Stenosis of the subclavian vein. An unknown cause of resistant reflex sympathetic dystrophy.

Abstract

The striking similarity of certain pain symptoms and neurologic changes in RSD and the findings of severe thoracic outlet and inlet syndrome were the reason why clinical diagnostic studies of this dystrophy were also completed by radiologic examinations of the vessel system. Surprisingly, more or less striking and differently configurated stenoses in the area of the subclavian vein, with a resulting impairment of the venous run-off, were found. Those findings have been documented in 20 of 21 patients with RSD since 1984 by functional venography and, in the meantime, they were confirmed intraoperatively in nine resistant cases. The stenoses led to a lesion-caused disproportion between increased arterial inflow and decreased venous outflow, with venous stasis. Consequently, they acted as a primary cause of an edema of the hand, with corresponding regional results, mainly on the function of the sympathetic nervous system. That shows a primarily increased activity in RSD that under the influence of local factors results in a pathologic positive feedback mechanism, as already was known. The stenosis of the subclavian vein, in my opinion, is the long-searched for cause of the so-called "individual predisposition." The use of functional venogram in diagnosis is essential because it gives important hints at the diagnostic and prognostic outlook for a possible surgical treatment of resistant RSD. It is also very important in understanding the pathogenesis. To improve the venous flow and diminish or interrupt the sympathetic efferences, we performed transaxillary decompression of the neurovascular bundle with additional upper thoracic sympathectomy in resistant cases of RSD. Nine patients experienced immediate improvement of the pain syndrome and edema, as well as the entire postoperative course. After an average follow-up of 7.5 years, we found an excellent result in seven patients, a good result in one, and a fair result in one. Intraoperative findings and the arteriograms we performed on seven surgically treated patients indicate the primarily increased sympathetic activity in RSD is mainly caused by irritations and compressions of the lower plexus roots as well as the postganglionic fibers in the area of the subclavian artery, mainly by the inner rim of the first rib and fibromuscular structures. So the two main pathogenetic factors of RSD are known, and now can be localized and documented radiologically. It now should be possible to study the pathophysiology of RSD in an appropriate animal model.