Currently, long-term outcomes are significant because health care system changes will likely lead to a single payment for each occurrence of care, including readmissions-the "bundled payment" system. Therefore, it is essential to understand the outcomes of trauma patients discharged alive from trauma centers. This article reviews the current knowledge base on the timing and causes of deaths after trauma. The trimodal mortality model (immediate deaths, early deaths, and late deaths) is utilized as the early research describing trimodal distribution is discussed. Also covered is the successive work as trauma systems matured, showing a shift toward a bimodal distribution with a decline in late deaths. Finally, studies of long-term outcomes are highlighted. Deaths occurring within minutes or a few hours of injury are largely unchanged, which underscores the enormity of injuries to the central nervous and cardiovascular systems. Late deaths caused by multiple organ failure and sepsis have declined considerably, however. Also, the causes of death in this patient population remain constant. Lastly, a considerable number of deaths after discharge may be due to nontraumatic causes.

Object Evidence-based management (EBM) guidelines for severe traumatic brain injuries (TBIs) were promulgated decades ago. However, the extent of their adoption into bedside clinical practices is not known. The purpose of this study was to measure compliance with EBM guidelines for management of severe TBI and its impact on patient outcome. Methods This was a retrospective study of blunt TBI (11 Level I trauma centers, study period 2008–2009, n = 2056 patients). Inclusion criteria were an admission Glasgow Coma Scale score ≤ 8 and a CT scan showing TBI, excluding patients with nonsurvivable injuries—that is, head Abbreviated Injury Scale score of 6. The authors measured compliance with 6 nonoperative EBM processes (endotracheal intubation, resuscitation, correction of coagulopathy, intracranial pressure monitoring, maintaining cerebral perfusion pressure ≥ 50 cm H2O, and discharge to rehabilitation). Compliance rates were calculated for each center using multivariate regression to adjust for patient demographics, physiology, injury severity, and TBI severity. Results The overall compliance rate was 73%, and there was wide variation among centers. Only 3 centers achieved a compliance rate exceeding 80%. Risk-adjusted compliance was worse than average at 2 centers, better than average at 1, and the remainder were average. Multivariate analysis showed that increased adoption of EBM was associated with a reduced mortality rate (OR 0.88; 95% CI 0.81–0.96, p < 0.005). Conclusions Despite widespread dissemination of EBM guidelines, patients with severe TBI continue to receive inconsistent care. Barriers to adoption of EBM need to be identified and mitigated to improve patient outcomes.

Objectives: Little is known about recent trends in U.S. emergency department (ED) visits for acute exacerbation of chronic obstructive pulmonary disease (AECOPD) or about ED management of AECOPD. This study aimed to describe the epidemiology of ED visits for AECOPD and to evaluate concordance with guideline-recommended care.Methods: Data were obtained from National Hospital Ambulatory Medical Care Survey (NHAMCS). ED visits for AECOPD, during 1993 to 2005, were identified using the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) codes. Concordance with guideline recommendations was evaluated using process measures.Results: Over the 13-year study period, there was an average annual 0.6 million ED visits for AECOPD, and the visit rates for AECOPD were consistently high (3.2 per 1,000 U.S. population; P trend = 0.13). The trends in the use of chest radiograph, pulse oximetry, or bronchodilator remained stable (all P trend > 0.5). By contrast, the use of systemic corticosteroids increased from 29% in 1993-1994 to 60% in 2005, antibiotics increased from 14% to 42%, and methylxanthines decreased from 15% to <1% (all P trend < 0.001). Multivariable analysis showed patients in the South (vs. the Northeast) were less likely to receive systemic corticosteroids (odds ratio [OR] = 0.6; 95% confidence interval [CI] = 0.4 to 0.9). Conclusions:The high burden of ED visits for AECOPD persisted. Overall concordance with guidelinerecommended care for AECOPD was moderate, and some emergency treatments had improved over time.

A new method has been developed to accurately measure apurinic and apyrimidinic (AP) DNA damage sites, which are lesions in DNA formed by loss of a nucleobase from oxidative stress or carcinogen adducts. If AP sites are left unrepaired (or if improperly repaired), these sites can lead to DNA mutations that may ultimately result in the formation of cancer. Hence, detection of AP sites may provide a useful indicator of exposure and susceptibility to chemical carcinogens and oxidative stress. AP detection is currently accomplished by immunodetection methods using an aldehyde reactive probe [Nakamura, J., Walker, V. E., Upton, P. B., Chiang, S.-Y., Kow, Y. W., and Swenberg, J. A. (1998) Cancer Res. 58, 222-225; Atamna, H., Cheung, I., and Ames, B. N. (2000) Proc. Natl. Acad. Sci. U.S.A. 97, 686-691]; however, these approaches lack the specificity required for unequivocal identification of the AP site. Therefore, we have developed an accurate method based on mass spectrometry detection of AP sites from AP DNA that have been prelabeled with O-4-nitrobenzylhydroxylamine (NBHA). Once labeled and once the excess labeling agent has been removed, enzymatic digestion of DNA to monomeric subunits can be accomplished, followed by isolation and detection with high-performance liquid chromatography coupled to electrospray ionization tandem mass spectrometry (HPLC-ESI-MS/MS). Optimization and validation of the experimental procedures and detection limits have been established using a model DNA oligomer (11-mer) containing uracil. Enzymatic removal of uracil with uracil glycosylase generates well-defined AP sites in both single- and double-stranded DNA. The addition of NBHA labels the AP site in the oligomer, creating a labeled 11-mer. HPLC-ESI-MS/MS in the negative ionization mode was used to monitor and confirm binding of NBHA to the AP oligomer. The NBHA-tagged oligomer underwent endo- and exonuclease digestion to the 5'-deoxyribose monophosphate (5'-dRp) level, thereby releasing free 5'-dRp-NBHA. The 5'-dRp-NBHA product was partially purified by solid phase extraction and quantified by LC-MS/MS using several transitions of the deprotonated molecule ([M - H]- at m/z 363) and isotopically labeled 5'-dRp-NBHA as an internal standard. Further experiments with 5',3'-bisphosphate-deoxyribose and heat/acid-treated calf thymus DNA showed similar labeling, digestion, and detection results. Initial results show a quantification limit with 100 mug of DNA to be 100 fmol (three abasic sites per 10(7) bases).

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