Durham J R, Yao J S, Pearce W H, Nuber G M, McCarthy W J
Department of Surgery, Northwestern University Medical School, Chicago, Illinois 60611.
J Vasc Surg. 1995 Jan;21(1):57-69; discussion 70. doi: 10.1016/s0741-5214(95)70244-x.
This article reviews experience with arterial injury caused by thoracic outlet syndrome. Special emphasis is placed on the influence of athletic or work activities on the axillary-subclavian artery system and the mechanism by which the humeral head compresses the axillary artery and the circumflex humeral arterial branches.
Retrospective review identified 34 patients (age range 13 to 67 years) treated for upper extremity symptoms or ischemic complications of thoracic outlet syndrome from 1983 to 1993. Evaluation included assessment of occupational and recreational activities plus duplex ultrasonography and contrast arteriography with positional maneuvers.
Twenty-two patients (27 arms) had subclavian artery injury, which was most commonly caused by compression by a bony abnormality (cervical rib, 16; anomalous first rib, two; cervical rib and anomalous first rib, two). Fourteen of the 27 arms had distal embolization. All 27 had surgical decompression of the subclavian artery; 15 required concomitant arterial reconstruction. Twelve additional patients (nine athletes) had axillary artery involvement, all from arterial compression by the head of the humerus during abduction maneuvers; all had concomitant compression of the posterior circumflex humeral artery. Axillary arterial injury included thrombosis (one), aneurysm (two), and symptomatic extrinsic compression only (nine). Five patients with axillary artery involvement were treated without a surgical procedure; of the remainder, three underwent decompression procedures only, and four had direct arterial repair. In both groups all subclavian and axillary artery reconstructions were patent at last follow-up examination (mean 31 months).
Most patients with thoracic outlet syndrome who have arterial involvement have a bony anomaly causing subclavian artery compression. This study demonstrates that humeral head compression of the axillary artery and its circumflex branches is a surprisingly common pathologic mechanism. Awareness of this condition affords a better therapeutic approach to arterial injuries caused by thoracic outlet syndrome.
本文回顾了胸廓出口综合征所致动脉损伤的治疗经验。特别强调了运动或工作活动对腋-锁骨下动脉系统的影响，以及肱骨头压迫腋动脉和旋肱动脉分支的机制。
回顾性分析1983年至1993年因上肢症状或胸廓出口综合征缺血性并发症接受治疗的34例患者（年龄范围13至67岁）。评估包括职业和娱乐活动评估，以及双功超声检查和带体位操作的造影动脉造影。
22例患者（27侧上肢）有锁骨下动脉损伤，最常见的原因是骨异常压迫（颈肋，16例；第一肋异常，2例；颈肋和第一肋异常，2例）。27侧上肢中有14侧发生远端栓塞。所有27例均接受了锁骨下动脉手术减压；15例需要同时进行动脉重建。另外12例患者（9名运动员）有腋动脉受累，均因外展动作时肱骨头压迫动脉所致；均伴有旋肱后动脉受压。腋动脉损伤包括血栓形成（1例）、动脉瘤（2例）和仅为有症状的外部压迫（9例）。5例腋动脉受累患者未接受手术治疗；其余患者中，3例仅接受减压手术，4例进行了直接动脉修复。两组患者最后一次随访检查（平均31个月）时所有锁骨下和腋动脉重建均通畅。
大多数有动脉受累的胸廓出口综合征患者存在导致锁骨下动脉受压的骨异常。本研究表明，肱骨头对腋动脉及其旋支的压迫是一种出人意料的常见病理机制。认识到这种情况有助于为胸廓出口综合征所致动脉损伤提供更好的治疗方法。
