Thoracic outlet syndrome (TOS) is a group of disorders all having in common compression at the thoracic outlet. Three structures are at risk: the brachial plexus, the subclavian vein, and the subclavian artery, producing neurogenic (NTOS), venous (VTOS), and arterial (ATOS) thoracic outlet syndromes, respectively. Each of these three are separate entities, though they can coexist and possibly overlap. The treatment of NTOS, in particular, has been hampered by lack of data, which in turn is the result of inconsistent definitions and diagnosis, uncertainty with regard to treatment options, and lack of consistent outcome measures. The Committee has defined NTOS as being present when three of the following four criteria are present: signs and symptoms of pathology occurring at the thoracic outlet (pain and/or tenderness), signs and symptoms of nerve compression (distal neurologic changes, often worse with arms overhead or dangling), absence of other pathology potentially explaining the symptoms, and a positive response to a properly performed scalene muscle test injection. Reporting standards for workup, treatment, and assessment of results are presented, as are reporting standards for all phases of VTOS and ATOS. The overall goal is to produce consistency in diagnosis, description of treatment, and assessment of results, in turn then allowing more valuable data to be presented.

Aortic endograft infection can be eradicated by excision and in situ or extra-anatomic replacement but is often associated with early postoperative morbidity and mortality and occasionally with a need for late removal for reinfection. Prosthetic graft replacement after explanation is associated with higher reinfection and graft-related complications and decreased survival compared with autogenous reconstruction.

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The expansion rate of CIAAs is 0.29 cm/y, and hypertension predicts faster expansion. Because no rupture of a CIAA <3.8 cm was observed, elective repair of asymptomatic patients with CIAA >or=3.5 cm seems justified. Although buttock claudication after EVAR remains a concern, results at 3 years support EVAR as a first-line treatment for most anatomically suitable patients who require CIAA repair. Patients with compressive symptoms or those with AVF should preferentially be treated with OR.

Open surgical repair of JAA is associated with low mortality and remains the gold standard. Although 18% had renal complications, only one patient had permanent renal failure. Patients with a combination of physiologic and anatomic risk factors identified on multivariate analysis may benefit from fenestrated endograft repair.