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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
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

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.
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