Successful paraclavicular surgical decompression for recurrent venous thoracic outlet syndrome following transaxillary first rib resection in an elite athlete.

OBJECTIVES: Recurrent effort thrombosis after prior surgical intervention for venous thoracic outlet syndrome (TOS) is an uncommon problem, and there are multiple alternative surgical approaches in the management of recurrent venous TOS. METHODS: We present a case of a 23 year-old female professional athlete who presented with arm swelling, pain, and recurrent effort thrombosis after prior transaxillary rib resection. Imaging at our institution revealed subclavian vein thrombosis, confirmed with dynamic venography, as well as a remnant first rib. RESULTS: Thrombolysis of the subclavian vein and balloon angioplasty was followed by paraclavicular thoracic outlet decompression with complete first rib resection. Success was confirmed with intraoperative dynamic venography demonstrating a patent subclavian vein and resulted in complete elimination of symptoms. CONCLUSION: Additional surgical decompression with complete medial first rib resection of remnant rib, which was potentially causing compression of the subclavian vein, may be necessary to prevent recurrent venous compression and thrombosis for venous TOS.

Reappraisal of H2S/sulfide concentration in vertebrate blood and its potential significance in ischemic preconditioning and vascular signaling.

Hydrogen sulfide (H(2)S) is rapidly emerging as a biologically significant signaling molecule. Studies published before 2000 report low or undetectable H(2)S (usually as total sulfide) levels in blood or plasma, whereas recent work has reported sulfide concentrations between 10 and 300 microM, suggesting it acts as a circulating signal. In the first series of experiments, we used a recently developed polarographic sensor to measure the baseline level of endogenous H(2)S gas and turnover of exogenous H(2)S gas in real time in blood from numerous animals, including lamprey, trout, mouse, rat, pig, and cow. We found that, contrary to recent reports, H(2)S gas was essentially undetectable (<100 nM total sulfide) in all animals. Furthermore, exogenous sulfide was rapidly removed from blood, plasma, or 5% bovine serum albumin in vitro and from intact trout in vivo. To determine if blood H(2)S could transiently increase, we measured oxygen-dependent H(2)S production by trout hearts in vitro and in vivo. H(2)S has been shown to mediate ischemic preconditioning (IPC) in mammals. IPC is present in trout and, unlike mammals, the trout myocardium obtains its oxygen from relatively hypoxic systemic venous blood. In vitro, myocardial H(2)S production was inversely related to Po(2), whereas we failed to detect H(2)S in ventral aortic blood from either normoxic or hypoxic fish in vivo. These results provide an autocrine or paracrine mechanism for myocardial coupling of hypoxia to H(2)S in IPC, i.e., oxygen sensing, but they fail to provide any evidence that H(2)S signaling is mediated by the circulation.