Gelabert H A, Machleder H I
University of California Los Angeles (UCLA) School of Medicine, USA.
Ann Vasc Surg. 1997 Jul;11(4):359-66. doi: 10.1007/s100169900061.
Neurovascular compression syndromes at the thoracic outlet generally present with predominantly arterial, venous, or neurogenic symptoms. The arterial abnormalities produce unique problems in diagnosis and management, and usually affect young, otherwise healthy, active individuals. Between 1984 and 1995 23 patients presented to our facility, with acute symptoms of arterial occlusion or embolization, found to be originating from the axillosubclavian arterial segment. The group comprised 14 females and nine males, ranging from 15 to 74 years, with an average age of 37 years. There were seven competitive athletes, three industrial workers, and 13 home, office, or service workers. The most severe presenting symptoms, occurring alone or in combination, and ranked in order of frequency observed, were: arm 'claudication' (74%), hand ischemia (48%), and digital gangrene (44%). Transaxillary thoracic outlet decompression was undertaken in 22 cases. This was combined with arterial reconstruction in 11 cases and sympathectomy for ischemic causalgia in seven cases. Transaxillary resection of a cervical rib was accomplished in 8 cases. There was one postoperative graft occlusion (PTFE), corrected by thrombectomy, with cumulative secondary patency (to 64 months), and one secondary embolic occlusion. Excepting the two secondary procedures, no patient had recurrent symptoms at a mean follow-up of 61 months. Effective and durable correction of the axillosubclavian arterial compressive abnormalities requires adequate thoracic outlet decompression, and anatomic vascular reconstruction when necessary. Failed prior procedures were a consequence of inaccurate diagnosis, failure to identify and correct the proximal embolizing arterial lesion, or inadequate decompression. Unilateral Raynaud's symptoms require meticulous investigation for arterial compression at the thoracic outlet with careful interpretation of subtle angiographic findings.
胸廓出口处的神经血管压迫综合征通常主要表现为动脉、静脉或神经源性症状。动脉异常在诊断和治疗方面会产生独特的问题,且通常影响年轻、原本健康且活跃的个体。1984年至1995年间,有23例患者因急性动脉闭塞或栓塞症状前来我院就诊,发现病变起源于腋-锁骨下动脉段。该组包括14名女性和9名男性,年龄在15岁至74岁之间,平均年龄为37岁。其中有7名竞技运动员、3名产业工人以及13名家庭、办公室或服务业工作者。最严重的首发症状,单独出现或合并出现,并按观察到的频率排序依次为:手臂“间歇性跛行”(74%)、手部缺血(48%)和手指坏疽(44%)。22例患者接受了经腋胸廓出口减压术。其中11例联合动脉重建术,7例因缺血性灼痛行交感神经切除术。8例完成了经腋颈椎肋切除术。术后有1例移植血管闭塞(聚四氟乙烯),通过取栓术纠正,累积二次通畅率(至64个月),还有1例继发性栓塞闭塞。除了这两次二次手术外,平均随访61个月时,没有患者出现复发症状。有效且持久地纠正腋-锁骨下动脉压迫异常需要充分的胸廓出口减压,必要时进行解剖学血管重建。既往手术失败是由于诊断不准确、未能识别和纠正近端栓塞性动脉病变或减压不充分。单侧雷诺氏症状需要对胸廓出口处的动脉压迫进行细致检查,并仔细解读细微的血管造影结果。