SECTION II: PATHOGENESIS OF BURN INJURY (INITIAL AND DELAYED)

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.

A. INITIAL INJURY

HEAT INJURY

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. 

INFLAMMATORY MEDIATOR INJURY (First to Third Day)

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.

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Mid Dermal Burn Injury
Treated with Topical Antibiotics

ISCHEMIA INDUCED INJURY

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.

MID-DERMAL BURN (Admission)

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

MID-DERMAL BURN (2 Days later)

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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.

Sect. ISect. III