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Pubmed for Handhelds

PUBMED FOR HANDHELDS

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  • Title: [Thoracic outlet syndrome and its significance for surgery of the hand (on the etiology and pathogenesis of epicondylitis, tendovaginitis, median nerve compression and trophic disorders of the hand)].
    Author: Wilhelm A, Wilhelm F.
    Journal: Handchir Mikrochir Plast Chir; 1985 Jul; 17(4):173-87. PubMed ID: 4029761.
    Abstract:
    At present, the term "thoracic outlet syndrome" (TOS) is used as a term to include all factors compressing the nerves and vessels situated in the outlet of the thorax and the costo-clavicular area. It is marked by neurological and vascular disorders; their manifestation can be either spontaneous or posttraumatic. In case of surgical treatment the transaxillary approach (according to Roos) proved to be the best, and is indicated in therapy-resistant TOS, in certain cases of arterial complications and in outlet obstructions of the subclavian vein. Complete resection of the first rib and the most careful removal of all fibro-muscular structures affecting the artery, vein and brachial plexus are of importance to the result of the operation. In the evaluation of cases we found surprising success with cases of lateral epicondylitis. Thus, the nerve irritation asserted as a cause in 1962 is once more confirmed. The postoperative development of 38 median nerve compressions proved to be particularly astonishing. Twenty-five of those vanished without any need for additional measures, and in eight cases definite improvement was achieved. Another important fact was observed when five median nerve compressions, previously operated upon, disappeared only after a secondary TOS-operation. These observations led to a new pathogenetic concept of median nerve compression. Apart from the common causes, the primary predisposing factor for median nerve compression is a chronic oedema due to a functional blockage of the subclavian vein, clinically and radiologically substantiated. This oedema eventually leads to a carpal tunnel syndrome, either directly on account of swelling of fibrous structures or via metabolic disorders and oxygen deficiency, thereby causing an infiltrative and proliferative reaction. In this connection, it seems interesting that the results of recent pathohistological researches suggest that the chronic oedema is the greater pathogenetic factor. The improvement of painful tendovaginitis and different disturbances in wound healing after surgical treatment of the TOS shows the importance of subclavian vein compressions. Phlebographic examination of patients who suffer from Sudeck's atrophy demonstrates significant narrowing of the subclavian vein. The increasing pressure in the subfascial space and the irritation of the lower cervical plexus and the subclavian artery can promote Sudeck's atrophy.
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