Hydrogel-impregnated dressings for graft fixation: a case series.

OBJECTIVE: Infection is the second most common cause of graft loss after skin grafting. Cutimed Sorbact is a range of dressings coated with a hydrophobic fatty acid that irreversibly binds to the bacterial surface and mechanically removes bacteria from the wound. The dressing is a hydrogel-impregnated material, which prevents wounds from drying. Here, we report on cases in which we used the gel instead of the widely used petrolatum gauze or paraffin gauze in a tie-over dressing for the fixation of grafted skin. METHOD: Patients treated for skin grafting between March 2013 and July 2013 were treated with the hydrogel-impregnated dressings and a tie over dressing. The wounds were opened five days after treatment. RESULTS: In total seven patients were treated with an age range of 23-86 years old. No infections were seen and the method was effective regardless of wound size, the thickness of the skin harvested and condition of the defect. CONCLUSION: Using this hydrogel-impregnated dressings, provide antibacterial and moisturising effects simultaneously, which a petrolatum or paraffin gauze cannot provide. DECLARATION OF INTEREST: There were no external sources of funding for this study. The authors have no conflicts of interest to declare.

Unusual cause of a facial pressure ulcer: the helmet securing the Sengstaken-Blakemore tube.

Many medical devices, such as pulse oximetry, ventilation masks and other splints are put on critically ill patients. Although these devices are designed to deliver relatively low physical pressure to the skin of the patient, they can still cause pressure ulcers (PUs) in critically ill patients. There are reports of medical device-related PUs on the face. Here we describe forehead skin necrosis caused by the securing helmet for the Sengstaken-Blakemore tube. It is difficult to detect this kind of PU early, because most of the patients have decreased mental status or delirium due to varix bleeding. For this reason, medical staff should be aware of the risk of developing a PU by the device and take preventive measures accordingly.

Differential expression of 11ß-hydroxysteroid dehydrogenase type 1 and 2 in mild and moderate/severe persistent allergic nasal mucosa and regulation of their expression by Th2 cytokines: asthma and rhinitis.

BACKGROUND: Glucocorticoids are used to treat allergic rhinitis, but the mechanisms by which they induce disease remission are unclear. 11ß-hydroxysteroid dehydrogenase (11ß-HSD) is a tissue-specific regulator of glucocorticoid responses, inducing the interconversion of inactive and active glucocorticoids. OBJECTIVE: We analysed the expression and distribution patterns of 11ß-HSD1, 11ß-HSD2, and steroidogenic enzymes in normal and allergic nasal mucosa, and cytokine-driven regulation of their expression. The production levels of cortisol in normal, allergic nasal mucosa and in cultured epithelial cells stimulated with cytokines were also determined. METHODS: The expression levels of 11ß-HSD1, 11ß-HSD2, steroidogenic enzymes (CYP11B1, CYP11A1), and cortisol in normal, mild, and moderate/severe persistent allergic nasal mucosa were assessed by real-time PCR, Western blot, immunohistochemistry, and ELISA. The expression levels of 11ß-HSD1, 11ß-HSD2, CYP11B1, CYP11A1, and cortisol were also determined in cultured nasal epithelial cell treated with IL-4, IL-5, IL-13, IL-17A, and IFN-γ. Conversion ratio of cortisone to cortisol was evaluated using siRNA technique, 11ß-HSD1 inhibitor, and the measurement of 11ß-HSD1 activity. RESULTS: The expression levels of 11ß-HSD1, CYP11B1, and cortisol were up-regulated in mild and moderate/severe persistent allergic nasal mucosa. By contrast, 11ß-HSD2 expression was decreased in allergic nasal mucosa. In cultured epithelial cells treated with IL-4, IL-5, IL-13, and IL-17A, 11ß-HSD1 expression and activity increased in parallel with the expression levels of CYP11B1 and cortisol, but the production of 11ß-HSD2 decreased. CYP11A1 expression level was not changed in allergic nasal mucosa or in response to stimulation with cytokines. SiRNA technique or the measurement of 11ß-HSD1 activity showed that nasal epithelium activates cortisone to cortisol in a 11ß-HSD-dependent manner. CONCLUSIONS AND CLINICAL RELEVANCE: These results indicate that the localized anti-inflammatory effects of glucocorticoids are regulated by inflammatory cytokines, which can modulate the expression of 11ß-HSD1, 11ß-HSD2, and CYP11B1, and by the intracellular concentrations of bioactive glucocorticoids.