The burn wound is defined in terms of the evolving injury that occurs. Therefore the histological description is defined in terms of specific areas of pathologic change called zones. Three zones have been classically described. The actual pathophysiology is now recognized to be much more complex than the terms used for defining the zones.

A.   Zone of coagulation

This zone is comprised of the surface tissue necrosis of the initial burn eschar. The surface injury is caused mainly by the heat or chemical insult. Obviously this zone has an irreversible injury.

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Full thickness burn (admission)
Zone of coagulation is the depth of tissue necrosis which, in this patient, compress both s layers of skin

INSERT IMAGE OF Mixed Depth Burn

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Zone of coagulation varies markedly from center of burn which is full thickness, to the very periphery where all necrotic tissue has been removed

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Zone of necrosis has been removed. Wound bed is viable tissue although injured (zone of injury) beneath the surface

B.  Zone of Injury (Stasis)

Deep and peripheral to the zone of coagulation, there is a sizable area of tissue injury where cells are viable but can easily be further damaged. The terms "stasis" or "ischemia" were used because the progressive injury in this area was thought to be due to capillary thrombosis from injured endothelium, leading to ischemia-induced cell death. Fibrin deposition, vasoconstriction, and thrombosis indeed do occur, most likely as a result of continued release of mediators. However, early epithelial cell death in this area, unrelated to blood flow, is reported to be quite high, leading to slowing of healing. Epithelial cells are particularly prone to environmental insults such as desiccation- and inflammation-induced injury. This zone is most prominent in mid-to-deep-dermal burns where there is less reserve in the remaining viable cells and less blood flow.

Peripheral to and below the zone of stasis is the zone of hyperemia. The area is characterized by minimal cell injury but with vasodilatation due to neighboring inflammation-induced mediators. Completed recovery of this tissue is expected unless there is an additional severe insult such as an invasive infection or profound tissue inflammation.

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This mid-dermal burn has larger zone of injury than a more superficial burn

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DEEP DERMAL BACK BURN

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Deep dermal back burn (with full thickness on flank) Dry white to dry red appearance reflective of lack of surface blood flow. The zone of injury below the surface is at high risk for conversion to a full thickness wound.

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IMAGE OF FULL THICKNESS BURN TO BACK

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In a full thickness burn, the zone of injury can readily extend below the skin into subcutaneous tissues. The zone of hyperemia develops in the subeschar area being most evident beginning about 7 days post burn.

IMAGE OF ZONE OF HYPEREMIA

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Zone of hyperemia is very evident in this wound excised at day 10. The blood flow to this fatty tissue is markedly increased over normal sub-dermis vascularity.

D.  Wound Conversion

This term refers to the dynamic process whereby the Zone of Injury progresses to the Zone of Tissue Necrosis thereby deepening the wound. Conversion is more likely with a mid to deep dermal injury because of less blood flow, longer time to healing and increased risk of excess inflammation and infection. Also environmental hazards can readily lead to conversion of an open wound.

PARTIAL THICKNESS BURN

E.   ZONES OF INJURY IN TWO BURN DEPTHS

THE ZONES OF STASIS OR INJURY AND HYPEREMIA (reaction) are much larger in a mid dermal burn compared to a superficial burn. This larger zone of injury exceeds the increase in size of the zone of coagulation (necrosis) between the two depths. 

The reason is that 1) the best blood flow is present in the superficial dermis and ischemia is a greater risk beyond that point, 2) once through the epidermis, the heat transfer increases into the dermis such that a deeper area of heat and inflammatory injury results. A mid (or deep) dermal is much more prone to further injury during the treatment period.

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Partial Thickness Burn Image

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Mid to Deep Dermal Burn Treated with Silver Sulfadiazine

Admission: Post-cleaning

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Conversion can be noted on post-burn - Day 7

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Note: Increased thickness of eschar with exudate build-up

F.   BURN EDEMA

A layer of protein-rich edema fluid develops between the eschar (zone of coagulation) and the per fused, heat-injured micro vessels as a result of increased (heat and mediator-induced) micro vascular permeability. The leak is most prominent in the first 8-12 hours but can persist for days. In superficial burns, the edema actually physically separates viable and non-viable tissue, producing blisters, so that mechanical cleaning can remove the dead tissues. In deep second-degree and third-degree burns, the edema occurs throughout the injured tissue. However, the necrotic dermis remains physically adherent to the sub dermal space and requires sharp dissection (debridement) to remove the dead tissue or the process of necrolysis must occur. This process is deleterious due to the risk of infection and degree of tissue inflammation, as well as absorption of dead tissue. The degree of tissue edema is dependent on the amount of resuscitation fluid given and the vascular pressures perfusing the area.

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Note: Edema developing below the zone of coagulation is very prominent in facial burns

Sect. IISect. IV