title: Vacuum-assisted closure therapy increases local interleukin-8 and vascular endothelial growth factor levels in traumatic wounds.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Division of Trauma Surgery, Department of Surgery, University Hospital Zürich, Zürich, Switzerland.
authors.forename: Ludwig
authors.initials: L
authors.lastname: Labler
authors.forename: Mario
authors.initials: M
authors.lastname: Rancan
authors.forename: Ladislav
authors.initials: L
authors.lastname: Mica
authors.forename: Luc
authors.initials: L
authors.lastname: Härter
authors.forename: Daniela
authors.initials: D
authors.lastname: Mihic-Probst
authors.forename: Marius
authors.initials: M
authors.lastname: Keel
mesh_terms: D000328:Adult; D000673:Amputation, Traumatic / Q000276:immunology / Q000473:pathology / Q000628:therapy; D001134:Arm Injuries / Q000276:immunology / Q000473:pathology / Q000628:therapy; D001706:Biopsy; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000097:blood; D005465:Fluorocarbon Polymers; D005597:Fractures, Open / Q000276:immunology / Q000473:pathology / Q000628:therapy; D006801:Humans; D015601:Injury Severity Score; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood*; D007869:Leg Injuries / Q000276:immunology / Q000473:pathology / Q000628:therapy; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D054843:Negative-Pressure Wound Therapy; D009389:Neovascularization, Pathologic / Q000276:immunology / Q000473:pathology; D009504:Neutrophils / Q000276:immunology; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000097:blood; D016038:Skin Transplantation; D017695:Soft Tissue Injuries / Q000276:immunology / Q000473:pathology / Q000628:therapy; D013524:Surgical Flaps; D042461:Vascular Endothelial Growth Factor A / Q000097:blood*; D014945:Wound Healing / Q000276:immunology; D014947:Wounds and Injuries / Q000276:immunology* / Q000473:pathology / Q000628:therapy*; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D005465:Fluorocarbon Polymers; D015850:Interleukin-6; D016209:Interleukin-8; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D042461:Vascular Endothelial Growth Factor A; D014841:von Willebrand Factor; D016222:Fibroblast Growth Factor 2; C010946:polytetrafluoroethane