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The objective of this study was to report on the safety, efficacy and clinical outcomes of the Polyax Locked Plating System (Biomet, Warsaw, IN, USA) in the management of acute (non-implant related and periprosthetic) distal femoral fractures. We retrospectively reviewed 71 patients with 73 distal femoral fractures. Thirty-three of the included fractures occurred around previously placed implants. The average patients' age was 67 years (range 18-98). There were 7 early postoperative complications (9.5%) including one deep surgical site infection, 2 pulmonary embolisms and 4 urinary or respiratory infections. At final follow-up (mean 12, range 9-55 months) all fractures progressed to clinical and radiological union. However, major revision surgery for healing problems was required in 5 cases (6.8%) and minor in 3 cases (4.1%). The average time to healing was 6 (range 3-23) months. Angulation less than 5 degrees in any plane was observed in 66 cases (89.7%), within 5-10 degrees in 5 cases (7.3%) and within 10-15 degrees in 2 cases (2.9%). The mean pre-injury and final follow-up values of Glasgow Outcome Scale were 1.5(1-3) and 1.7(1-3) respectively. Overall 61 patients (83.53%) retained their pre-injury activity status. The Polyax Locked Plating System offers a safe and efficient fixation in distal femoral fractures., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Single-pass, whole-body computed tomography (pan-CT) was proposed in the late 1990s as a new concept for the diagnostic work-up of severely injured patients. Since its introduction, it has led to considerable debate among clinicians and scientists, triggered by concerns about its immediate safety, questionable therapeutic advantages and exposure to radiation. However, it was recently shown that pan-CT scanning may be associated with a reduction in trauma mortality. In this article, we provide an overview of current knowledge of the value of this compelling concept. The diagnostic accuracy of multidetector row CT (MDCT) for clearing various anatomical regions in trauma patients is, at best, unclear. Little is known about the accuracy of pan-CT as a whole, which weakens statements about its effectiveness and prevents inferences about survival advantages. This last point may be explained by a stage-migration or "Will Rogers" phenomenon: Pan-CT increases injury severity by detecting lesions that would not have been recognized by conventional methods but still do not affect treatment decisions, thus artificially lowering the ratio of observed to expected deaths. In order to maintain the credibility of pan-CT technology for trauma, a rigorous, large-scale evaluation of its accuracy is required. Such an evaluation requires consensus about the definition of true and false positive and negative findings in the setting of blunt multiple trauma. In addition, triage criteria need to be refined to increase specificity and reduce the number of unnecessary scans.

We previously reported that chronic exposure of adult male rats to morphine by pellet implantation has no effect on corticosterone secretion but causes a marked testosterone-dependent increase in CBG. In the studies reported here, we examined the effects of chronic morphine on the pituitary-adrenocortical axis of male rats prior to the developmental rise in testosterone. In contrast to adults, morphine had little effect on CBG in peripubertal males. We found nothing remarkable with regard to basal hormone levels; morphine caused only a transient increase in ACTH and corticosterone in juveniles. However, while the pituitary-adrenocortical response to mild stress was normal in adults exposed to morphine, it was markedly increased in juveniles. After 7 days of morphine exposure, the stress response was as much as 2.5 times greater than normal in morphine-treated juveniles. This exaggerated response to stress did not appear to be due to the passive withdrawal of morphine or to an additive effect of stress plus morphine. Instead, morphine may either increase the perceived severity of stressors or decrease sensitivity to the negative feedback effects of stress levels of corticosterone in juvenile males. Either way, there is a striking shift in morphine's effects on the pituitary-adrenocortical axis across development.

We previously reported that morphine increases the concentration of corticosteroid-binding globulin (CBG) in blood of male, but not female, rats. This pronounced sexual dimorphism suggested that CBG upregulation by morphine might be androgen-dependent. In the current studies, we found that castration, whether performed just before or just after puberty or in adulthood, increased the concentration of CBG in adult male rats. Naltrexone did not prevent this increase and, therefore, it does not appear to be attributable to the release of endogenous opioids. Exposure to morphine for 1 week in adulthood increased ( approximately 100%) the concentration of CBG in intact, i.e., sham-castrated, males. The CBG levels of castrated rats treated with morphine did not differ from those of intact rats treated with morphine. However, because castration increased the concentration of CBG, the difference between the placebo and morphine groups decreased with time after castration. At 4 weeks after castration, the difference between the morphine and placebo groups (19%) was no longer statistically significant. Testosterone replacement prevented the rise in CBG levels following castration and maintained the magnitude of the difference between placebo and morphine-treated rats within the normal range. Thus, testosterone appears necessary for morphine effects on CBG to be fully manifested.