Abstract
In the absence of ischemic events, arterial pathology at the thoracic outlet (TO) is rarely identified because findings of chronic arterial pathology may be masked by symptoms of neurogenic compression. This study describes the clinical presentations and significance of arterial compression at the TO. This was a retrospective analysis of the clinical records and imaging studies of 41 patients with objective findings of arterial compression at the TO. Sixteen were diagnosed from 1990 to 2003, during which 284 patients underwent surgery for TO decompression with selective arterial imaging; 25 were diagnosed from 2003 to 2009, and 62 underwent TO surgical decompressions. Subclavian artery stenosis, with or without poststenotic dilatation (PSD), was found in 26 patients (63%), subclavian artery aneurysms in 12 (29%), chronic subclavian occlusion in 1(2.4%), and axillary artery compression in 2 (5%). Chronic symptoms difficult to discern from neurogenic compression were present in 27 patients (66%; 24 had subclavian stenoses or PSD, or both, 1 had subclavian occlusion, and 2 had axillary artery compression); 13 (32%) presented with acute ischemia (11 had aneurysms and 2 had PSDs), and 1 asymptomatic patient had a subclavian aneurysm. Osteoarticular anomalies were found in 27 patients (66%), including 19 cervical ribs, 4 first rib anomalies, and 4 clavicular or first rib fractures, or both. Among 27 patients with subclavian aneurysms or PSD, 21 (78%) had a bone anomaly. Arterial pathology was deemed significant in 30 patients (73%) and mild or moderate in 11 (21%). Symptoms in 23 of these patients were compatible with neurogenic compression without clinical suspicion of arterial pathology, but 13 (56%) harbored a significant arterial anomaly. The incidence of arterial pathology secondary to compression at the TO may be underestimated, and in the absence of obvious ischemia, significant arterial pathology may not be suspected. Two-thirds of patients with arterial compression have associated bone anomalies. Therefore, routine arterial imaging seems advisable for patients evaluated for TO syndrome in the presence of a bone anomaly at the TO or an examination that shows an arterial abnormality. In the absence of these signs, however, arterial pathology may be overlooked in patients with symptoms suggestive of neurogenic compression. Further study is needed to elucidate the incidence, natural history, and clinical relevance of arterial compression and PSD at the TO.
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