Current opinion regarding indications for emergency department thoracotomy.

BACKGROUND: Emergency department thoracotomy (EDT) is a dramatic but rarely lifesaving intervention. Clinical variability regarding indications for EDT has yet to be quantified. Members of the Eastern and American Associations for the Surgery of Trauma were questioned by mail to evaluate which clinical and demographic factors influence the decision to perform EDT and whether physicians perform EDT in accordance with current practice guidelines. METHODS: A single mailing of an anonymous survey was sent to 1,124 surgeons to collect institutional and physician demographics as well as indications for EDT on the basis of variable mechanisms of trauma, duration of arrest, and signs of life (SOL). Statistical analysis included the Pearson and linear-by-linear association chi(2) tests, independent samples t test, and univariate and multivariate analyses of variance; p values of < 0.05 were considered significant. RESULTS: Completed surveys were received from 358 respondents. After 54 surveys were excluded that were incomplete, late, or from noneligible respondents, 304 surveys were analyzed. There were no significant differences in EDT indications among institutions of differing caseload volume, exposure to penetrating trauma, trauma level designation, American College of Surgeons verification status, or residency program affiliation. In addition, neither the respondent's position nor whether attendings versus residents performed the majority of EDTs influenced clinical decision-making. Performance criteria for EDT were liberal in comparison with established guidelines, especially for blunt trauma. The presence or recent loss of SOL influenced responses, but respondents varied greatly in their definition of SOL. CONCLUSION: A lack of agreement exists regarding the indications for EDT in multiple clinical scenarios as well as in defining SOL. Indications for EDT were liberal, especially for blunt trauma-related indications, and were determined by clinical parameters, not by physician or institutional factors. Our results suggest that clinical practice is at variance with Advanced Trauma Life Support guidelines. We recommend that practice guidelines for EDT be established on the basis of a consensus definition of SOL to allow for a more uniform and selective approach to EDT.

Normal lymphoid homeostasis and lack of lethal autoimmunity in mice containing mature T cells with severely impaired IL-2 receptors.

The importance of IL-2Rbeta function for immune regulation is highlighted by the severe impairment in lymphoid cell function in IL-2Rbeta-deficient mice. It has been speculated that failed IL-2/IL-2R signaling in peripheral T cells causes the associated autoimmunity, imbalanced peripheral lymphoid homeostasis, and defective T cell function. This study explored the requirement for IL-2Rbeta function in mature T lymphocytes. We show that transgenic thymic expression of the IL-2R beta-chain in IL-2Rbeta-deficient mice prevents lethal autoimmunity, restores normal production of B lymphocytes, and results in a peripheral T cell compartment that is responsive to triggering through the TCR, but not the IL-2R. The dysfunction of the IL-2R is illustrated by the near complete failure of mature T cells to proliferate to IL-2 in vitro and in vivo, to differentiate into CTL, and to up-regulate IL-2Ralpha expression. These data indicate that lymphoid homeostasis is largely maintained despite a nonfunctional IL-2R in mature T lymphocytes and suggest that IL-2Rbeta provides an essential signal during thymic development to regulate self-reactivity.

Prostaglandin E2 inhibits T cell activation-induced apoptosis and Fas-mediated cellular cytotoxicity by blockade of Fas-ligand induction.

Prostanoids exhibit both pro-apoptotic and anti-apoptotic functions depending on the maturation stage and tissue localization of target cells. Prostaglandin (PG) E2 has been shown to protect T lymphocytes from TCR-mediated activation-induced cell death, but the mechanism by which PGE2 inhibits apoptosis of T cells has not been established. We show that this protection involves the down-regulation of Fas-ligand (Fas-L) mRNA levels in T cells. Modulation of cell surface Fas-L expression by physiological concentrations of PGE2 was shown to be both anti-apoptotic as well as capable of inhibiting Fas-L-mediated cytotoxicity of Fas-transfected P815 target cells. Thus, this study provides direct evidence of the likely biological means by which PGE2 down-regulates T cell apoptosis.