The Burn Wound

The damage to epidermis and dermal elements from a burn is the result of several key insults which can be divided also into initial and delayed insults.

The most immediate and obvious injury is that due to heat. Excess heat causes rapid protein denaturation and cell damage. The depth of heat injury is dependent on the depth of heat penetration. Wet heat (scald) travels more rapidly into tissue than dry heat (flame). A surface Cl- temperature of over 60' C produces immediate cell death as well as vessel thrombosis. The dead skin tissue on the surface is known as eschar. The depth of burn is dependent on the temperature of the heat insult, the contact time and the medium (air-water). In addition, the depth of the skin layer is critical as the thinner the skin, the deeper the burn.

It is now clear that much of the tissue damage, especially in the perfused subsurface burn, is caused by toxic mediators of inflammation which are activated with the burn. Although onset of inflammation is required for healing, excess production of mediators especially oxidants and proteases will cause more capillary endothelial and skin cell damage. Early release of oxidants and increased proteolytic activity in the burn is now well recognized. C rent x ur evidence indicates that the inflammatory response initiated by the heat injury is responsible for further early tissue damage, increased capillary permeability and in large part responsible for the later wound conversion if inflammation becomes excessive. This now well established concept allows the care providers to intervene early and control the further mediator injury thereby limiting the final injury. The early use of both mediator inhibitors and skin substitutes is based on this concept. The clinician therefore has the potential of significantly modifying the degree of injury

Dermal Molecules Influencing Burn Wound Closure
Molecule	Source	Location
Collagen type I	Fibroblast	Dermis Supports epidermal cell attachment and migration
Collagen type IV	Epidermal cell, fibroblasts	Lamina densa Supports epidermal cell attachment and spreading
Collagen type V Fibronectin	Epidermal cells Fibroblasts	Basement membrane zone Basement membrane zone and wound surface with adhesion properties
Laminin	Epidermal cell	Epidermal cell adherence
Vitronectin	Serum	Promotes cell adhesion and spreading

INFLAMMATION INDUCED WOUND INJURY

Protease Release Injuring Healing Tissue and Deactivating Growth Factors
Oxidants Release Injuring Cells, Denaturing Proteins, and Activating Inflammation
Consumption of Wound Oxygen by Neutrophils Leading to Tissue Hypoxia
Increasing Stimulus to Fibrosis

Instant surface vascular thrombosis occurs along with cell death from the heat insult. Ischemia does not play a role in the initial surface necrosis. However, the injured capillaries below the surface, where tissue is still viable, can continue to thrombose due to initial heat and subsequent mediator injury, to endothelial cells, causing further ischemia and further tissue necrosis. Systemic hypovolemia or local impairment in perfusion due to constricting eschar or edema will produce the same effect.

B. DELAYED INJURY

Continued tissue damage can occur in the burn wound after the initial heat and mediator damage. The common element is ongoing inflammation perpetuated by surface eschar, bacterial colonization, mechanical trauma or that caused by topically applied antibacterial agents. Increased neutrophils, especially in exudate on the surface, results in increased damage to viable tissue by both neutrophil proteases and oxidants and neutrophil consumption of oxygen. Wound surface protease activity, particularly metalloprotease, has been noted to be markedly increased on open burn wounds. Of great importance is the fact that there is recent evidence that the proteolytic activity, on the normal partial thickness human burn, is markedly increased. This results in a net ongoing proteolysis in the burn both on the surface and in the matrix. Besides injury to new tissue formation, these proteases deactivate locally released growth factors, further impairing healing. This constant impediment to wound healing will stimulate further collagen synthesis, with subsequent increased scar, even in a mid-dermal burn. Eliminating surface exudate is a major goal of the use of occlusion dressing but active surface inflammation will persist.

However, only a wound closure using an adherent membrane or skin substitute will decrease the degree of surface inflammation as well as prevent surface exudate. Dead tissue or any residual exudate needs to be removed prior to an attempt at wound closure since this approach will not work unless the wound has a viable tissue wound surface to allow adherence.

CONTINUING BURN WOUND INJURY

ongoing inflammation caused by
- neurotic tissue
- bacteria on surface
- caustic topical agents
- surface exudate
excess wound proteolytic activity
- activated by surface insults
- continued damage to viable cells and new tissue growth
- damage to wound surface and matrix denaturation of growth factors
excess oxidant release
- injuring viable cells

Note red dermal surface free of exudate after initial cleaning prior to placement of topical antibiotic silver sulfadiazine

Note presence of eschar or pseudo eschar. Surface exudate is adherent and composed of denatured protein, inflammatory cells, and rich in surface metalloproteinase activity which can denature growth factors and increase the degree of injury.