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Objectives: Haemorrhage remains among the most preventable causes of trauma death. Massive transfusion protocols, as part of 'haemostatic resuscitation', have been implemented in most trauma centres. Relative to the attention to the ideal ratio of red blood cells to fresh frozen plasma and platelets, cryoprecipitate treatment has been infrequently discussed. We aimed to outline the use of cryoprecipitate during trauma resuscitation and analyse outcomes in patients who received cryoprecipitate after hypofibrinogenaemia detection., Methods: A retrospective review of registry data on all major trauma patients (Injury Severity Score>15) presenting to a level I trauma centre over a 4-year period (2008-2011) was conducted. We selected all patients who had received cryoprecipitate and then analysed patients who had received cryoprecipitate following the detection of hypofibrinogenaemia (<1.0 g/l). Mortality at hospital discharge among hypofibrinogenaemic patients who had received cryoprecipitate was compared with that among patients who had not received cryoprecipitate., Results: Of 3996 trauma patients, 3571 had fibrinogen levels recorded. Most patients (n=3517, 98.5%) had initial fibrinogen counts of 1.0 g/l or higher, and cryoprecipitate was administered to a small proportion of these patients (n=126, 3.6%). Of the 54 patients with hypofibrinogenaemia on arrival, one patient died immediately and was excluded from further analysis. Of the 53 patients, 30 received cryoprecipitate and 28/53 died (53%). There was no difference in mortality between those who had received and those who had not received cryoprecipitate (14/30 vs. 14/23, P=0.31)., Conclusion: Administration of cryoprecipitate was uncommon during trauma resuscitation, even among patients with hypofibrinogenaemia on presentation. This study provides no evidence towards improved outcomes from administration of cryoprecipitate.

Objective: To describe the burden of road transport-related serious injury in Victoria, Australia, over a 10-year period, after the introduction of an integrated trauma system., Background: Road traffic injury is a leading cause of death and disability worldwide. Efforts to improve care of the injured are important for reducing burden, but the impact of trauma care systems on burden and cost of road traffic injury has not been evaluated., Methods: All road transport-related deaths and major trauma (injury severity score >12) cases were extracted from population-based coroner and trauma registry data sets for July 2001 to June 2011. Modeling was used to assess changes in population incidence rates and odds of in-hospital mortality. Disability-adjusted life years, combining years of life lost and years lived with disability, were calculated. Cost of health loss was calculated from estimates of the value of a disability-adjusted life year., Results: Incidence of road transport-related deaths decreased (incidence rate ratio 0.95, 95% confidence interval: 0.94-0.96), whereas the incidence of hospitalized major trauma increased (incidence rate ratio 1.03, 95% confidence interval: 1.02-1.04). Years of life lost decreased by 43%, and years lived with disability increased by 32%, with an overall 28% reduction in disability-adjusted life years over the decade. There was a cost saving per case of A$633,446 in 2010-2011 compared with the 2001-2002 financial year., Conclusions: Since introduction of the trauma system in Victoria, Australia, the burden of road transport-related serious injury has decreased. Hospitalized major trauma cases increased, whereas disability burden per case declined. Increased survival does not necessarily result in an overall increase in nonfatal injury burden.

Study Design: Retrospective review on prospective cohort and explicit chart review., Objective: To identify early spine trauma predictors of functional disability and to assess management compliance to established spine trauma treatment algorithms., Summary of Background Data: Identification of early (within 48 hours) spine trauma predictors of functional disability is novel and may assist in the management of patients with trauma. Also, with significant global variation, spine trauma treatment algorithms are essential., Methods: Analysis was performed on patients with spine trauma from May 1, 2009, to January 1, 2011. Functional outcomes were determined using the Glasgow Outcome Scale (GOS) at 1 year. Univariate and multivariate regressions were applied to investigate the effects of the injury severity score, age, blood sugar level, vital signs, traumatic brain injury, comorbidities, coagulation profile, neurology, and spine injury characteristics. A compliance study was performed using the SLIC and TLICS spine trauma algorithms., Results: The completion rate for the GOS was 58.8%. The completed GOS cohort was 4.2 years younger in terms of mean age, had more number of patients with severe polytrauma, but less number of patients with severe spinal cord injuries (ASIA [American Spinal Injury Association] A, B, and C) in comparison with the uncompleted GOS cohort. Multivariate logistic regression revealed 3 independent early spine trauma predictors of functional disability with statistical significance (P < 0.05). They were (1) hypotension (OR [odds ratio] = 1.98; CI [confidence interval] = 1.13-3.49), (2) hyperglycemia (OR = 1.67; CI = 1.09-2.56), and (3) moderate/severe traumatic brain injury (OR = 5.88; CI = 1.71-20.16). There were 305 patients with subaxial cervical spine injuries and 653 patients with thoracolumbar spine injuries. The subaxial cervical spine injury classification and thoracolumbar injury classification and severity score compliance studies returned agreements of 96.1% and 98.9%, respectively., Conclusion: Early independent spine trauma predictors of functional disability identified in a level 1 trauma center with high compliance to the subaxial cervical spine injury classification and thoracolumbar injury classification and severity score algorithms were hypotension, hyperglycemia, and moderate or severe traumatic brain injury. Spine trauma injury variables alone were shown not to be predictive of functional disability., Level of Evidence: 3.

Study Design: Retrospective cohort study., Objective: To identify early independent mortality predictors after spine trauma., Summary of Background Data: Spine trauma consists of spinal cord and spine column injury. The ability to identify early (within 24 hours) risk factors predictive of mortality in spine trauma has the potential to reduce mortality and improve spine trauma management., Methods: Analysis was performed on 215 spine column and/or spinal cord injured patients from July 2008 to August 2011. Univariate and multivariate logistic regression models were applied to investigate the effects of the Injury Severity Score, age, mechanism of injury, blood glucose level, vital signs, brain trauma severity, morbidity before trauma, coagulation profile, neurological status, and spine injuries on the risk of in-hospital death., Results: Applying a multivariate logistic regression model, there were 7 independent early predictive factors for mortality after spine injury. They were (1) Injury Severity Score more than 15 (odds ratio [OR] = 3.67; P = 0.009), (2) abnormal coagulation profile (OR = 6; P < 0.0001), (3) patients 65 years or older (OR = 3.49; P = 0.007), (4) hypotension (OR = 2.9; P = 0.033), (5) tachycardia (OR = 4.04; P = 0.005), (6) hypoxia (OR = 2.9; P = 0.033), and (7) multiple comorbidities (OR = 3.49; P = 0.007). Severe traumatic brain injury was also associated with mortality but was excluded from multivariate analysis because there were no patients with this variable in the comparison group., Conclusion: Mortality predictors for spine trauma patients are similar to those for general trauma patients. Spine injury variables were shown not to be independent predictors of spine trauma mortality.

Objective: To describe outcomes of major trauma survivors managed in an organized trauma system, including the association between levels of care and outcomes over time., Background: Trauma care systems aim to reduce deaths and disability. Studies have found that regionalization of trauma care reduces mortality but the impact on quality of survival is unknown. Evaluation of a trauma system should include mortality and morbidity., Methods: Predictors of 12-month functional (Glasgow Outcome Scale-Extended) outcomes after blunt major trauma (Injury Severity Score >15) in an organized trauma system were explored using ordered logistic regression for the period October 2006 to June 2009. Data from the population-based Victorian State Trauma Registry were used., Results: There were 4986 patients older than 18 years. In-hospital mortality decreased from 11.9% in 2006-2007 to 9.9% in 2008-2009. The follow-up rate at 12 months was 86% (n = 3824). Eighty percent reported functional limitations. Odds of better functional outcome increased in the 2007-2008 [adjusted odds ratio (AOR): 1.22; 95% CI: 1.05, 1.41] and 2008-2009 (AOR: 1.16; 95% CI: 1.01, 1.34) years compared with 2006-2007. Cases managed at major trauma services (MTS) achieved better functional outcome (AOR: 1.22; 95% CI: 1.03, 1.45). Female gender, older age, and lower levels of education demonstrated lower adjusted odds of better outcome., Conclusions: Despite an annual decline in mortality, risk-adjusted functional outcomes improved over time, and cases managed at MTS (level-1 trauma centers) demonstrated better functional outcomes. The findings provide early evidence that this inclusive, regionalized trauma system is achieving its aims.

The anti-estrogenic drug tamoxifen, which is used therapeutically for treatment and prevention of breast cancer, can lead to the development of thrombosis. We found that tamoxifen rapidly increased intracellular free calcium [Ca2+]i in human platelets from both male and female donors. Thus 10 microM tamoxifen increased [Ca2+]i above the resting level by 197 +/- 19%. Tamoxifen acted synergistically with thrombin, ADP, and vasopressin to increase [Ca2+]i. The anti-estrogen ICI 182780 did not attenuate the effects of tamoxifen to increase [Ca2+]i; however, phospholipase C inhibitor U-73122 blocked this effect. 4-hydroxytamoxifen, a major metabolite of tamoxifen, also increased [Ca2+]i, but other tamoxifen metabolites and synthetic derivatives did not. Three hydroxylated derivatives of triphenylethylene (corresponding to the hydrophobic core of tamoxifen) which are transitional structures between tamoxifen (Ca agonist) and diethylstilbestrol (Ca antagonist) increased [Ca2+]i slightly (6% to 24%) and partially inhibited thrombin-induced [Ca2+]i elevation (68% to 79%). Therefore the dimethylaminoethyl moiety is responsible for tamoxifen being a Ca agonist rather than antagonist. 4-Hydroxytamoxifen and polymer-conjugated derivatives of 4-hydroxytamoxifen increased [Ca2+]i, with similar efficacy. The ability of tamoxifen to increase [Ca2+]i in platelets, leading to platelet activation, and its ability to act synergistically with other platelet agonists may contribute to development of tamoxifen-induced thrombosis.