Management of Atrophic scars
Goal is to make the scar unseeable or less conspicuous and erase the scar-related unpleasant memories.
Factors of Atrophic Scar Formation The formation of atrophic scar may be caused by multiple reasons. The following are a number of factors provoking the formation of atrophic scar:
- Loss of integrity the deep layers of the skin (dermis)
- Moderate edema and inﬂammation
- Low-intensity inﬂammation during phase 1 of cicatrization
- Particular areas of localization
- Scars resulting from animal or human bites (salivary ferments)
- Postsurgery/manipulation scars (e.g., cryodestruction of hemangioma)
- Acne scars
- Initial debridement errors (non ﬁxation of wound edges)
- Deﬁciency of oxygen, vitamin C, and other cofactors of collagen synthesis
Cascade of atrophic scarring
- Sluggish inflammation
- Low concentration of chemically active substances (TGF-β1 and TGF-β2)
- Low quantity of active fibroblasts
- Insufficient collagen synthesis
- Atrophic scar
The facial muscles are mostly mimetic; therefore, atrophic scarring of the facial tissues is observed in 90% of cases after injury or surgery Scar edges are in constant movement during muscle work, which gradually leads to dehiscence and sinking of skin. Atrophic scarring is frequently observed in children as a result of the work of the muscles of expression (laughter, crying, masticating, grimacing, etc.
Atrophic scars are most likely to be formed after animal bites. Apparently, this is because the saliva rich in enzymes (including proteolytic ones) get into the wound. Bite wounds take a long time to heal, are often infected, and are hard to treat. Scar edges in children and young people often dehisce because of the work of the expression muscles, whereas in elderly people the bottom of the scar sinks into the dermis , retracts, and forms solid ﬁbrous tissue.
Unlike bites, scratches leave a small, narrow, and delicate atrophic scar. Such scars are not deep; their bottom is typically on the papillary dermis level and might descend to the reticular dermis in sporadic cases. Their width supersedes the depth. Such scars are hard to resurface; any resurfacing results in spreading of the scar edges, with their depth remaining unchanged because resolution of collagen tissue continuity did not take place. Consequently, there is nothing to be restored. Operative surgery is conducted within the limits of sound tissues. Thus, the postsurgery scar is wider than the one before surgery. Notwithstanding the tenuity of such scars, they tend to cause more trouble and anguish than thick scars caused by accident or surgery.
Methods of Treatment for Fresh Scars
Scars are deemed fresh if they are less than 1 year old. Such scars are the most responsive to treatment: They respond to all types of therapy. With the process of maturation, viable connective tissue is developed in the scar, becoming rougher and less responsive to treatment. The ﬁrst 7–9 months are regarded as the most favorable period for treatment. The scar becomes fully formed after 12 months, subject to correction rather than treatment. Treatment starts with simpler methods, shifting toward more complex ones. Usually, treatment consists of several stages, and provided that adequate methods are chosen, the scar becomes practically indiscernible to the eye.
When treating fresh scars, commonly more than one method is applied. It is stipulated by the scar etiology, mechanism of origin, and the processes in the skin at the stages of its maturation. Identical scars never occur, even in one person. Therefore, there are no treatment patterns. With scar maturation, the treatment strategy also alters
The following are methods of treatment:
- Cryotherapy (cryohatching)
- Laser correction
More than 3,000 enzymes are being synthesized by the human body, with three to ﬁve involved in scar treatment. Predominantly, these are proteolytic enzymes and hyaluronidase. Proteolytic enzymes dilute necrotic mass, whereas hyaluronidase depolymerizes hyaluronic acid. Thereby, the wound quickly puriﬁes and intercellular matrix deliquesces, resulting in the formation of a soft elastic scar.
Hydration of wound
Hydrogel Local application for 2 months
The purposes of such applications are as follows:
- Maximal hydration of the scar formation zone
- Reduction of transepidermal water loss
- Acceleration of cell migration
- Increase of ﬁbroblast proliferation and synthetic
Facial injuries and post derma abrasion local application of hydrogel significantly reduces scarring.
The most common procedure among the machine skin treatment methods of fresh atrophic scars is dermabrasion with aluminum oxide microcrystals. Advantages of dermabrasion compared with other treatment methods are beyond dispute in view of the following:
First, it evens and improves the scar surface
Second, it clears away the epidermal (lipidic) skin barrier of the scar area along with epidermis, which enables medicinal products to penetrate freely into the skin.
Third, the scar bottom is elevated by the vacuum to the surrounding skin level, thus producing counteraction to myoﬁbroblasts, which draw the scar into derma.
Therefore, a scar close to normotrophic is being formed.
Early repeated microdermabrasion carried out within the shortest period of time after injury, inﬂammation, or postsurgery stitch removal is of great interest here. The procedure is performed multiple times (three to ﬁve times) at 3- 4-week intervals. Persistent scar fraction during the procedure enables elevating its bottom to the level of surrounding skin. Along with scar maturation, connective tissues are formed, with the scar becoming less ﬂexible and microdermabrasion losing its relevance. This is the reason for early repeated microdermabrasion being the most valuable.
For a microdermabrasion procedure to be effective, the processed area should be stretched between the thumb and pointer ﬁnger. The parameters are to be set so that the microcrystal ﬂow penetrates to the papillary derma level, namely, to pinpoint bleeding (−0.4 bar = −6 psi).
Microdermabrasion Side Effects and Complications
Because aluminum oxide microcrystal ﬂow penetrates into the skin to the papillary derma level, crusting is formed in the processed areas the following day . This is normal. Such crusts typically last 3–4 days and are eliminated independently. However, procedure-induced hyperemia may remain for several months. It is highly important to protect the skin from direct ultraviolet rays during this period. The procedure is repeated after 3–4 weeks, if applicable, despite the preserved hyperemia. Another frequent microdermabrasion side effect apart from hyperemia and crusting is secondary hyperpigmentation. It occurs 1–1.5 months after the procedure . Such pigmentation commonly subsides within 6–8 months without any treatment.
Microdermabrasion is not to be performed in hyperpigmentation-inclined patients and IV–VI skin phototypes (Fitzpatrick skin phototypes).
Fruit acid surface peelings (alpha hydroxy acid) do not produce signiﬁcant effect because they affect epidermis cells only. Medium and deep peelings are an effective method of fresh scar treatment. On acid burn, the skin receives a powerful stimulus for regeneration caused by the ﬂow of stem cells required for regeneration. However, there is an opinion that the stem cell resource is limited, and the more frequently peelings are performed, the more their resource is exhausted. One to three sessions commonly suffice for fresh scar treatment at 1.5- 2-month intervals.
Trichloroacetic acid (TCA) application is performed using local anesthesia with EMLA cream. Before acid application, the remaining cream is to removed with a dry cotton pad. Fresh 30–50 % trichloracetic acid solution is applied on the surface. Thorough and precise therapy requires that the acid shall be applied in two crisscross directions. The emergence of “frost” is stipulated by protein coagulation on the papillary derma level. This coagulated protein coating prevents the deeper layers of derma from acid penetration. Therefore, deacidiﬁcation is not applicable.
Nonablative lasers (585-nm pulsed dye laser [PDL]; 1,450nm diode; 1,320-nm Nd:YAG [neodymium-yttrium- aluminum-garnet], etc.) should only be used in fresh atrophic scar treatment. Epidermis remains intact after such a laser procedure. It is not necessary to apply ablative lasers in fresh scar treatment. It is not expedient because the risks of their application exceed the anticipated result. The potential source of skin regeneration is big enough. There are other methods of fresh scar treatment that are less aggressive but more efﬁcient.
Two sessions of vascular laser (PDL) treatment are given at 1.5-month intervals. The course of treatment is 3 months. The mechanism of elimination of the scar vascular component lies in red blood cell (RBC) exposure to high energy in the capillary lumen. These are capillaries that act as substrate for an erythematic scar. Light quantum erodes the RBCs in the capillary lumen by heating. Sort of a “microexplosion” occurs at the moment the capillary walls weld together. Gradually, the capillaries fade and resolve. The scar starts turning pale.
Collagen Induction Therapy
Dermaroller and dermapen therapy are most effective for atrophic scars
Mechanism of Action
When applying (rolling) the dermaroller, thousands of microscopic channels are formed on the skin. Such channels induce a chain of healing processes (hemostasis, inﬂammation, proliferation, remodeling). As a result of complex consecutive reactions, the ﬁbroblasts “patch” microscopic channels, and a powerful supporting block (patch) is formed from its own collagen islets.
Dissolution of collagen tissue continuity is induced by injury, hormonal changes, or destructive in ﬂ ammation in deep skin layers. In the areas with defective collagen ﬁbers, the skin sinks; thus, atrophic scars or stretch marks are formed. With the help of the dermaroller, an abundance of perforations 0.08–0.22 mm in diameter are formed. The depth of microneedle penetration ranges from 0.2 to 2.5 mm, depending on the problem intensity and its localization. One hundred and ﬁfty perforations may be performed per 1 cm 2. Abundant ﬁbroblast proliferation and collagen synthesis occurs in the puncture areas. Collagen islets gravitate to each other, gradually nearing the scar or stretch mark edges. An elastic supporting block is formed from fresh collagen tissue, and the size of atrophic scars and stretch marks is reduced because of retraction of their bottoms to the skin surface.
“Some products containing onion extract or Allium cepa (e.g., Contractubex, Mederma) shall not be applied in the treatment of atrophic scars and stretch marks. The onion extract has an antiproliferative effect on ﬁbroblasts. Such effect is unacceptable for atrophic scars with impaired collagen synthesis. Application of these products on the atrophic scars and stretch marks will further their retraction.”
Methods of Old Atrophic Scar Correction
Scars are deemed old if over 1 year. Such scars are capricious; their correction is more time consuming and requires more aggressive procedures. Along with scar maturation, an indurated connective tissue develops in the scar; it becomes more callous and less responsive to treatment, and it makes no difference whether the scar is 1 or 10 years old. They are equally hard to correct with any methods. Therefore, scars over 1 year are commonly subjected to surgical correction, although it is not always expedient. The newly formed scar is often worse than the presurgery one.
- Dermabrasion (Micro-)
- Auto ﬁbroblasts
- Laser correction
Fillers are all substances injected into an atrophic scar to align its relief . All ﬁller are divided into two groups: biological and alloplastic.
Biological implants include bovine collagen, autocollagen, allogenic collagen, autologic ﬁ broblasts, and fat. The alloplastic group incorporates silicone, micronized alloderma, polymethyl methacrylate, and polytetra Fuoroethylene. Filler injections are performed as a ﬁnal stage of atrophic scar correction. Peeling, dermabrasion, and electrophoresis are not to be performed after ﬁller injections as these procedures may boost destruction of biodegradable ﬁller and induce their complete resorption in the shortest timeframe.
Old postacne ice-pick scars and postchickenpox scars practically do not respond to this correction method. That is why by the time the scar fully matures, that is, scars are over 1 year old, bridles are formed in the scar bottom area, ﬁxing it in the derma. Whatever ﬁller is injected into derma, it will fail to elevate the scar bottom until ﬁbrosis ﬁbers are destroyed. In view of this information, initially subcision is to made with subsequent ﬁller injection, if applicable.
The subcision method was developed by David Orentreich, an American dermatologist. Its concept is as follows: Connective tissues are being developed by way of scar maturation, ﬁ xating its bottom to keep it in the derma. Scar subcision is performed by Nokor needle, preferably 18G. The bottom of the scar releases and draws to the surface after bridle subcision. The deﬁciency aligns.
In subcision, scar edges are ﬁxed with thumb and index ﬁnger. The needle entry is 3–4 mm away from the targeted subcision location. The needle is to enter slowly, slightly parallel to the skin surface, with reciprocating movements. The needle moves from side to side, releasing the tied scar bottom from the connective bridle. When cutting connective bridle, a characteristic clicking is heard, which indicates that the procedure is being properly conducted. A recess ﬁlled with blood is formed in the course of subcision. Fillers such as Restylane or Juvederm may be injected into the recess. Fillers of excipients are absorbed afterward, and in their place collagen is synthesize.
Punch excision (resection by punch, a circular knife) is applied in correction of deep ice-pick and boxcar atrophic scars after acne disease or chickenpox. The size of the punch must be slightly bigger than the scar. Under local anesthesia with 2 % lidocaine solution, the punch is entered into the skin with circular movements 1.0–2.0 mm vertical to the skin surface . The resected skin cylinder is elevated by mouse-tooth forceps and cut off by scissors. The edges of the de ﬁ ciency can be sutured by one stitch, glued by tissue adhesive (i.e., Dermabond) or stripped (Steri-Strip) in parallel to skin tension lines.
All laser systems (ablative, nonablative, pulsed, combined, plasma, etc.) are applied in old scar correction with a varying success rate. The majority induce collagen tissue recombination and stimulate new collagen synthesis in the skin.
Pulsed CO 2 Laser (10,600 nm)
The 10,600-nm pulsed CO 2 laser is applied mainly for correction of retracted postacne and chickenpox scars. Fresh scar treatment (6–10 weeks) shows better results compared to that for old scars. When exposed to high energy, epidermis vaporization and partial collagen coagulation in derma are induced. Collagen ﬁ brillae dehydrate and decrease. Because of these factors, skin tightening occurs. The tightening effect facilitates further induction of collagen synthesis.
Fractional lasers are a type of СО 2 lasers
The only difference is that the pulsed laser vaporizes all the surface exposed to the laser beam, whereas a fractional laser creates microchannels in the skin that are interspersed with intact skin. Fibroblasts are activated at the bottom of these channels, synthesizing collagen. These lasers are less traumatic and more efﬁcient in atrophic scar correction.
Short-Pulse Erbium: Yttrium-Aluminum-Garnet Laser (2,940 nm)
When vaporizing water from the reticular derma layer, collagen becomes more compact (consolidated), and ﬁbroblasts synthesize collagen in the freed space. Unlike СО 2 lasers, YAG lasers are characterized with signiﬁcantly low thermal effect. This is the so-called cold ablation with minimal thermal damage, enabling minimization of the risk of new scar formation and pain.
Duration and strength of postsurgery erythema is less expressed with the erbium laser compared to a СО 2 laser. An erbium or fractional laser is better to apply in small atrophic scar correction. These cause fewer adverse effects. A СО 2 laser is to be applied in correcting stretch marks, wide atrophic scars, and postchickenpox scars, which require collagen synthesis stimulation. Even though СО 2 laser application does not fully solve the problem of either scars or stretch marks, it does not incur high risks of adverse effects.
Pulsed Dye Laser
The PDLs at 585 or 595 nm wavelength are used in erythematic atrophic scar correction . Erythematic striae at the early stage of formation also provide a better response to laser treatment than in the ﬁnal stage. The mechanism of scar vascular component removal lies in the RBC high-energy exposure in the lumen, which is the red scar substrate. A PDL is better applied as a ﬁnal correction stage after resurfacing, cryodestruction, and so on, that is, after relief aligning. Because all machine-based relief correction methods facilitate the development of a venous capillary network in the scar, laser treatment of scar vessels is to be performed after the said procedures.
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