Burn Wound Healing
INCREASE OF THE HEALING RATE OF BURN PATIENTS BY IMPROVING BURN WOUND MANAGEMENT METHODS.
Common causes of burn death include internal organ failure, severe infection, and inhalation injury, and burn wound management is closely correlated with these three complications, especially severe systemic infection. As a primary route of burn infection, burns wound, and especially deep burn wounds, are significantly related to the prognosis of burn victims.
Both tissue ischaemia and hypoxia develop in infected epidermal tissue in deep burn wounds, which may lead to fascial space syndrome, owing to compression of the extremities by necrotic eschar, and/or dyspnoea, due to chest compression. Ischaemic and hypoxic burn tissue is liable to be infected by bacteria and toxin.
The burn eschar is essentially necrotic tissue that is beneficial to the growth and proliferation of bacteria. In addition, burn toxin and multiple putrefied products can be released from necrotic eschar, leading to the development of systemic infection and intoxication. Special attention to the hazardousness of deep burn wounds and their removal and active and effective coverage as early as possible are therefore key steps if we are to free burn patients from the threat of infection and to raise their cure rate.
Tremendous advancements have been made in understanding the processes of wound healing. The cell types and the order in which they appear in the wound have been established; many growth factors and their functions have been elucidated. Despite the advances in understanding the science of wound healing, many more steps have yet to be discovered and elucidated. The frontier of this field includes the prevention of hypertrophic and keloid scar formation and, ultimately, any visual remnant of the wound.
An incision created by a scalpel, trauma resulting from a bullet, or tissue death caused by a myocardial infarction all undergo a similar and predictable reparative process. Understanding how the body repairs damaged tissue and what factors influence the wound healing process helps the surgeon ensure an acceptable outcome from surgery.
Wound Healing Growth Factors
Synonyms and related keywords: primary healing, wound closure, secondary healing, re-epithelialization, reepithelialization, tertiary wound closure, delayed primary closure, debridement, suture, inflammatory phase, proliferative phase, maturational phase, hemostasis, inflammation, collagen, clotting cascade, clotting, thromboxane A2, prostaglandin 2a, prostaglandin 2-alpha, vasoconstrictor, hemorrhage, vasodilatation, histamine, platelet, chemokine, epidermal growth factor, EGF, fibronectin, fibrinogen, histamine, platelet derived growth factor, platelet-derived growth factor, PDGF, serotonin, von Willebrand factor, clot formation, platelet degranulation, complement cascade, neutrophil, leukocyte, macrophage, monocyte, collagenase, interleukin, tumor necrosis factor, TNF, fibroblasts, transforming growth factor, TGF, keratinocyte, epithelialization, angiogenesis, granulation tissue formation, collagen deposition, insulin-like growth factor, insulinlike growth factor
| TYPES OF WOUND HEALING | Section 3 of 6    |
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The 3 categories of wound closure are primary, secondary, and tertiary. Primary healing involves closure of a wound within hours of its creation. Secondary healing involves no formal wound closure; the wound closes spontaneously by contraction and reepithelialization. Tertiary wound closure, also known as delayed primary closure, involves initial debridement of the wound for an extended period and then formal closure with suturing or by another mechanism.
| PHASES OF WOUND HEALING | Section 4 of 6 |
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The wound healing process has 3 phases. They are the inflammatory phase, the proliferative phase, and the maturational phase. The inflammatory phase is characterized by hemostasis and inflammation. Collagen exposed during wound formation activates the clotting cascade (both the intrinsic and extrinsic pathways), initiating the inflammatory phase. After injury to tissue occurs, the cell membranes, damaged from the wound formation, release thromboxane A2 and prostaglandin 2-alpha, potent vasoconstrictors. This initial response helps to limit hemorrhage. After a short period, capillary vasodilatation occurs secondary to local histamine release, and the cells of inflammation are able to migrate to the wound bed. The timeline for cell migration in a normal wound healing process is predictable (see Image 1).
Platelets, the first response cell, release multiple chemokines, including epidermal growth factor (EGF), fibronectin, fibrinogen, histamine, platelet-derived growth factor (PDGF), serotonin, and von Willebrand factor. These factors help stabilize the wound through clot formation. These mediators act to control bleeding and limit the extent of injury. Platelet degranulation also activates the complement cascade, specifically C5a, which is a potent chemoattractant for neutrophils.
The inflammatory phase continues, and more immune response cells migrate to the wound. The second response cell to migrate to the wound, the neutrophil, is responsible for debris scavenging, complement-mediated opsonization of bacteria, and bacteria destruction via oxidative burst mechanisms (ie, superoxide and hydrogen peroxide formation). The neutrophils kill bacteria and decontaminate the wound from foreign debris.
The next cells present in the wound are the leukocytes and the macrophages (monocytes). The macrophage, referred to as the orchestrator, is essential for wound healing. Numerous enzymes and cytokines are secreted by the macrophage. These include collagenases, which debride the wound; interleukins and tumor necrosis factor (TNF), which stimulate fibroblasts (produce collagen) and promote angiogenesis; and transforming growth factor (TGF), which stimulates keratinocytes. This step marks the transition into the process of tissue reconstruction, ie, the proliferative phase.
The second stage of wound healing is the proliferative phase. Epithelialization, angiogenesis, granulation tissue formation, and collagen deposition are the principal steps in this anabolic portion of wound healing. Epithelialization occurs early in wound repair. If the basement membrane remains intact, the epithelial cells migrate upwards in the normal pattern. This is equivalent to a first-degree skin burn. The epithelial progenitor cells remain intact below the wound, and the normal layers of epidermis are restored in 2-3 days. If the basement membrane has been destroyed, similar to a second- or third-degree burn, then the wound is reepithelialized from the normal cells in the periphery and from the skin appendages, if intact (eg, hair follicles, sweat glands).
Angiogenesis, stimulated by TNF-alpha, is marked by endothelial cell migration and capillary formation. The new capillaries deliver nutrients to the wound and help maintain the granulation tissue bed. The migration of capillaries into the wound bed is critical for proper wound healing. The granulation phase and tissue deposition require nutrients supplied by the capillaries, and failure for this to occur results in a chronically unhealed wound. Mechanisms for modifying angiogenesis are under study and have significant potential to improve the healing process.
The final part of the proliferative phase is granulation tissue formation. Fibroblasts differentiate and produce ground substance and then collagen. The ground substance is deposited into the wound bed; collagen is then deposited as the wound undergoes the final phase of repair. Many different cytokines are involved in the proliferative phase of wound repair. The steps and the exact mechanism of control have not been elucidated. Some of the cytokines include PDGF, insulinlike growth factor (IGF), and EGF. All are necessary for collagen formation (see Table).
The final phase of wound healing is the maturational phase. The wound undergoes contraction, ultimately resulting in a smaller amount of apparent scar tissue. The entire process is a dynamic continuum with an overlap of each phase and continued remodeling. The wound reaches maximal strength at one year, with a tensile strength that is 30% of normal skin. Collagen deposition continues for a prolonged period, but the net increase in collagen deposition plateaus after 21 days.
Currently, cytokines have a limited role in clinical practice. The only currently available commercial product proven to be efficacious in randomized, double blind-studies is PDGF, available as recombinant human PDGF-BB. In multiple studies, recombinant human PDGF-BB has been demonstrated to reduce healing time and improve the incidence of complete wound healing in stage III and IV ulcers. Many other cytokines currently under study in vitro include TGF-beta, EGF, and IGF-1.
Proper wound healing involves a complex interaction of cells and cytokines working in concert. In recent years, more chemical mediators integral to this process have been identified. The sequential steps and specific processes have not been fully differentiated. When examining the process of wound healing, one should identify the major steps and know the important mediators.
Collagen types and locations are as follows:
- Type I - Located in all connective tissue except hyaline cartilage and basement membranes
- Type II - Located in hyaline cartilage
- Type III - Located in distensible connective tissue (blood vessels)
- Type IV - Located in basement membranes
- Type V - Located in all tissues
- Type VI - Located in all tissues
- Type VII - Located in the dermal-epidermal junction
- Type VIII - Located in the Descemet membrane
- Type IX - Located in hyaline cartilage
- Type X - Located in hypertrophic cartilage and hyaline cartilage
Adapted from Bone et al, Cohen et al, and Sabiston et al
Burn Wound Healing
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