Hypertrophic scars are usually difficult to eradicate when treated by traditional
destructive methods. Cosmetically unsatisfactory or inadequate results have been produced from treatments advocated in the past,
including dermabrasion, laser abrasion, excisional surgery with closure, skin grafting, intralesional steroid injections, cryosurgery,
radiotherapy, topical retinoids, collagen injections, silicone gel sheeting and pressure dressings.
The complexity of wound healing may culminate in the reappearence or even worsening of hypertrophic
scars when treated with the above methods. While there is no definitive treatment approach, laser scar revision using pulsed dye laser
technology has been shown to result in prolonged positive clinical outcomes.
An estimated 4.5% to 16% of the population are affected by hypertrophic scars and keloids. These
scars often develop on the anterior chest in pressure- or movement- dependent areas (e.g., scapula) and on body areas that respond with
slow wound healing. Although an increased susceptibility to hypertrophic scars and keloid formation occurs in individuals with darker
skin tones or in those who have defects in their ability to repair or synthesize collagen (i.e., Ehlers-Danlos or Marfan syndromes), they
may develop in anyone following surgery or trauma.
Little is known of the evolution of hypertrophic scaring. By definition, a hypertrophic scar is raised, erythematous,
and remains within the boundaries of the original trauma or wound. A keloid, on the other hand, extends beyond the confines of the wound and
is more nodular. The time of onset of either varies from weeks to years. Hypertrophic scars differ from keloids because of their tendency for
spontaneous regression over time.
Histologically, both are comprised of thick, hyalinized collagen bundles arranged in nodules consisting of small fibroblasts
and fibrocytes. Multiple microvessels often appear occluded by an excess of endothelial cells. An increased amount of hyaluronidase is present
in keloids, while a decreased expression of collagenase occurs in hypertrophic scars. The clinical presentation of hypertrophic scars and keloids
overlap, making differentiation a difficult task.
The etiology of scar formation remains unclear, although several theories have been advanced. The cascade of wound healing
involves a complex interplay of steps which have been impossible to separate in a satisfactory manner and thus a single cell type or other responsible
factor has not been implicated.
The vascular-specific 585-nm pulsed dye laser was the first pulsed laser system used to successfully treat hypertrophic scars and
keloids. It was known that vascular-specific laser irradiation would improve the persistent erythema present in most hypertrophic scars and keloids.
Improved skin texture and color resulted from the initial testing of the pulsed dye laser in argon laser-induced port-wine stain scars. Furthermore,
there was no recurrence or worsening of the scar at the 6-month or 4-year examination interval.
Other investigations also have demonstrated positive clinical results with improved pliability, texture, color, and bulk with one
or two pulsed dye laser treatments in patients with surgical or traumatic hypertrophic scars. In addition, pulsed dye laser treatment has been shown to
improve burn scars and hypertrophic and keloid median sternotomy scars with no evidence of recurrence.
The definitive mechanism whereby hypertrophic and keloid scars are improved is not known. However, explanations include laser-induced
tissue hypoxia (leading to collagenolysis from decreased microvascular perfusilon), collagen fiber heating with dissociation of disulfide bonds and subsequent
collagen fiber realignment, selective photothermolysis of vasculature, and mast cell factors (including histamine) that could affect collagen metabolism.
The optimal candidates for pulsed dye laser treatments are individuals with lighter skin phototypes (Fitzpatrick types I-III) because less
epidermal pigment (melanin) is present to compete with hemoglobin for absorption of the laser energy. Treatment in individuals with darker skin tones may be
successful, although hypopigmentation may result and patients should be forewarned of this possibility.
There is no consensus of optimal timing to initiate pulsed dye laser treatment. Following integumental injury, hypertrophic scars may
spontaneously improve (especially erythema) during the initial 6 to 12-month period. Anecdotal evidence suggests that hypertrophy may be prevented in individuals
who are prone to developing keloids if the pulsed dye laser treatment is initated within 1 month of injury. It is plausible that scar proliferation may be stopped
with early laser irradiation (e.g. within the first few weeks) following trauma or surgery and thus decrease the number of laser treatments that are necessary.
TREATMENT PROTOCOL (PULSED DYE LASER)
Pulsed dye laser treatments are generally performed in an outpatient setting. Neither general nor intravenous anesthesia typically is needed
since there is limited discomfort associated with the treatment. Topical or intralesional anesthesia may be desirable in patients undergoing treatments to sensitive
body areas (e.g., lips, breasts, perineum, fingers) as well as when treating younger patients. Topical lidocaine cream (e.g., EMLA, ElaMax) can be applied for 30 to
60 minutes to achieve adequate anesthesia. As with other laser procedures, hair-bearing areas within the treatment field should be dampened with water or saline and
protective eyewear should be worn by operating room personnel as well as the patient.
During each laser session, the entire scar is treated with adjacent, nonoverlapping laser pulses at appropriate energy densities (or fluences).
The spot size used, the color and thickness of the scar, and its location determine the choice of energy density. During the early sessions, lower fluences are generally
used. Depending upon the scar response, the fluences are adjusted upward during subsequent treatments. Slightly higher fluences may be used to treat thicker or darker
scars while lower energy densities are used to treat pale, less fibrotic scars in sensitive or thin-skinned areas (e.g., anterior chest, neck). Immediately after the
pulsed dye treatment, a purpuric tissue response is seen (bruising). Vesiculation, crusting, or bleeding are indicative of excessive fluences or overlapping of laser
pulses which should be avoided in subsequent treatments.
Within 1 to 2 weeks the purpura or bruises disappear. The patient should be instructed to perform daily gentle cleansing of the area with mild
fragrance-free soap and water and to apply a topical antibiotic ointment and nonstick dressing. The treatment site is evaluated 6 to 8 weeks later. If residual scar
erythema or hypertrophy is noted, the laser treatment may be repeated.
The patient's response to previous laser treatments determines subsequent treatment fluences. The energy density generally remains the same if
there is adequate improvement (i.e., reduced scar erythema and bulk with increased pliability). If improvement is fair to nonexistent, an increase of 10% in the treatment
fluence should be chosen. A lower fluence should be used when individuals report posttreatment vesiculation or crusting, and careful attention should be paid to treatment
technique with avoidance of overlapping pulses.
SIDE EFFECTS AND COMPLICATIONS
Hyperpigmentation of the irradiated skin is the most common side effect following laser treatment of scars with the 585-nm flashlamp-pumped pulsed
dye laser. With adequate protection and avoidance of the sun, the hyperpigmentation spontaneously fades over time. The fading process can be hastened with daily application
of hydroquinone (or other bleach) cream.
Subsequent laser treatments on hyperpigmented scars should be postponed and resumed only after the pigmentation has completely resolved in order for the
laser to exert its optimal effect without interference from a competing chromophore (or target) such as melanin.
Other complications such as blister formation and scar worsening (due to excessive thermal damage to the skin) can be mediated with the use of proper
energy densitites and nonoverlapping laser pulses. An allergic contact dermatitis may occasionally result from the prescribed topical antibiotic, as may irritant dermatitis
from the dressing adhesive. The type of vesiculation (e.g., non-purpuric and not relating to the laser spot "footprint") and the presence of pruritis (commonly associated with
dermatitis) are identifiable markers facilitating the determination of proper care and patient management (e.g., discontinuation of the ointment or dressing and application of
a mild corticosteroid cream such as hydrocortisone, until the problem resolves).
In most hypertrophic scars, a mean improvement exceeding 80% is seen following two or three laser treatments. Treated scars are less erythematous and flatter,
and exhibit an appearance similar to the normal surrounding skin. Scars that are more fibrotic or keloid-like typically require additional treatment sessions in order to achieve the
desired cosmetic effect (i.e., lightening and flattening of the scar). Optimal inter-treatment intervals of 6 to 8 weeks are necessary to allow for adequate skin healing between laser
Hypertrophic scarring commonly occurs following surgery or trauma and has been exceedingly difficult to treat in the past. The use of the 585-nm flashlamp-pumped
pulsed dye laser is an effective treatment for hypertrophic scars and keloids. The clinical appearance, surface texture, pliability, and symptoms of scars can improve following a few
treatment sessions. Results are long-lasting and scar recurrences are rare. The ease of treatment enhances viability and patient acceptance.
Although the exact mechanism of action responsible for the laser's effects is unknown, laser stimulated release of histamine or other factors may play an integral role
in scar fibroblast activity. The effect of adjuvant treatments such as intralesional corticosteroids should be studied in future investigations to determine whether there is a synergistic
therapeutic benefit and improvement in clinical outcome.