The injury area of burns skin is divided into necrotic and reaction layers from superficial to interior. 

The former results from physical injury, the latter from chemical reactions following thermal injury.

In accordance with pathogenesis characteristic of burns, the tissue in the thermal chemical reaction layer is gradually transformed to the progressive necrosis and inflammatory reaction layers, thus the unique morphological appearance of local pathology following burns injury is formed. 

There are three concentric zones of thermal injury from superficial to internal which exist in burns wounds (excepting first-degree burns).

1. The central ‘zone of necrosis’ is directly injured by the heat source, causing immediate cell death. 
2. Outside this zone is the ‘zone of stasis’ which is due to indirect thermal injury and chemical injury resulting from the circulatory stasis and tissue degeneration caused by progressive microcirculatory thrombosis. 
3. The outermost zone is the ‘zone of hyperemia’ where skin tissue experiences an inflammatory reaction caused by local thermal and chemical injury. This zone is characterized by a series of fully reversible pathomorphological changes including tissue edema, hyperemia, anoxia and exudation.

The pathological injury changes within the three zones reveal the most complicated biodynamics of all traumatic wounds. Apart from the natural changes among the three zones, their changes are also closely related to the administration of different clinical therapies. The application of a therapy which causes further injury to local wound may worsen the viability of all three zones. 

If no secondary injury is caused, the three zones may resolve in a natural process. 

However, if one uses a therapy which is protective and therapeutically effective to the tissue beneath the necrotic tissues, the progressive injury of the tissue in the zone of stasis may be prevented or reversed.

Though the necrotic layer of the burns wound surface is impossible to rescue, the management of necrotic tissue of burns wounds affects viable tissue in the deep layer. 

If the necrotic layer is left alone, a nonphysiological pressure exerted upon the underlying tissue results due to tissue dehydration and lack of normal skin elasticity. 

The pressure and increased microcirculatory blood concentration may lead to pressure ischemia with consequent anoxia thus aggravating the progressive necrosis of the underlying tissue.

Application of therapy characterized by dry, coagulation, formation of crust or eschar will cause lethal injury to stasis and hyperemia tissues, and thereby cause extension of the depth of the burn wound even to full-thickness necrosis.

However, if measures for losing the necrotic layer or preventing pressure to the underlying tissue are adopted, this full-thickness necrosis can be prevented and reversible changes of underlying stasis and hyperemia tissue may be attained.

Besides the aforementioned indirect factors, treatment of the zone of stasis is also affected by various direct factors. 

For example, the application method of crust/eschar formation characterized by drying, dehydration and protein coagulation, or maceration method may speed up the microcirculatory progressive thrombosis.

Alternatively, options exist for protecting the deep tissue which optimize the recovery of the tissue.

Repeated observation has taught the astute observer that the zone of hyperemia may recover naturally if no further injury occurs to the stasis tissues. 

Unfortunately, most typical burns treatments inadvertently allow progression of burn to necrotic tissue due to serious ischemia, anoxia and cell death.