{'fraction_non_alphanumeric': 0.022191400832177532, 'fraction_numerical': 0.0013869625520110957, 'mean_word_length': 5.061624649859944, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Is stenting for superior vena cava syndrome supercalifragilisticexpialidocious?

Superior vena cava (SVC) syndrome presents with symptoms of poor venous return from the head and upper extremities as more blood is routed from the deep veins to collateral pathways. Objective evidence of this in most patients is demonstrated as dilated skin surface veins, an erythrocyanotic appearance to the skin, swelling of the face and arms, and the skin is warmer to the touch. The more abrupt the occlusion and extensive the involvement of the SVC is, particularly when the azygous vein is compromised, the more dramatic the symptoms are. In this article, head or neck distention was noted in only 29%. This must be a reflection of either the chronicity of the occlusion or perhaps the patients really did not have SVC syndrome. The two patients with ‘‘thoracic outlet syndrome’’ (TOS) are a case in point. It would be most unusual for thrombus to propagate from the clavicle/ first rib junction through the innominate vein and into the SVC. Clot propagation would be distal to the compression but not ‘‘in front of it.’’ The flow of the ipsilateral internal jugular (important in TOS) and contralateral innominate vein should limit the proximal extent of thrombus from the site of compression. TOS may be present but cannot explain the complete picture of SVC syndrome. So, the physician needs to consider other diagnostic entities that range from primary thrombophilia to mediastinal fibrosis to cancer. This should be highly scrutinized because the etiologic mechanism for SVC syndrome is the most important variable to consider when it comes to treatment. Many decades ago, syphilitic aortic aneurismal disease was a common cause for extrinsic compression of the SVC. This cause is almost never seen now. Currently, lung cancers and lymphoma are commonly responsible for the malignant forms of SVC syndrome [1]. Longterm indwelling catheters and pacemaker/defibrillator leads cause most of the nonmalignant cases of this syndrome. To the practicing clinician, cancer leads to extrinsic compression, whereas indwelling catheters lead to intrinsic fibrosis and thrombosis.