[libribook.com] Traumatic Scar Tissue Management 1st Edition

Excessive Scarring
Excessive scarring was first described in the Smith papyrus around 1700 BC
(Berman & Bieley 1995). A few millennia later, Mancini & Quaife (1962) and
Peacock et al. (1970) differentiated excessive scarring into hypertrophic and
keloid scar formation and defined their distinguishing characteristics: both scar
types rise above skin level, but while hypertrophic scars do not extend beyond
the initial site of injury, keloids typically project beyond the original wound
margins (Gauglitz et al. 2011).
Excessive or pathophysiological scars form as a result of prolongations or
aberrations of physiologic wound healing and may develop following any injury
to the deep dermis, including burn injury, lacerations, abrasions, surgery,
piercings and vaccinations. Wound healing in pathophysiological scars is
characterized by a prolonged and stronger inflammation phase with
inappropriately released cytokines followed by a subsequent delay in the healing
response (Huang et al. 2013). Excessive scarring resulting in pain, pruritus,
adherences and contractures can affect quality of life, physically, physiologically
and psychologically (Gauglitz et al. 2011). Scar depth can have a negative
impact on the healing process and, subsequently, impact the functions of the
dermal layer and deeper layers of tissue (e.g. muscle, fascia).
Each year in industrialized nations, 100 million people develop scars as a result
of 55 million elective operations and 25 million operations due to trauma
(Gauglitz et al. 2011). From 55% to 100% of surgical patients will experience
postsurgical scar/adhesion complications that may not become evident until
months or years later (Diamond 2012).
Although there is extensive research on the pathophysiologic process of wound
healing and scar formation, there is still no consensus on the best treatment
strategy for preventing and reducing the issues associated with
pathophysiological scars (Van der Veer et al. 2009, Cho et al. 2014).