Summary Patient preparation for hand surgery often necessitates skin preparation via the use of an assistant to hold the arm to be operated on in mid-air while disinfectant is applied. This study introduces a three-dimensional printed arm stand that decreases dead time during skin preparation, while also enabling the more efficient use of an assistant. The arm stand devices were customized on the anatomy of the patients and then successfully used on patients having general or regional anesthesia. A practical, reusable, and effective three-dimensional printed arm stand has been developed and applied on both adult and pediatric patients. We have found the bespoke device to be beneficial in terms of reducing theater dead time and overall costs, while increasing the efficiency of an upper limb operating theater list. The rapid prototyping cycle afforded by 3D printing renders this technology a valuable tool for developing medical devices with patient-precise dimensions.

In this study we collected and analysed data of the severe burn patients at our institution over an 11-year period in order to shed light on the controversial role of bloodstream infection (BSI) as a predictive factor for mortality in this burn population. The factors examined were age, total body surface area, smoke inhalation, presence of BSI, and BSI with resistant bacteria. In total 1081 burn patients were hospitalized from 2001 to 2011, of whom 4% died. We focused here on 158 severe burn patients, 74 of whom developed BSI, and 35 who died. Using univariate analysis, it appeared that the BSI group had a threefold greater chance of mortality compared to the non-BSI group. Patients with a Ryan score 3 had a 100% chance of mortality and those with a score 0 had 0%. Thus, focusing only on Ryan score 1 and score 2 patients, BSI did not contribute to mortality, nor was it shown to contribute to mortality in a multivariate analysis in which the score and BSI were included together. When BSI did occur, it predicted longer hospitalization periods. We conclude that BSI predicts longer length of hospitalization stay but does not contribute to the prediction of mortality beyond that offered by the Ryan score in a severe burn population.

Background:Fat grafting is an increasingly popular method of augmentation/reconstruction of soft tissue defects. However, the clinical unpredictability and high resorption rates of the grafts remain problematic. Cellular stress from the harvest and the ensuing ischemic episode may be the cause of this. Cellular stress activates the p38 mitogen–activated protein kinase (MAPK) signaling pathway. In response to cellular stress, the p38 pathway can lead to apoptosis and can negatively regulate cell proliferation. Inhibition of p38 in ex vivo experiments has been shown to promote the expansion of human cord blood hematopoietic stem cell and improve the adipogenesis process through its upstream regulator, Shp2. Because of its wide-ranging cell regulation and antiinflammatory properties, large-scale clinical trials using p38 inhibitors are also currently being performed, especially for therapeutic effect in chronic obstructive pulmonary disease and asthma. The rationale for our study was that the treatment of fat grafts with p38 inhibitor would (a) prevent apoptosis of adipose-derived stem cells in the fat grafts, (b) increase adipose-derived stem cells proliferation, and (c) stimulate the release of several angiogenic factors and promote revascularization.Methods:Clinical and histological testing was performed on 5 fat-transplanted (1 mL) CD-1 nude mice compared with the test group of 5 mice, which were injected with a p38 MAPK inhibitor at 1, 3, 6, and 9 days after the fat transplantation.Results:The weights and volumes of the control group grafts were significantly higher than those of the p38 MAPK inhibitor–treated grafts. Average volume resorption was 36% in the control group and 92% in the test group. Histological evaluation of the grafts revealed significantly improved integration, with a significant reduction of fibrosis and inflammation in the control group versus the treated group.Conclusions:This preliminary study suggests that as opposed to our hypothesis, inhibition of p38 significantly increases fat graft resorption. The dramatic effects observed in our study may suggest that p38 may act differently on the numerous cell types that constitute the fat graft, and further investigation is necessary.

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