Popliteal Artery Adventitial Cystic Disease Justin K. Nelms, David G. Neschis and William R. Flinn Adventitial cystic disease of the popliteal artery is a relatively rare cause of lower limb ischemia in which single or multiloculated cysts develop within the adventitial layer of the wall of the popliteal artery. As the typical gelatinous secretions of the intramural adventitial cyst accumulate, the cyst produces progressive obliteration of the adjacent arterial lumen. The reduction of arterial flow leads to the subsequent development of ischemic symptoms, most often intermittent claudication. The term adventitial cystic disease has been almost universally associated with the popliteal artery, but the first case of adventitial cystic disease was actually observed in the external iliac artery by Atkins and Key in 1947. They observed a 7-cm cystic lesion reminiscent of a sausage and thought it to be a myxomatous tumor of the adventitia. The first description of adventitial cystic disease of the popliteal artery was that of Ejrup and Heirtonn in 1954. They reported the incision of a mass filled with gelatinous material in a thickened area of the popliteal artery, which they believed at the time represented mucoid degeneration of the media. Subsequently, more than 400 case reports have been published in the world literature that describe adventitial cystic disease in the radial, ulnar, and femoral arteries, but the vast majority of cases have involved the popliteal artery. There have also been rare reports of adventitial cystic disease involving the iliofemoral and saphenous veins. Etiology The precise cause of popliteal artery adventitial cystic disease remains uncertain. Disparate reports of the findings from surgical exploration and from pathologic examination of cysts have resulted in several different theories. The first was the theory of microtrauma, in which repetitive stretch injury to the arterial wall or injury from surrounding musculotendinous structures was thought to cause cystic myxomatous degeneration of the adventitia. Past reports have noted that the young men afflicted were often heavy laborers or were athletically active. However, if trauma alone were the cause, it would be expected that the condition would be seen more often. Cases of adventitial cystic disease have also been reported in children in whom chronic trauma as a primary cause would be unlikely. A second theory proposed an extraarterial origin for the adventitial cysts. Adventitial cysts closely resemble ganglion cysts and can originate from pericapsular joint tissue and then extend outward to involve the arterial wall. Advocates of this theory have noted that adventitial cystic disease has always been found adjacent to joint spaces and never in the mid thigh or mid calf. A ganglion arising from the tibiofibular joint has been reported to extend to and compress the lateral popliteal nerve, indicating the potential for these articular lesions to involve anatomically proximate structures. Some cases of adventitial disease of the popliteal artery have been reported to have a communication to the knee joint documented by an arthrogram or discovered at the time of surgical exploration. More evidence has emerged to contradict the extraarterial or ganglion theory. The cyst contents in adventitial cystic disease of the popliteal artery are essentially identical to that of typical ganglion cysts. The viscid, gel-like material is rich in mucopolysaccharides with a high content of hyaluronic acid and is markedly dissimilar to synovial fluid. A microanalysis of a cystic adventitial lesion performed by Oi and colleagues detected only one of the two types of synoviocytes that compose normal synovium, suggesting that the lesion was not derived from synovial fluid. Additionally, in most reported cases, microscopic examination has not identified a lining of synovial cells in the adventitial cyst. This has led many investigators to doubt an extraarterial origin of adventitial cysts from adjacent joint tissue. A third theory of pathogenesis for adventitial cystic disease suggests a systemic process. Adventitial cysts are thought to develop as a result of spontaneous ganglionic degeneration of the intrinsic tissue within the adventitia of the artery itself. This theory has fallen out of favor because pathologic and epidemiologic supporting evidence has been scarce, and multicentric disease has proved to be extremely rare. A final proposed etiology is the developmental theory, which at this time appears to have the most widespread acceptance and supporting evidence. The theory suggests that mucin-secreting mesenchymal cells from nearby joints are inadvertently deposited in the adventitia of vessels during embryogenesis and then secrete mucin later in life. Levien and coworkers recognized that all reported cases of adventitial cystic disease occurred in nonaxial vessels that are formed adjacent to developing joint structures in gestational weeks 15 to 22. During this time, mesenchymal tissue destined to form joints can become trapped in nearby developing nonaxial vessels and proceed to secrete mucoid material years later. Whatever the precise origin of these unusual lesions, they appear to have a relatively benign clinical source overall. Once accurately diagnosed, most have been successfully treated. The cyst wall can be resected in most patients. When involvement of the artery is extensive or arterial thrombosis has occurred, resection with vein graft interposition has been successful. Recurrence of these cysts is infrequent, and limb loss or other serious morbidity is rare. Clinical Presentation Adventitial cystic disease of the popliteal artery characteristically occurs in young, healthy, nonsmoking men without evidence of atherosclerosis or other vascular disease. Previous reviews of this disorder have noted a 5:1 predominance of men over women and a mean age of approximately 40 years. The typical patient has a relatively sudden onset of intermittent, unilateral calf claudication. Severe limb-threatening ischemia has been rare. Patients usually report symptoms of claudication early because of the abrupt onset and relatively disabling nature in these young men who have previously been very active in work or athletics. However, because of their young age and the absence of other risk factors, symptoms are often initially interpreted to be neurogenic or musculoskeletal, which can delay definitive diagnosis. The clinical picture may be further confused by the spontaneous resolution of symptoms and the disappearance of abnormal physical findings in the some patients. In young adults with intermittent claudication or symptoms suggesting claudication, adventitial cystic disease should be considered because there are now reliable noninvasive methods available to confirm the diagnosis in most patients. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Technical Aspects of Percutaneous Carotid Angioplasty and Stenting for Arteriosclerotic Disease In-Situ Treatment of Aortic Graft Infection with Prosthetic Grafts and Allografts Treatment of Acute Upper Extremity Venous Occlusion Intraoperative Assessment of the Technical Adequacy of Carotid Endarterectomy Stay updated, free articles. 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Popliteal Artery Adventitial Cystic Disease Justin K. Nelms, David G. Neschis and William R. Flinn Adventitial cystic disease of the popliteal artery is a relatively rare cause of lower limb ischemia in which single or multiloculated cysts develop within the adventitial layer of the wall of the popliteal artery. As the typical gelatinous secretions of the intramural adventitial cyst accumulate, the cyst produces progressive obliteration of the adjacent arterial lumen. The reduction of arterial flow leads to the subsequent development of ischemic symptoms, most often intermittent claudication. The term adventitial cystic disease has been almost universally associated with the popliteal artery, but the first case of adventitial cystic disease was actually observed in the external iliac artery by Atkins and Key in 1947. They observed a 7-cm cystic lesion reminiscent of a sausage and thought it to be a myxomatous tumor of the adventitia. The first description of adventitial cystic disease of the popliteal artery was that of Ejrup and Heirtonn in 1954. They reported the incision of a mass filled with gelatinous material in a thickened area of the popliteal artery, which they believed at the time represented mucoid degeneration of the media. Subsequently, more than 400 case reports have been published in the world literature that describe adventitial cystic disease in the radial, ulnar, and femoral arteries, but the vast majority of cases have involved the popliteal artery. There have also been rare reports of adventitial cystic disease involving the iliofemoral and saphenous veins. Etiology The precise cause of popliteal artery adventitial cystic disease remains uncertain. Disparate reports of the findings from surgical exploration and from pathologic examination of cysts have resulted in several different theories. The first was the theory of microtrauma, in which repetitive stretch injury to the arterial wall or injury from surrounding musculotendinous structures was thought to cause cystic myxomatous degeneration of the adventitia. Past reports have noted that the young men afflicted were often heavy laborers or were athletically active. However, if trauma alone were the cause, it would be expected that the condition would be seen more often. Cases of adventitial cystic disease have also been reported in children in whom chronic trauma as a primary cause would be unlikely. A second theory proposed an extraarterial origin for the adventitial cysts. Adventitial cysts closely resemble ganglion cysts and can originate from pericapsular joint tissue and then extend outward to involve the arterial wall. Advocates of this theory have noted that adventitial cystic disease has always been found adjacent to joint spaces and never in the mid thigh or mid calf. A ganglion arising from the tibiofibular joint has been reported to extend to and compress the lateral popliteal nerve, indicating the potential for these articular lesions to involve anatomically proximate structures. Some cases of adventitial disease of the popliteal artery have been reported to have a communication to the knee joint documented by an arthrogram or discovered at the time of surgical exploration. More evidence has emerged to contradict the extraarterial or ganglion theory. The cyst contents in adventitial cystic disease of the popliteal artery are essentially identical to that of typical ganglion cysts. The viscid, gel-like material is rich in mucopolysaccharides with a high content of hyaluronic acid and is markedly dissimilar to synovial fluid. A microanalysis of a cystic adventitial lesion performed by Oi and colleagues detected only one of the two types of synoviocytes that compose normal synovium, suggesting that the lesion was not derived from synovial fluid. Additionally, in most reported cases, microscopic examination has not identified a lining of synovial cells in the adventitial cyst. This has led many investigators to doubt an extraarterial origin of adventitial cysts from adjacent joint tissue. A third theory of pathogenesis for adventitial cystic disease suggests a systemic process. Adventitial cysts are thought to develop as a result of spontaneous ganglionic degeneration of the intrinsic tissue within the adventitia of the artery itself. This theory has fallen out of favor because pathologic and epidemiologic supporting evidence has been scarce, and multicentric disease has proved to be extremely rare. A final proposed etiology is the developmental theory, which at this time appears to have the most widespread acceptance and supporting evidence. The theory suggests that mucin-secreting mesenchymal cells from nearby joints are inadvertently deposited in the adventitia of vessels during embryogenesis and then secrete mucin later in life. Levien and coworkers recognized that all reported cases of adventitial cystic disease occurred in nonaxial vessels that are formed adjacent to developing joint structures in gestational weeks 15 to 22. During this time, mesenchymal tissue destined to form joints can become trapped in nearby developing nonaxial vessels and proceed to secrete mucoid material years later. Whatever the precise origin of these unusual lesions, they appear to have a relatively benign clinical source overall. Once accurately diagnosed, most have been successfully treated. The cyst wall can be resected in most patients. When involvement of the artery is extensive or arterial thrombosis has occurred, resection with vein graft interposition has been successful. Recurrence of these cysts is infrequent, and limb loss or other serious morbidity is rare. Clinical Presentation Adventitial cystic disease of the popliteal artery characteristically occurs in young, healthy, nonsmoking men without evidence of atherosclerosis or other vascular disease. Previous reviews of this disorder have noted a 5:1 predominance of men over women and a mean age of approximately 40 years. The typical patient has a relatively sudden onset of intermittent, unilateral calf claudication. Severe limb-threatening ischemia has been rare. Patients usually report symptoms of claudication early because of the abrupt onset and relatively disabling nature in these young men who have previously been very active in work or athletics. However, because of their young age and the absence of other risk factors, symptoms are often initially interpreted to be neurogenic or musculoskeletal, which can delay definitive diagnosis. The clinical picture may be further confused by the spontaneous resolution of symptoms and the disappearance of abnormal physical findings in the some patients. In young adults with intermittent claudication or symptoms suggesting claudication, adventitial cystic disease should be considered because there are now reliable noninvasive methods available to confirm the diagnosis in most patients. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Technical Aspects of Percutaneous Carotid Angioplasty and Stenting for Arteriosclerotic Disease In-Situ Treatment of Aortic Graft Infection with Prosthetic Grafts and Allografts Treatment of Acute Upper Extremity Venous Occlusion Intraoperative Assessment of the Technical Adequacy of Carotid Endarterectomy Stay updated, free articles. Join our Telegram channel Join
