Prior to the advent of laser technology, fine-wire cautery, cryotherapy, and sclerotherapy were used to treat facial telangiectasia.1 fine-wire radiosurgery can be very effective, but is operator sensitive.2 In addition, it can be painful, and it destroys normal tissue surrounding the vessels. Because of the nonspecific tissue destruction, a significant risk of scarring exists.
The use of cautery or radiofrequency also causes acute hemorrhaging of the vessels that is difficult to control and complicates visualization of surrounding telangiectasias. Some of the earliest laser treatments for facial telangiectasia were performed with continuous wave CO2 (10600 nm) and argon (488 and 514 nm) lasers, as well as Nd:YAG (1064 nm) systems.3,4 Although successful outcomes were reported, the CO2 laser destroyed the ectatic vascular tissue as well as the overlying epidermis in a nonselective fashion.5 The argon laser, which emits a mixed blue and green light selective for hemoglobin and melanin, also destroyed ectatic vessels and the overlying epidermis.5 This nonselective heat dissipation resulted in a high incidence of scarring and hypopigmentation or hyperpigmentation.6 These lasers were, in effect, sophisticated forms of electrocautery.
In 1983 when Anderson and collegues,8 in a classic paper, described the concept of selective photothermolysis, they hypothesized that selective thermolysis could be predicted by choosing the appropriate wavelength, pulse duration, and pulse energy for a particular chromophore target.9 This simple theory revolutionized laser surgery. The 2 key conclusions were that the wavelength of the laser light must be absorbed by the target in order to have a treatment effect and that the laser energy must be confined to the intended target to spare the surrounding tissue from damage. As previously stated, the target for vascular lesions is oxyhemoglobin. The absorption peaks for oxyhemoglobin are approximately 418, 542, and 577 nm.
The theory of selective photothermolysis spurred the development of flashlamp-pumped, pulsed-dye, and copper-vapor lasers. These lasers emit light between 577 and 585 nm.
These wavelengths are selectively absorbed by oxyhemoglobin, thus destroying the ectatic vessel with minimal damage to the underlying tissue. This type of laser differs from previous lasers by emitting light in pulses rather than a continuous beam.7 In addition to the pulses, the time between each pulse allows thermal cooling of the target chromophore. If the pulse width is equal to or less than the thermal relaxation time (TRT) of the telangiectatic vessel (the time during which 50% of the incident heat has transferred out of the vessel to adjacent tissues), the resultant thermal damage will be confined to the vessel.10 Having a pulse duration that is shorter than the TRT of the treated vessel prevents the energy from dissipating too far beyond the targeted vessel. For vessels as small as 50–75 mm in diameter, the TRT is approximately 1 millisecond.10 Larger vessels, such as those found on the ala, have a much longer TRT.
A vessel with a diameter of 300 mm has a TRT of approximately 42 milliseconds, about 10 times that of a vessel one third its size. Vessels with a diameter of 1000 mm (1 mm) have a TRT of about 500 milliseconds.10 The 585-nm flashlamp-pumped, pulsed-dye laser has become the gold standard by which other vascular lasers are judged. The flashlamp-pumped, pulsed-dye laser has the significant drawback of posttreatment purpura, which is difficult to conceal and can persist for up to 14 days. Other clinical drawbacks of the pulsed-dye laser include costly field service for tube or dye replacements, mirror collimation, and overheating of the machine and the treatment room.
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