Burn is a complex trauma which severity is function of the total extent and proportion of deep burn the localization of the lesion and in particular the impairment of functional zones and finally the age of the patient Petite phrase qui dit que compare à d autres trauma la brulure a pour caractéristique d induire des dommages aux tissues qui complique la cicatrisation classique des tissus destruction cellulaire et du reseau vasculaire pas de flux sanguin Burn induces a local response with coagulative necrosis due to denaturation of protein and plasma membrane integrity Arturson 1996 211 Keck 2009 214 The gravity depends on the transferred energy the etiology of the burn and the time of exposure
After burn the evolution of the wound follows a gradient of severity from the center of the wound to the periphery Jackson 1953 69 with a zone of tissue loss coagulation zone at the center of the wound with a surrounding zone than can convert to necrosis due to poor tissue perfusion and with an outer periphery zone of the wound containing viable cells and characterized by hyperemia where vasodilation is mediated by local inflammatory mediator The two last zones can heal depending on wound care management and fluid resuscitation to avoiding burn wound progression due to progressive ischemia and increased capillary permeability Mettre un point sur burn conversion Necrotic burned tissues release large amount of toxic lipid protein Allgower 2008 72 and locally signaling molecules from extracellular matrix or necrotic cells named Damage Associated Molecular Patterns DAMPs DAMPS via the activation of TLR NF κ B pathway activate inflammasome leading to the production of large amount of inflammatory molecules Jeschke 2011 215 Manson 2012 217 Islam 2016 216 D Arpa 2017 220
This systemic inflammatory response can lead to shock with an increased in capillary permeability edema formation in the interstitial space increased systemic vascular resistance and a reduced metabolism cardiac output and hypovolemia requiring fluid resuscitation Figure xxx After around 3 days hypermetabolism response is observed in burn patients characterized by glycolysis lipolysis and proteolysis and finally loss of total body mass that are driven by catecholamines stress hormones and inflammatory mediators Hypermetabolim and hyper inflammation can persist for year and result in insulin resistance muscle catabolism immune suppression and organ dysfunction Jeschke 2011 215 while wound healing is delayed Elevated level of pro inflammatory cytokine consequently to sepsis interfere with local inflammatory response and has been related to delayed wound healing Sommer 2013 218 which is highly correlated with hypertrophic scarring in burn patients Cubison 2006 237 Lonie 2017 219 Independently of surface and depth cutaneous injury initiates a cascade of events that subtly regulate wound healing in term of timing and actors inflammation phase proliferation and re epithelialization phase and remodeling phase Eming 2014 212 Singer 1999 213
After injury debris and clotting reaction initiate inflammation phase essential to activate innate immune system This activation can prevent infection and allow degradation of necrotic tissue and also release cytokines and factors able to initiate proliferation phase During this second phase new tissue is formed with the deposition of extracellular matrix the formation of new vessels and re epithelialization begins from the edge of the wound Once re epithelialization is complete angiogenesis ECM deposition are decreased and myofibroblast enter in apoptosis while process of matrix remodeling begin figure XX Deregulation of one of this phase might alter tissue repair Immune response play a key role during wound healing and control the quality of the reparation to avoid fibrosis Eming 2009 227 Eming 2017 226 While inflammatory response is necessary for healing severe burns are characterized by a huge localized and systemic inflammatory response and a hypermetabolism that persist for more than a year with a significant increase of inflammatory cytokine cortisol and catecholamines Jeschke 2011 215 Figure xx As a consequence delay in repair of burn patient often occur mainly due to poor vascularity at wound site and high susceptibility to infection leading to often poor skin graft engraftment Several studies have also shown that in severe trauma such as burn Th1 response is diminished and Th2 response is enhanced and could be one reason of immunosuppressed state observed in severe burn patient Rani 2014 230 Jewo 2015 231 Kim 2017 229 In fact TNF α IL 10 ratio a TH2 response is inversely correlated to burn severity Tsurumi 2016 228 Another point that interfere with normal healing is that this inflammatory persistence are also correlated to late hypertrophic scarring Zhu 2016 232 In fact Kwan et al showed that early serum levels of IL 1 β and decorin and late serum levels of TGF β 1 can predict hypertrophic scar formation Kwan 2015 234 Other study of Tredget team showed that depletion of macrophages in subacute phase of healing following skin graft can limit hypertrophic scar formation Zhu 2016
233 This data were in correlation with Lucas results indicating that macrophage deletion during inflammatory phase lead to reduce granulation tissue formation angiogenesis and myofibroblast activation Lucas 2010 235 As a consequence proliferation phase Figure XX in severe burn patient seem to be delayed but persist a long time while remodeling phase is decreased compared to normal wound healing Gauglitz 2011 238
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