Scars are produced as the end result of wound healing. Instead of replacing damaged tissue with regenerated identical tissue, humans and most animals heal wounds by filling the wound with scar. In theory, this allows faster yet less perfect wound healing. However, today most people would rather their wounds heal without scarring, even if this requires more time.
Scars can be limiting and disfiguring, particularly when the injury is extensive. The amount of scar produced is a consequence of many factors including: the extent of traumatized tissue around the wound, how long the wound remains open, the anatomic location, and genetically determined healing factors. When more scar forms than is desirable, the scar is considered hypertrophic. Initial rapid growth, then gradual fading and shrinkage characterize hypertrophic scars over several years. This often leads to widened, unattractive skin defects.
Some individuals have a genetically inherited disease characterized by extreme excess scar production. These scars are called keloid scars. Keloid scars are very different than hypertrophic scars, although they do share some common features. Keloid scars tend to become much larger than the original wound. They usually persist and reoccur after surgical excision.
Avoid: direct sun exposure, mechanical trauma, harsh perfume soaps, irritating chemicals such as alcohol or peroxide.
Do not soak the incision with creams and moisturizers
Use topical anti-inflammatory agents: NSAIDs (i.e. Avosil) have fewer side effects than steroids (i.e. cortisol). Antihistamines (i.e. diphenhydramine) can be effective as well.
Maintains health hydration and raises scar temperature.
Adhesive gel sheeting, elastic wraps or snug sportswear immobilize and reduce mechanical tension
In order to discuss the prevention and treatment of hypertrophic and keloid scars, a discussion of important aspects of wound healing is essential. There are three principal phases in the wound healing process: inflammation, transitional repair, and maturation.
Immediately following tissue injury, proteins released from the injured tissue and blood initiate the first stage of wound healing called the inflammation phase. The amount of blood released, extent of tissue damage and bacteria content are the primary determinants of the intensity of inflammation. The major object of this phase is to gain immunologic control of the wound. In general, wounds do not become sterile until it regains an epidermal cover. Thus, the length of time until wound closure is also important in determining the extent of wound inflammation.
The next phase is called transitional repair. During the transitional repair phase, the density of cells in the tissue around the wound increases. Under normal conditions, this stage begins several days after the injury and lasts several weeks. However, if injury is severe this phase will persist longer. New vessels and epithelium are formed as rapidly as possible to maximize the tissue replacement dynamics. Most wound cells are maximally active and are very sensitive to factors that regulate cell growth and tissue matrix synthesis. Also, enzymes are released into the extra-cellular fluid to activate a simultaneous matrix breakdown process. The balance between tissue degradation and biosynthesis permits remodeling of the temporary tissue matrix of collagen and other proteins and also determines the net amount of scar tissue produced.
The maturation phase is the final phase of wound healing and it begins in 6-12 weeks after wounding. When enough transitional matrix is produced, a turn-off signal is received, which initiates the maturation stage characterized by cellular apoptosis and a shift in balance of scar remodeling toward scar degradation. This process is accompanied by extracellular matrix reorganization and degradation. Tissue degrading enzymes released during the transitional repair phase continue to breakdown the extracellular matrix at a rate largely determined by physical and biochemical factors in the matrix. Additional extra-cellular matrix biosynthesis is controlled by the need for tissue strength and other operational parameters. Mechanical stress is an important deterministic parameter in the amount of scar production.
In summary, the most important known determinate of the amount of scar production are the magnitude and duration of inflammation, the magnitude of mechanical tension acting on the scar, and the genetic phenotype of the individual.
The terminology used to describe scarring remains confusing. Generally, a hypertrophic scar is a thick, disfiguring scar that is usually raised above the skin surface. The criteria are very qualitative. A keloid scar is a scar that forms in a person that has keloid disease; a disease which leads to tumor-like scars whenever a wound forms.
Basically, factors that increase or prolong wound inflammation or wound tension predispose an individual to hypertrophic scar formation. These factors include wound infection, prolonged healing by secondary intention or foreign materials in the wound. Several reports concluded that there are substantial increased risks for hypertrophic scarring in burn wounds that take longer than 21 days to heal. The incidence of hypertrophic scarring following surgery is about 40-70%, whereas it is higher (up to 91%) following burns.
Too much mechanical skin tension on the healing wound is another major non-genetic cause of excess scarring. Therefore, scars located in certain areas of the body (e.g. sternum, deltoid and upper back) are frequently hypertrophic. This anatomic dependency seems to correlate with anatomic patterns of skin tension.
A hereditary pattern in hypertrophic scarring is not described, although populations with higher skin melanin content are known to have a higher incidence of hypertrophic scars. These populations include African, Asian and Hispanic people. A hormonal etiology is also known to be a factor, with hypertrophic scarring often initiated at the start of puberty or during pregnancy. The natural history of hypertrophic scars is that they regress with time after injury, leaving behind an unsightly wide gap of thinned dermis between wound edges.