The Problem Being Treated
Universally, nearly everyone has or will experience a scar at some point in their life. Irrespective of the cause of the scar, the wound-healing process may result in either a “normal” scar or, in some, a pathologic scar, such as a hypertrophic, keloid, or atrophic scar. Initially, normal scars appear erythematous with an irregular surface. As the wound-healing process continues, the mature scar may acquire a skin-colored tone, and its surface may become more even and flat. Histology of normal scars shows hyalinized collagen lying parallel to the surface of the skin, with a decreased amount of elastic fibers.
Patients with scars usually seek treatment due to their unfavorable cosmetic appearance, which may result in psychologic burden and social withdrawal. The additional presence of associated symptoms, specifically in patients with hypertrophic scars and keloids, as well as contractures and functional compromise, may also incite the patient to seek treatment.
Hypertrophic Scars and Keloids
Hypertrophic scars arise as red, raised, firm scars that are limited to the incision or original injury site ( Fig. 5.1 ). They are frequently linear, and a significant percentage are accompanied by sensation abnormalities, such as pruritus. Hypertrophic scars may be located anywhere on the body, although areas under constant pressure and stretching are more commonly affected.
Keloids are clinically described as erythematous, hyperpigmented, or even purple nodules that extend beyond the boundaries of the original injury ( Fig. 5.2 ) and can be associated with abnormal sensations. They are frequently disfiguring and may result in functional impairment. Keloids can appear within weeks or years following the original cutaneous insult. The most common locations for keloids are the earlobes, anterior chest, shoulders, and upper back. Besides the usual cutaneous injuries that cause scarring, keloids may also result from ear piercing, abrasions, tattooing, and vaccinations. Complete resolution of keloids is very difficult, as they do not spontaneously regress and have high recurrence rates with most therapies, reappearing even years later. There is a familial and ethnic predisposition to the formation of keloids, with darker-skinned individuals having a higher incidence.
Although the precise mechanism has not been established, multiple disturbances in the wound-healing process have been implicated in the development of hypertrophic scars and keloids. The development of excessive scar tissue seen in these types of pathologic scars may be due to either excessive matrix deposition, reduced collagen degradation, or both. Fibroblasts from keloids show an abnormal response to stimulation, producing high levels of collagen, especially type I. On the other hand, fibroblasts in hypertrophic scars exhibit a normal response when exposed to growth factors and show a moderate increase in collagen synthesis.
Transforming growth factor-β linkage to increased collagen and fibronectin deposition has also been involved in the pathogenesis of excessive scarring. Furthermore, collagen fibers in these types of scars are arranged as whorled, hyalinized bundles. Other factors implicated in the development of hypertrophic scars and keloids are hyaluronic acid, proteoglycans, and mast cells, among others.
Atrophic Scars
Although atrophic scars are commonly seen in patients with a history of acne ( Fig. 5.3 ), other conditions such as varicella, surgery, and trauma may also result in atrophic scarring. Striae distensae (or “stretch marks”) are also types of atrophic scars; initially, they can appear as pink, erythematous areas of thinned skin (striae rubra) that gradually darken ( Fig. 5.4A ). As the striae mature, they acquire a white coloration (striae alba) parallel to skin tension lines ( Fig. 5.4B ).
Atrophic acne scars result from active acne lesions arising within the pilosebaceous follicles. The presence of Cutibacterium acnes is essential in the development of inflammatory acne, and the degree of inflammation determines the risk and amount of postacne scarring. Acne scarring typically originates from deep inflammatory reactions that involve the destruction or loss of connective tissue with dermal atrophy and fibrosis. During the maturation phase, the scar contracts and pulls the surface layers, causing skin indentation.
Acne Scars
Based on the acne scar’s width, depth, and three-dimensional architecture, a classification of acne scars into three types is utilized: icepick scars, rolling scars, and boxcar scars ( Fig. 5.5 ). Icepick scars are seen as narrow and deep with decreasing width as they extend into the dermis ( Fig. 5.6 ) and are typically managed with the trichloroacetic acid (TCA) chemical reconstruction of skin scars (CROSS) technique rather than light and energy-based devices. Rolling scars have a wide surface with margins that give a “rolling” appearance to the skin. Also with a wide surface, the boxcar scar type is limited by well-demarcated vertical borders. Rolled and boxcar atrophic acne scarring often coexist ( Fig. 5.3 ) and can be managed with light and energy-based devices.
Even though atrophic scars are the most common type of postacne scarring, some patients may also present with hypertrophic scars and keloids ( Fig. 5.7 ). In contrast to hypertrophic scars and keloids, which result from excessive collagen deposition and scar tissue formation, atrophic scars result from connective tissue destruction with dermal atrophy and fibrosis.
Erythematous Scars
Erythema refers to the excessive redness or hyperemic appearance of skin. Erythema is a common feature of scars ( Fig. 5.8 ), signifying capillary dilation during wound healing and angiogenesis, or proliferation of new vessels, in the maturation phase of scar formation. Although capillary dilation and angiogenesis typically regresses as scars mature, keloids and other hypertrophic scars are characterized by persistent erythema due to the constant presence of new vessels in the area. Persistent erythema is an important feature and guides decision making in scar management.
Scar Dyspigmentation
Scar hyperpigmentation is a result of hemosiderin or, more commonly, melanin deposition ( Fig. 5.9 ). Though not fully understood, scar hyperpigmentation is believed to occur via a mechanism unrelated to that of ultraviolet-induced skin hyperpigmentation. Focal hyperpigmentation is commonly seen in the form of traumatic tattooing. Traumatic tattoos have a typical black or blue-gray appearance and occur when foreign material is embedded into the skin following injury ( Fig. 5.10 ).
Hypopigmented and depigmented scarring often accompanies hyperpigmentation ( Fig. 5.11 ) and is typical of traumatic, burn, and surgical scars but can also be seen after fully ablative resurfacing and deep chemical peeling. The pathophysiology of scar hypopigmentation or depigmentation is thought to be due to a mechanism other than melanocyte deficiency.
The psychological burden of a scar, no matter which type, goes beyond its cosmetic appearance. Both patients and physicians alike are consistently seeking new scar treatment strategies that may further improve outcomes.
Lasers for Scar Management
Light Amplification by Stimulated Emission of Radiation (LASER) technology utilizes collimated, coherent, monochromatic light to target chromophores (hemoglobin, pigment, and water) in the skin. Based on the theory of selective photothermolysis, laser parameters, such as wavelength, pulse duration, and fluence, determine successful absorption of target chromophore and clinical effect. Vascular, pigment, nonablative, and ablative lasers can be used for the management of scars.
Lasers have been used in the management of scars since the 1990s with the first description of the pulsed dye laser (PDL) for the treatment of erythematous and hypertrophic scars. Shortly after, fully ablative carbon dioxide (CO 2 ) and erbium:yttrium-aluminum-garnet (Er:YAG) resurfacing lasers were popularized for facial scars. In the early 2000s, the innovation of fractional ablative resurfacing laser technology allowed for effective treatment of scars with minimal risk, even in glabrous skin. More recently, the discovery of laser-assisted drug delivery (LADD) has further metamorphosed the landscape of laser management of scars.
Over the years, different treatment options have been offered, some of which have decreased in popularity due to their side effects and poor outcome, whereas many are still used alone or in combination with other interventions. Currently, the PDL, often in combination with intralesional (IL) triamcinolone acetonide (TAC), is considered the treatment of choice for hypertrophic scars and keloids. Fractional lasers, such as CO 2 and Er:YAG lasers, have the capability of treating multiple scar features and are commonly used for atrophic postacne scarring.
Based on the scars’ features, laser modalities are often combined or incorporated with nonlaser treatment approaches, such as surgical scar revision, IL 5-fluorouracil (5-FU), IL TAC, topical imiquimod, punch excisions, and subcision ( Table 5.1 ) to achieve desired effects. Conservative treatments, such as silicone sheets and scar massage, should be encouraged concomitantly with laser and nonlaser interventions.
| Scar Feature | Devices | Adjuvant Treatments | |
|---|---|---|---|
| Adnexa-poor location | Vascular laser | PDL (585- or 595-nm) | Conservative measures a |
| KTP (532-nm) | |||
| NAFL | Erbium (1540-, 1550-, 1565-, or 1400-nm) | ||
| Thulium (1927-nm) | |||
| High tension location | Vascular laser | PDL (585- or 595-nm) | Conservative measures a Consider botulinum toxin A |
| KTP (532-nm) | |||
| NAFL | Erbium (1540-, 1550-, 1565-, or 1400-nm) | ||
| Thulium (1927-nm) | |||
| Erythema | Vascular Laser | PDL (585- or 595-nm) | Conservative measures a |
| KTP (532-nm) | |||
| Energy-based device | IPL (500- to 1300-nm with vascular filters) | ||
| Mild hypertrophy (<3 mm) | Vascular laser | PDL (585- or 595-nm) | Conservative measures a TAC, intralesional or LADD 5-FU, intralesional or LADD |
| KTP (532-nm) | |||
| Energy-based device | TMFI | ||
| Moderate/severe hypertrophy (>3 mm), unstable b | NAFL | Erbium (1540-, 1550-, 1565-, or 1400-nm) | Conservative measures a TAC, intralesional or LADD 5-FU, intralesional or LADD |
| Thulium (1927-nm) | |||
| Moderate/severe hypertrophy (>3 mm), stable c | AFL | CO 2 (10,600-nm) | Conservative measures a TAC, intralesional or LADD 5-FU, intralesional or LADD |
| Er:YAG (2940-nm) | |||
| Atrophy | NAFL | Erbium (1540-, 1550-, 1565-, or 1400-nm) | Punch excision Punch elevation Subcision PLLA, injected or LADD Other dermal fillers Chemical peeling Dermal grafting Microdermabrasion |
| Thulium (1927-nm) | |||
| AFL | CO 2 (10,600-nm) | ||
| Er:YAG (2940-nm) | |||
| Energy-based device | RFMN | ||
| TMFI | |||
| Plasma resurfacing | |||
| Striae distensae | Vascular laser | PDL (585- or 595-nm) | Peeling agents (glycolic acid, tretinoin, L-ascorbic acid) Microdermabrasion PRP |
| KTP (532-nm) | |||
| Infrared lasers | QS Nd:YAG (1064-nm) | ||
| Nd:YAG (1320-nm) | |||
| Diode (1450-nm) | |||
| Erbium:Glass (1540-nm) | |||
| NAFL | Erbium (1540-, 1550-, 1565-, or 1400-nm) | ||
| Thulium (1927-nm) | |||
| Energy-based device | IPL ( 500- to 1300-nm with vascular filters) | ||
| RFMN | |||
| Hyperpigmentation | Pigment lasers | QS Ruby (694-nm) | Bleaching creams |
| QS Alexandrite (755-nm) | |||
| QS Nd:YAG (1064-nm) | |||
| Hypopigmentation | AFL | CO 2 (10,600-nm) | Prostaglandin analogs, LADD +/– retinoids |
| Er:YAG (2940-nm) | |||
| Contraction | AFL | CO 2 (10,600-nm) | Conservative measures a TAC, intralesional or LADD 5-FU, intralesional or LADD |
| Er:YAG (2940-nm) | |||
a Conservative measures include scar massage, occlusion, and silicone sheets.
b Unstable scars exhibit symptoms (pain or pruritus), growth, or prolonged erythema.
c Stable scars are asymptomatic, not growing, and generally flesh colored (not erythematous).
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