All breakages of the skin cause a cascade of biological reactions with the skin where the objective is to reestablish its functionality to the best quality and as quickly as possible. Scarring is unfortunately often a complex and unpredictable process, and it is not rare to see defective hypertrophic or keloid scarring processes develop.
In this way, all surgical acts or physical trauma to the skin raise the problem of scarring. It is unpredictable and requires careful consideration of the risk of developing hypertrophic or keloid scars, especially for those who are especially at risk.
The different phases of scarring
The skin is a physical envelope for our body. It plays a vital role, acting as a barrier and a regulating influence between the outside environment and the inside environment. In the presence of an acute of chronic wound, the body triggers a complex scarring process where the only objective is to succeed in closing the injured skin. We can distinguish 4 phases in the scarring process:
- The vascular phase or haemostasis
- The inflammatory phase
- The budding or epithelialization phase
- Development and remodeling phase
Most acute wounds (traumas, superficial burns, surgical...) evolve towards a normal scarring process, where the scarring time depends on the area, the depth and the texture.
Chronic wounds (ulcers, diabetic vascular lesions...) evolve towards a complicated scarring process where prevention tends to be the best treatment. Managing and caring for (chronic) wounds must be done under medical care because of the large risk of necrosis.
Many studies have demonstrated that scarring is much quicker in a damp atmosphere than in a dry atmosphere. A 2.5cm² pig wound under occlusive bandaging maintaining a humid atmosphere achieved 90% of scarring in 3 days, whilst scarring was only at 50% for a dry wound in open air. The wound treated with a current of warm air only achieved 18%.
The last stage of treatment for an acute wound is to exclude all systematic usage of local antiseptics or antibiotics.
The value of using antiseptics on injured skin is minimal compared to their potential side effects (systemic toxicity, germ selection, allergies, causticity...). Washing with saline solution or clear water and soap is sufficient.
With respect to antibiotics, it must be clarified that the bacterial flora, except for excess, is not detrimental, it even helps with cleaning. This detersion phase, essentially relates to gram-negative or anaerobic bacteria, which will spontaneously decrease with scarring, to be replaced by gram-positive cocci at the sprouting and epidermisation stages. Local antibiotics are therefore generally useless. Only silver sulfadiazine continues to be regularly used, in particular in burn centres.
Plasma exudation (escape of plasma from a cut or wound on the skin) initially constitutes an excellent culture environment due to the fibroblast and epidermis cells, and this must not be disturbed by an overly aggressive attitude (use of certain antiseptics or heavily aggressive bandaging).
Bandages, of all varieties, are the best assets for encouraging, or at least not disturbing, the scarring process, to protect the wound, to control pain, for their breathability, for being well tolerated by the skin, for being easy to change, comfortable, with an acceptable cost/efficiency benefit.
Bandages are classed into 3 large categories which are:
To this day, the different bandages available on the marker are spread out between the following large family groups:
Keloid scarring is defined as a fibrous proliferation from the skin’s root extensions in the form of “crab claws” developing for over 2 years. This is very common for black people and is a real nightmare for young women, especially when they are situated on exposed areas of the skin. The risk factors for keloids are strong pigmentation of the skin (for those with black or dark skin), blood groups (notably type A), age (from puberty to 30) and the location of physical aggression to the skin (sternum, ear lobe, lower part of the face, shoulder blade, neck, pubis), sun exposure of scars.
We have seen above that scarring develops in 4 phases: Hemostasis, Inflammation, Sprouting & Epithelisation, and finally Development and Remodeling. In a keloid, the Sprouting & Epithelialisation phase, also known as the proliferative phase, has an extended duration. This duration extends from the 21 maximum days for normal scars, to several months for a keloid scar. This hyperactivity of the fibroblasts will cause an overproduction of collagen. The absence of collagenase (the enzyme responsible for the destruction of collagen), combined with this overproduction of collagen will cause blistering in the area of the scar. The thus synthesised collagen fibres are 20 times more abundant than in normal skin.
Although the formation of keloid scars is shrouded in controversy, the TGF-β seems to be the principal factor in this abnormal proliferation of fibroblasts and production of collagen. This abnormal production of TGF-β is associated with an abnormally elevated concentration of T lymphocytes, macrophages and Langerhans cells resulting from the differentiation of keratinocytes.
Keloid scarring is a pathology specific to human beings (no other animal has developed keloids). This therefore explains the difficulties in understanding the physiopathology of this scarring anomaly, since there are no animal examples.
Although certain treatments exist to reduce the severity, at this time there are no satisfactory therapeutic solutions for this pathology.
The treatment of keloids must be, at best, preventative post surgery, for those who frequently suffer from keloids. After the appearance of the keloid, the most effective treatment generally lies in the combination of various complementary surgical, radio therapy and medical procedures (corticosteroid therapy).
Furthermore, diagnosing a keloid scar poses problems, and this dictates which therapeutic response to make. It’s similarity to hypertrophic scarring make it difficult to make decisions on which therapeutic route to take in the early stages, where it’s development can be the most effectively confused.
- Topical silicone gel
There is no real consensus for caring for keloids. The first choice is still intralesional corticoid injections. If this treatment is ineffective, intra-marginal surgery with or without corticoid injections or other molecules can be attempted. Radiotherapy must be reserved for only the most difficult cases. Pressotherapy and silicone gels will mainly be used as a preventative measure.
In general, the only way to defend against keloids, especially for the black population who are at risk, is to avoid all non-essential acts of aggression on the skin, especially on the sternum, ear lobe, the lower part of the face, shoulder blade, neck and pubis.