A Review of the Local Pathophysiologic Bases of Burn Wound Progression

Abstract

Burn wound progression refers to the phenomenon of continued tissue necrosis in the zone of stasis after abatement of the initial thermal insult. A multitude of chemical and mechanical factors contribute to the local pathophysiologic process of burn wound progression. Prolonged inflammation results in an accumulation of cytotoxic cytokines and free radicals, along with neutrophil plugging of dermal venules. Increased vascular permeability and augmentations of interstitial hydrostatic pressure lead to edema with vascular congestion. Hypercoagulability with thrombosis further impairs blood flow, while oxidative stress damages endothelial cells and compromises vascular patency. A number of studies have investigated the utility of various agents in modulating these mechanisms of burn wound progression. However, as many of studies have used animal models of burn injury, often with administration of therapy preburn, obscuring the clinical applicability of the results to burn patients is of questionable benefit. An understanding of the complex, interrelated mediators of burn wound progression and their ultimate point of convergence in effecting tissue necrosis—cell apoptosis or oncosis—will allow for the future development of therapeutic interventions.

Quantitative assessment of graded burn wounds in a porcine model using spatial frequency domain imaging (SFDI) and laser speckle imaging (LSI)

“…Partial thickness burns (both superficial and deep) appeared pale/blanched throughout the spatial extent of the wound. All burn wounds were delineated by a prominent red ring representing the zone of hyperemia [37]. Superficial partial thickness burns were indistinguishable from deep partial thickness burns based on visual inspection as both burns appeared pale/blanched (Fig.…”

Toll-Like Receptor Signaling in Burn Wound Healing and Scarring

“…This ''burn wound progression'' is thought to result from progressive ischemia due to thrombosed vessels, increased capillary permeability, hypoperfusion, and oxidative damage, which are exacerbated by locally released signaling molecules from extracellular matrix and ruptured necrotic cells (i.e., DAMPs and PAMPs) that activate surviving proximal cells to produce inflammatory mediators. 14 In addition, burn progression likely involves ischemia/reperfusion (I/R) injury because burnedtissue blood flow on the day of injury fluctuated repetitively (Laser Doppler Imaging) in parallel to changes in base deficit. 15 In other types of tissue damage involving I/R injury, the importance of TLR signaling, including HMGB1-TLR signaling, has been demonstrated in a large number of in vivo studies (see Ref.…”

Honey and Medicinal Plants in the Management of Certain Surgical Bovine Clow Affections

“…[37] or Leptospermum scoparium [38] is documented. According to its in vivo studies; honey topical application is recommended in difficult surgical wounds such as burns [39]; chronic leg wounds [25]; venous leg ulcers [40] or diabetic foot lesions [41]. Carnwath et al (2014) tested in vitro the antimicrobial activity of different honey batches against 10 different bacterial species concluding that it may be effective topical treatment up to 16 concentration.…”