery_Schwartz. DF, Glover JR, Dalsing MC, Silver D. The Ehlers-Danlos specter revisited. Vasc Endovascular Surg. 2002; 36(3):213-217. 211. Ho NC, Tran JR, Bektas A. Marfan’s syndrome. Lancet. 2005;366(9501):1978-1981. 212. Davies JE, Sundt TM. Surgery insight: the dilated ascending aorta—indications for surgical intervention. Nat Clin Pract Cardiovasc Med. 2007;4(6):330-339. 213. London NJ, Srinivasan R, Naylor AR, et al. Subintimal angio-plasty of femoropopliteal artery occlusions: the long-term results. Eur J Vasc Surg. 1994;8(2):148-155. 214. Chassaing N, Martin L, Calvas P, Le Bert M, Hovnanian A. Pseudoxanthoma elasticum: a clinical, pathophysiological and genetic update including 11 novel ABCC6 mutations. J Med Genet. 2005;42(12):881-892. 215. Yeung RS. Pathogenesis and treatment of Kawasaki’s disease. Curr Opin Rheumatol. 2005;17(5):617-623. 216. Greco A, De Virgilio A, Ralli M, et al. Behcet’s disease: new insights into pathophysiology, clinical features and treatment options. Autoimmun Rev. |
Surgery_Schwartz_6598 | Surgery_Schwartz | Curr Opin Rheumatol. 2005;17(5):617-623. 216. Greco A, De Virgilio A, Ralli M, et al. Behcet’s disease: new insights into pathophysiology, clinical features and treatment options. Autoimmun Rev. 2018;17(6):567-575. 217. Uygunoglu U, Siva A. Behcet’s syndrome and nervous system involvement. Curr Neurol Neurosci Rep. 2018;18(7):35. 218. Muhammad JS, Ishaq M, Ahmed K. Genetics and epigenetics pathogenesis of Behcet’s syndrome. Curr Rheumatol Rev. 2018. 219. Stanton M, Bhimji SS. Polyarteritis nodosa. StatPearls. Trea-sure Island (FL); 2018. 220. Temprano KK. A review of Raynaud’s disease. Mo Med. 2016; 113(2):123-126. 221. Hinojosa CA, Anaya-Ayala JE, Bermudez-Serrato K, et al. Surgical interventions for organ and limb ischemia associ-ated with primary and secondary antiphospholipid antibody syndrome with arterial involvement. Vasc Endovascular Surg. 2017;51(8):550-554. 222. Narula N, Kadian-Dodov D, Olin JW. Fibromuscular dyspla-sia: contemporary concepts and future directions. Prog | Surgery_Schwartz. Curr Opin Rheumatol. 2005;17(5):617-623. 216. Greco A, De Virgilio A, Ralli M, et al. Behcet’s disease: new insights into pathophysiology, clinical features and treatment options. Autoimmun Rev. 2018;17(6):567-575. 217. Uygunoglu U, Siva A. Behcet’s syndrome and nervous system involvement. Curr Neurol Neurosci Rep. 2018;18(7):35. 218. Muhammad JS, Ishaq M, Ahmed K. Genetics and epigenetics pathogenesis of Behcet’s syndrome. Curr Rheumatol Rev. 2018. 219. Stanton M, Bhimji SS. Polyarteritis nodosa. StatPearls. Trea-sure Island (FL); 2018. 220. Temprano KK. A review of Raynaud’s disease. Mo Med. 2016; 113(2):123-126. 221. Hinojosa CA, Anaya-Ayala JE, Bermudez-Serrato K, et al. Surgical interventions for organ and limb ischemia associ-ated with primary and secondary antiphospholipid antibody syndrome with arterial involvement. Vasc Endovascular Surg. 2017;51(8):550-554. 222. Narula N, Kadian-Dodov D, Olin JW. Fibromuscular dyspla-sia: contemporary concepts and future directions. Prog |
Surgery_Schwartz_6599 | Surgery_Schwartz | syndrome with arterial involvement. Vasc Endovascular Surg. 2017;51(8):550-554. 222. Narula N, Kadian-Dodov D, Olin JW. Fibromuscular dyspla-sia: contemporary concepts and future directions. Prog Car-diovasc Dis. 2018;60(6):580-585. 223. Baradhi KM, Bream P. Fibromuscular dysplasia. StatPearls. Treasure Island (FL); 2018. 224. Li S, King BN, Velasco N, Kumar Y, Gupta N. Cystic adven-titial disease-case series and review of literature. Ann Transl Med. 2017;5(16):327. 225. Lejay A, Ohana M, Lee JT, et al. Popliteal artery entrapment syndrome. J Cardiovasc Surg (Torino). 2014;55(2 suppl 1): 225-237. 226. Gokkus K, Sagtas E, Bakalim T, Taskaya E, Aydin AT. Pop-liteal entrapment syndrome. A systematic review of the lit-erature and case presentation. Muscles Ligaments Tendons J. 2014;4(2):141-148. 227. Rivera-Chavarria IJ, Brenes-Gutierrez JD. Thromboangiitis obliterans (Buerger’s disease). Ann Med Surg (Lond). 2016; 7:79-82. 228. Sugimoto M, Miyachi H, Morimae H, et al. Fate of ischemic | Surgery_Schwartz. syndrome with arterial involvement. Vasc Endovascular Surg. 2017;51(8):550-554. 222. Narula N, Kadian-Dodov D, Olin JW. Fibromuscular dyspla-sia: contemporary concepts and future directions. Prog Car-diovasc Dis. 2018;60(6):580-585. 223. Baradhi KM, Bream P. Fibromuscular dysplasia. StatPearls. Treasure Island (FL); 2018. 224. Li S, King BN, Velasco N, Kumar Y, Gupta N. Cystic adven-titial disease-case series and review of literature. Ann Transl Med. 2017;5(16):327. 225. Lejay A, Ohana M, Lee JT, et al. Popliteal artery entrapment syndrome. J Cardiovasc Surg (Torino). 2014;55(2 suppl 1): 225-237. 226. Gokkus K, Sagtas E, Bakalim T, Taskaya E, Aydin AT. Pop-liteal entrapment syndrome. A systematic review of the lit-erature and case presentation. Muscles Ligaments Tendons J. 2014;4(2):141-148. 227. Rivera-Chavarria IJ, Brenes-Gutierrez JD. Thromboangiitis obliterans (Buerger’s disease). Ann Med Surg (Lond). 2016; 7:79-82. 228. Sugimoto M, Miyachi H, Morimae H, et al. Fate of ischemic |
Surgery_Schwartz_6600 | Surgery_Schwartz | IJ, Brenes-Gutierrez JD. Thromboangiitis obliterans (Buerger’s disease). Ann Med Surg (Lond). 2016; 7:79-82. 228. Sugimoto M, Miyachi H, Morimae H, et al. Fate of ischemic limbs in patients with Buerger’s disease based on our 30-year experience: does smoking have a definitive impact on the late loss of limbs? Surg Today. 2015;45(4):466-470. 229. Mills JL Sr. Buerger’s disease in the 21st century: diagnosis, clinical features, and therapy. Semin Vasc Surg. 2003;16(3): 179-189.Brunicardi_Ch23_p0897-p0980.indd 98027/02/19 4:15 PM | Surgery_Schwartz. IJ, Brenes-Gutierrez JD. Thromboangiitis obliterans (Buerger’s disease). Ann Med Surg (Lond). 2016; 7:79-82. 228. Sugimoto M, Miyachi H, Morimae H, et al. Fate of ischemic limbs in patients with Buerger’s disease based on our 30-year experience: does smoking have a definitive impact on the late loss of limbs? Surg Today. 2015;45(4):466-470. 229. Mills JL Sr. Buerger’s disease in the 21st century: diagnosis, clinical features, and therapy. Semin Vasc Surg. 2003;16(3): 179-189.Brunicardi_Ch23_p0897-p0980.indd 98027/02/19 4:15 PM |
Surgery_Schwartz_6601 | Surgery_Schwartz | Venous and Lymphatic DiseaseAtish Chopra, Timothy K. Liem, and Gregory L. Moneta 24chapterVENOUS ANATOMYVeins are part of a dynamic and complex system that returns low-nutrient deoxygenated blood to the heart. Venous blood flow is dependent on multiple factors such as gravity, venous valves, the cardiac and respiratory cycles, blood volume, and the calf muscle and feet pumps. Alterations in the intricate balance of these factors can result in venous pathology.Structure of VeinsVeins are thin-walled, highly distensible, and collapsible. Their structure specifically supports the primary functions of veins to transport blood toward the heart and serve as a reservoir to prevent intravascular volume overload.The venous intima is composed of a nonthrombogenic endothelium with an underlying basement membrane and an elastic lamina. The endothelium produces endothelium-derived relaxing factors such as nitric oxide and prostacy-clin, which help maintain a nonthrombogenic surface through | Surgery_Schwartz. Venous and Lymphatic DiseaseAtish Chopra, Timothy K. Liem, and Gregory L. Moneta 24chapterVENOUS ANATOMYVeins are part of a dynamic and complex system that returns low-nutrient deoxygenated blood to the heart. Venous blood flow is dependent on multiple factors such as gravity, venous valves, the cardiac and respiratory cycles, blood volume, and the calf muscle and feet pumps. Alterations in the intricate balance of these factors can result in venous pathology.Structure of VeinsVeins are thin-walled, highly distensible, and collapsible. Their structure specifically supports the primary functions of veins to transport blood toward the heart and serve as a reservoir to prevent intravascular volume overload.The venous intima is composed of a nonthrombogenic endothelium with an underlying basement membrane and an elastic lamina. The endothelium produces endothelium-derived relaxing factors such as nitric oxide and prostacy-clin, which help maintain a nonthrombogenic surface through |
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