Vacuum-assisted closure therapy increases local interleukin-8 and vascular endothelial growth factor levels in traumatic wounds.

BACKGROUND: Clinical observations are suggesting accelerated granulation tissue formation in traumatic wounds treated with vacuum-assisted closure (VAC). Aim of this study was to determine the impact of VAC therapy versus alternative Epigard application on local inflammation and neovascularization in traumatic soft tissue wounds. METHODS: Thirty-two patients with traumatic wounds requiring temporary coverage (VAC n = 16; Epigard n = 16) were included. At each change of dressing, samples of wound fluid and serum were collected (n = 80). The cytokines interleukin (IL)-6, IL-8, vascular endothelial growth factor (VEGF), and fibroblast growth factor-2 were measured by ELISA. Wound biopsies were examined histologically for inflammatory cells and degree of neovascularization present. RESULTS: All cytokines were found to be elevated in wound fluids during both VAC and Epigard treatment, whereas serum concentrations were negligible or not detectable. In wound fluids, significantly higher IL-8 (p < 0.001) and VEGF (p < 0.05) levels were detected during VAC therapy. Furthermore, histologic examination revealed increased neovascularization (p < 0.05) illustrated by CD31 and von Willebrand factor immunohistochemistry in wound biopsies of VAC treatment. In addition, there was an accumulation of neutrophils as well as an augmented expression of VEGF (p < 0.005) in VAC wound biopsies. CONCLUSION: This study suggests that VAC therapy of traumatic wounds leads to increased local IL-8 and VEGF concentrations, which may trigger accumulation of neutrophils and angiogenesis and thus, accelerate neovascularization.

Bilateral hand transplantation: bone healing under immunosuppression with tacrolimus, mycophenolate mofetil, and prednisolone.

PURPOSE: Little is known about bone healing after composite tissue transplantation that requires pharmacologic immunosuppression. Bone integration and callus development were assessed in bilateral hand transplantation. METHODS: In this study the course of callus development and callus maturation were assessed by color Doppler sonography and radiography in a double hand transplant and compared with forearm replantation. RESULTS: After hand transplantation, ingrowth of small vessels at the bone junction was observed at week 3, calcified callus became visible at month 4, and bone union was completed at month 11. A similar time course of bone integration was observed after replantation. Plating offered sufficient stability. A recipient periostal flap is thought to have improved blood supply and favored development and induction of callus. CONCLUSIONS: Bone healing after hand transplantation under immunosuppression with tacrolimus, mycophenolate mofetil, and prednisolone is identical to that after forearm replantation.

Macrophage activation decreases macrophage prostaglandin E2 release in experimental trauma.

Prostaglandin E2 (PGE2) derived from macrophages following trauma may contribute to trauma-induced immunosuppression. This study evaluated the effect of glucan, a macrophage-activating agent, on macrophage PGE2 release in a murine trauma model. ICR/HSD mice were administered D5W, glucan pre-trauma, or glucan post-trauma, and subjected to hindlimb crush and amputation injury. Splenic macrophages were isolated 24 hours following trauma, cultured (24 hrs), and macrophage PGE2 levels were determined. In-vitro marrow proliferation was assessed as a measure of immune function. Crush-amputation injury increased (184%) macrophage PGE2 release. In contrast, glucan administration (pre or post) reduced PGE2 levels in macrophage supernatants (71% and 85%, respectively). A 52% decrease in in-vitro bone marrow proliferation was observed following trauma. Glucan pre- or post-trauma eliminated the suppression of bone marrow proliferation. In conclusion, macrophage-activating immunomodulators may exert beneficial effects following trauma by: 1) reducing macrophage PGE2 synthesis and release; and 2) reducing traumatic suppression of bone marrow proliferation.