Treatment of Leg Telangiectasias with Laser and High-Intensity Pulsed Light

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CHAPTER 13 Treatment of Leg Telangiectasias with Laser and High-Intensity Pulsed Light

The laser was first conceived in the imagination of H.G. Wells, who described the use of a light gun in 1896 as an outer-space weapon. Albert Einstein then transformed this vision into a theoretical possibility in the early 1900s. Einstein described the process of stimulated emission as an offshoot in his quest to show the inherent singular nature of the four basic forces of the universe. However, it was not until 1960 that the first laser was actually constructed.

The acronym LASER stands for Light Amplification by the Stimulated Emission of Radiation. In short, a laser emits a beam of monochromic, coherent, collimated photons of a specific wavelength. The emitted wavelength is produced by exciting an atom or molecule to release photons at a wavelength or wavelengths specific for that type of molecule. This ability to produce laser light at a specific wavelength is one key factor in the production of selective damage. By tuning the laser to the absorption spectrum of a particular target, such as oxygenated hemoglobin, theoretically only that target will be affected by the laser energy.

With proper use, lasers are very safe and have not been associated with long-term side effects. Most of the laser radiation used in medicine is within or near the range of visible light in the electromagnetic spectrum. Therefore, its radiant energy level is at a much longer wavelength than that of the high-energy ionizing radiation associated with X-rays and radiation therapy; as such, it is not associated with commonly perceived radiation hazards.1 In addition to determining the specificity of absorption, each laser’s emitted wavelength also dictates the depth of its penetration (Fig. 13.1). (A more thorough discussion of laser physics can be found in other sources.1,2)

Lasers have been used to treat leg telangiectasias for various reasons.3 First, lasers have a futuristic appeal. By virtue of their advanced technology, lasers are perceived as ‘state-of-the-art.’ The general public often equates ‘high tech’ with treatment safety and superiority. Unfortunately, as described later, this perception by both the general public and the physician has often resulted in unanticipated adverse sequelae (scarring and pain) and higher costs; lasers cost considerably more to purchase and maintain than a needle, syringe, and sclerosing solution.

In addition, lasers have theoretical advantages compared with sclerotherapy for treating leg telangiectasias. Sclerotherapy-induced pigmentation is caused by hemosiderin deposition through extravasated red blood cells (RBCs) (see Chapter 8). Laser coagulation of vessels should not have this effect. In the rabbit ear model, approximately 50% of vessels treated with an effective concentration of sclerosing solution demonstrated extravasated erythrocytes, compared with a 30% incidence when treated with the flashlamp-pumped pulsed dye laser (PDL) (Goldman MP, unpublished observations). Furthermore, telangiectatic matting (TM), which occurs in a significant percentage of sclerotherapy-treated patients, has also not been seen after laser treatment of vascular lesions. Finally, specific allergenic effects of sclerosing solutions are not a concern when treating telangiectasias with a laser.

Both lasers and intense pulsed light (IPL) have been used to treat leg telangiectasias. Each acts in a different manner to induce vessel destruction. Effective lasers and IPL are pulsed so that their effects act within the thermal relaxation times of blood vessels to produce specific destruction of vessels of various diameters based on the pulse duration. Lasers of various wavelengths and the broad-spectrum IPL are used to selectively treat blood vessels by taking advantage of the difference between the absorption of the components in a blood vessel (oxygenated and deoxygenated hemoglobin) and the overlying epidermis and surrounding dermis (as described below) to selectively thermocoagulate blood vessels. Each wavelength requires a specific fluence to cause vessel destruction. In addition, leg veins are not composed mostly of oxygenated hemoglobin, unlike port-wine stains (PWSs) and hemangiomas, but are filled with predominantly deoxygenated hemoglobin; hence their blue color. Selective wavelengths for deoxyhemoglobin as opposed to oxyhemoglobin include approximately 545 nm, 580 nm, and a broad peak between 650 and 800 nm.

Optical properties of blood are mainly determined by the absorption and scattering coefficients of its various oxyhemoglobin components. Oxyhemoglobin has three major absorption peaks at 418, 542, and 577 nm. A less selective and broader absorption peak spans from approximately 750 to 1100 nm. Figure 13.2 shows the oxyhemoglobin absorption and scattering coefficient depth of penetration into blood.4 The main feature to note in the curve is the strong absorption at wavelengths below 600 nm with less absorption at longer wavelengths. However, a vessel 1 mm in diameter absorbs more than 67% of light even at wavelengths longer than 600 nm. This absorption is even more significant for blood vessels 2 mm in diameter. Therefore, use of a light source above 600 nm would result in deeper penetration of thermal energy without negating absorption by oxyhemoglobin in vessels greater than 1 mm in diameter. This is because the absorption coefficient in blood is higher than that of surrounding tissue for wavelengths between 600 and 1000 nm (Figs 13.2 and 13.3). Shorter wavelengths heat only the portion of the vessel wall closest to the skin surface, which can result in incomplete thrombosis.5 The only caveat is that wavelengths greater than 900 nm are less specific and also target water, making higher fluences required to produce desired effects on oxyhemoglobin, the desired chromophore.6 However, these higher fluences can cause unnecessary damage to surrounding tissue unless adequate cooling measures are employed.

Patients seek treatment for a leg vein largely for cosmetic reasons.7 Bernstein8 has evaluated the clinical characteristics of 500 consecutive patients presenting for laser removal of lower extremity spider veins. Patients ranged in age from 20 to 70 years and had had noticeable spider veins for an average of 14 years. Twenty-eight percent of patients had leg veins less than 0.5 mm in diameter; 39% of patients had veins less than 1.5 mm in diameter. Fifty-six percent of patients who had had sclerotherapy (not stated how this was performed) developed TM. Any treatment that is effective should be relatively free of adverse sequelae. With recent advances, lasers or IPL have become methods for treating telangiectatic vessels with a minimum of adverse effects. However, for these advanced treatments to be effective and safe, they must be used appropriately.

As detailed in Chapter 8, sclerotherapy has a number of potential adverse effects. Up to 30% of patients treated with sclerotherapy develop postsclerosis pigmentation9 and/or TM.10 As discussed above, at least one study determined that TM developed in 56% of patients who presented for laser treatment of leg veins.8 These adverse effects can occur even with optimal treatment but are more common when an excessive inflammatory reaction occurs. To minimize risks of an inflammatory response, lasers and IPL act by producing thermal damage with the ultimate goal being vaporization of the targeted vessel. When used with appropriate fluences, pulse durations, and epidermal cooling, the thermal effects of lasers and IPL present minimal inflammatory response compared with chemical irritation of the vessel wall through sclerotherapy.

An understanding of the appropriate target vessel for each laser and/or IPL is important so that treatment is tailored to the appropriate target. As detailed elsewhere in this book, most telangiectasias arise from reticular veins. Therefore, the single most important concept for the treating physician is that feeding reticular veins must be treated completely before treating the telangiectasia. This minimizes adverse sequelae and enhances therapeutic results. When no apparent connection exists between deep collecting or reticular vessels, telangiectasia may arise from a terminal arteriole or arteriovenous anastomosis.11 In this latter scenario, the telangiectasia may be treated without consideration of underlying forces of hydrostatic pressure. Failure to treat ‘feeding’ reticular veins and short follow-up periods after the use of lasers may give inflated values to the success of laser treatment.12 This chapter reviews and evaluates the use of these nonspecific and specific laser and light systems in the treatment of leg venules and telangiectasias (Table 13.1).

Histology of Leg Telangiectasia

The choice of proper wavelength(s), degree of energy fluence, and pulse duration of light exposure are all related to the type and size of target vessel treated. Deeper vessels necessitate a longer wavelength to allow adequate penetration. Large diameter vessels necessitate a longer pulse duration to effectively thermocoagulate the entire vessel wall, allowing sufficient time for thermal energy to diffuse evenly throughout the vessel lumen. The correct choice of treatment parameters is aided by an understanding of the histology of the target telangiectasia.

Venules in the upper and middle dermis typically maintain a horizontal orientation. The diameter of the postcapillary venule ranges from 12 to 35 µm.13 Collecting venules range from 40 to 60 µm in the upper and middle dermis and enlarge to 100 to 400 µm in diameter in the deeper tissues. Histologic examination of simple telangiectasia demonstrates dilated blood channels in a normal dermal stroma with a single endothelial cell lining, limited muscularis, and adventitia.14,15 Most leg telangiectasias measure from 26 to 225 µm in diameter.14 Electron microscopic examination of ‘sunburst’ varicosities of the leg has demonstrated that these vessels are widened cutaneous veins.14 They are found 175 to 382 µm below the stratum granulosum. The thickened vessel walls are composed of endothelial cells covered with collagen and muscle fibers. Elastic fibers are also present.

Alternatively, arteriovenous anastomoses may be involved in the pathogenesis of telangiectasia. They have been demonstrated in 1 of 26 biopsy specimens of leg telangiectasias.11 Red telangiectasias have been found to have an oxygen saturation of 76%, compared with blue telangiectasias, which have an oxygen concentration of 69%.16 Thus each type of telangiectasia may have a slightly different optimal absorption wavelength based on its color in addition to its relative size and depth.

Unlike leg telangiectasias, the ectatic vessels of PWSs are arranged in a loose fashion throughout the superficial and deep dermis. They are more superficial (0.46 mm) and much smaller than leg telangiectasias, usually measuring 10 to 40 µm in diameter. This may explain the lack of efficacy reported by many physicians who treat leg telangiectasia with the same laser and parameters as they do with PWSs.

Laser Treatment of Leg Telangiectasia

Various lasers have been used in an effort to enhance clinical efficacy and to minimize the adverse sequelae of telangiectasia treatment. Unfortunately, most have also been associated with adverse responses far in excess of those associated with sclerotherapy. This is related both to the nonspecificity of the laser used and the lack of treatment of hydrostatic pressure from the ‘feeding’ venous system.

The optimal light source would have a wavelength specific for the vessel treated and would be able to penetrate to the depth of the vessel through its entire diameter. This wavelength has been proposed to be between 600 and 900 nm. Ideally, a light source should have a pulse duration that would allow the light energy to build up in the target vessel so that its entire diameter is thermocoagulated. Optimal pulse durations have been calculated for various diameter blood vessels (Table 13.2).

Table 13.2 Thermal relaxation times of blood vessels

Diameter of vessel (mm) Thermal Relaxation Time (sec)
0.1 0.01
0.2 0.04
0.4 0.16
0.8 0.6
2.0 4.0

Presented by R.A. Anderson at the Annual Meeting of the North American Society of Phlebology, Washington, DC, November, 1996.

During the process of delivering a sufficient packet of energy to thermocoagulate the target vessel, the overlying epidermis and perivascular tissue should be unharmed. This requires some form of epidermal cooling. A number of different laser and IPL systems have been developed toward this end, as discussed in subsequent sections. In addition to the information presented in the following sections, the reader is encouraged to refer to an excellent summary of various laser treatments for leg veins by Kunishige et al.6

Carbon dioxide laser

The carbon dioxide (CO2) laser has been used for obliterating venules and telangiectatic vessels.1721 One recent case report described the successful treatment of matted telangiectasias with fractional photothermolysis.22 The patient underwent five successive monthly treatments with the 1550 Fraxel SR laser (Solta Medical, Hayward, Calif.), at energies ranging from 10 to 12 mJ, to an area on her medial thigh. At 6 months after the final treatment session, the target areas showed more than 75% improvement. However, since the natural history of matted telangiectasias is usually to spontaneously resolve over the course of a year, it is uncertain how much of the improvement seen in the aforementioned case report was actually due to ‘the tincture of time’ as opposed to the CO2 laser treatment.

The rationale for using the CO2 laser in the treatment of telangiectasia is to produce ‘precise’ vaporization without significant damage to tissue structures adjacent to the penetrating laser beam. Also, since the CO2 laser does not specifically target melanin, it can be used on those of darker skin types, a subgroup of the population that cannot be safely treated with the pulse dye laser. However, with the CO2 laser, the epidermis and the dermis overlying the blood vessel are destroyed. CO2 laser disruption of vessels has also been reported to cause occasional brisk bleeding from the vessel, which required pressure bandages for 48 hours.20 Pain during treatment is moderate to severe, but of short duration. Most reported studies demonstrate unsatisfactory cosmetic results. Treated areas show multiple hypopigmented punctate scars with either minimum resolution of the treated vessel or neovascularization adjacent to the treatment site (Fig. 13.4). Because of this nonselective action, the CO2 laser is of no advantage over the electrodesiccation needle and has not been used successfully in treating leg telangiectasia.

Argon laser

The argon laser with output at 488 nm and 511 nm has wavelengths somewhat preferentially absorbed by hemoglobin and to a lesser, although significant, extent by water and melanin (Fig. 13.5). Its relatively short wavelength, combined with a spot size of 1 mm, prevents its penetration much beyond 0.5 mm. When the patient is pigmented or tanned, epidermal melanin will selectively absorb the laser energy, preventing penetration below the epidermis. Thus, the argon laser does not have ideal parameters for treating leg veins (Fig. 13.6).

Being continuous in nature, argon lasers do not allow for selective vessel heating, so scarring commonly occurs.23 Specifically, argon laser treatment of telangiectasia or superficial varicosities of the lower extremities may cause purple or depressed scars. In a report of 38 patients treated by Apfelberg et al,18 49% had either poor or no results from treatment, and only 16% had excellent or good results. In addition, almost half of the patients had hemosiderin bruising. In another series, Dixon et al24 noted significant improvement in only 49% of patients. They speculated that after initial improvement, incomplete thrombosis, recanalization, or new vein formation produced reappearance of the vessels after 6 to 12 months.

In an effort to enhance therapeutic success with leg vein sclerotherapy, the argon laser has been used to interrupt the telangiectasia every 2 to 3 cm before injection of a sclerosing agent.25 Eleven of 16 patients completed treatment. Two patients developed punctate depigmented scars, and three patients developed hyperpigmentation. However, 93.7% of patients were reported to have ‘satisfactory’ results.

Cooling the skin simultaneously with argon or tunable dye (577 nm, 585 nm) laser treatment has been demonstrated to produce improvement in 67% of leg telangiectasia 1 mm in diameter.26 This may be caused by temperature-related vasomotor changes in blood flow.27

Overall, argon laser therapy appears to be extremely technique dependent and not only relatively ineffective in treating leg telangiectasia but also associated with an unacceptably high risk of adverse sequelae.

Contact probe delivery

Directing the laser energy to the target vessel produces another method for more selective delivery of nonspecific laser energy. Keller28 reported on the use of a microcontact argon laser probe to treat ‘spray telangiectasias’ of the leg. Fifteen patients were treated with this device using an argon laser energy of 1 to 2 W with a pulse duration of 0.1 second. This treatment was performed as ‘spot welding’ along the course of the blood vessel; 100% effectiveness and no notable complications were reported. We have not achieved the same success rate as Keller,29 and further reports of this novel form of therapy have not occurred. Thus, at present, argon laser therapy apparently is a satisfactory method for treating selected facial telangiectasia but is much less effective in treating leg telangiectasia. Box 13.1 summarizes the disadvantages of the argon laser treatment.

Krypton triphosphate and frequency-doubled Nd:YAG (532 nm)

Modulated krypton triphosphate (KTP) lasers have been reported to be effective at removing leg telangiectasia, using pulse durations between 1 and 50 ms (see Table 13.1). The 532-nm wavelength is one of the hemoglobin absorption peaks (see Fig. 13.5). Although this wavelength does not penetrate deeply into the dermis (about 0.75 mm), relatively specific damage (compared with the argon laser) can occur in the vascular target by selection of an optimal pulse duration, enlargement of the spot size, and addition of epidermal cooling.

Effective results have been achieved by tracing vessels with a 1-mm projected spot. Typically, the laser is moved between adjacent 1-mm spots with vessels traced at 5 to 10 mm/second. Immediately after laser exposure, the epidermis is blanched. Lengthening of the pulse duration to match the diameter of the vessel is attempted to optimize treatment (see Table 13.2). With this method, West and Alster30 utilized this method to treat 12 patients with leg telangiectasia. They used a 10-ms pulse at 15 J/cm2 with a 1-mm handpiece at a repetition rate of two pulses per second. The average improvement was 25% to 50% (Fig. 13.7).

Quintana et al31 treated 19 leg veins that were less than 1.5 mm in diameter with the Laserscope KTP Dermastat (Laserscope, San Jose, Calif.). They used a 2-mm diameter handpiece at a fluence of 13 to 15 J/cm2 given at a rate of 10 to 15 milliseconds. Patients were treated at 4- to 6-week intervals on four separate visits, with results examined 6 months after the last visit. Of the 28% of patients evaluated, 15% percent achieved 100% clearance, 40% had 75% clearance, 35% had 50% clearance, and 10% had 25% clearance. No scarring was reported, and 25% had transient hyperpigmentation. Therefore, this laser is somewhat effective but requires multiple treatments.

We and others have found the long-pulse 532-nm laser (frequency-doubled Nd:YAG) (VersaPulse, Lumenis, Palo Alto, Calif.) to be effective in treating leg veins less than 1 mm in diameter that are not directly connected to a feeding reticular vein.32 When used with a 4°C chilled tip, a fluence of 12 to 15 J/cm2 is delivered as a train of pulses in a 3- to 4-mm diameter spot size in order to trace the vessel until spasm or thrombosis occurs. Some overlying epidermal scabbing is noted with hypopigmentation not uncommonly occurring in dark-skinned patients. Individual physicians report considerable variation in results. Usually, more than one treatment is necessary for maximum vessel improvement, with only rare reports of 100% resolution of the leg vein (Fig. 13.8). A summary of important clinical evaluations of this technology follows.

McMeekin33 treated 18 sites of leg veins ranging from 0.5 to 1.1 mm in diameter in 10 patients, using a VersaPulse with a 3-mm diameter spot, 5.5°C cooling, at 12 and 16 J/cm2 with one to three passes over each vessel at 2 Hz. He followed the patients for 1 year after a single treatment. Overall, 44% of patients had a greater than 50% clearance from a single treatment. Six percent of patients had complete clearance, 88% had partial clearance, and 6% had no change. Of the partial clearance group of patients, more cleared at 16 J/cm2 than at 12 J/cm2. At 16 J/cm2, 37% cleared 25% to 50%, 25% cleared 50% to 75%, and 37% cleared 75% to 100%. Ninety-four percent developed hyperpigmentation that took up to 6 months to resolve. One patient developed blisters and hypopigmented atrophic scars.

Bernstein et al34 achieved similar efficacy in a study of 15 women with leg telangiectasia less than 0.75 mm in diameter at 27 sites, using a 10-ms pulse duration 532-nm laser at 16 J/cm2 with a 3-mm diameter spot size at 4 Hz and using a chill tip with three passes over each vein twice, 6 weeks apart. Computer-based image analysis demonstrated more than 75% clearing. Ten of the 27 sites (37%) cleared completely after one treatment. Two of 15 patients (13.3%) reported blistering with minimal hyperpigmentation noted 6 weeks after treatment.

A longer pulse duration of 20 to 50 ms, accompanied by an increase in spot size to 5 mm with a higher total fluence of 20 J/cm2 became available, with improvement in efficacy and a reduction in pigment changes. Narukar35 evaluated patients with leg veins less than 1.5 mm in diameter, treated with 2- to 50-ms pulses up to 40 J/cm2 with a 3- to 6-mm diameter spot size and a 4°C chill tip. He treated patients at 6- to 8-week intervals two to three times. A 45% clearance was found. Interestingly, a 68% clearance was found in patients whose previous sclerotherapy showed a good response. A 32% clearance occurred in patients whose vessels responded poorly to sclerotherapy. At 2-month follow-up, 2% of patients had TM, 4% had hyperpigmentation, and 2% had hypopigmentation.

Massey and Katz36 bettered Narukar’s results using a spot size of 5 mm, a pulse width of 50 ms, fluences of 18 to 20 J/cm2, and a 1.5-Hz repetition rate. A 75%–100% reduction was achieved in 68% of vessels less than 1 mm and in 44% of vessels 1 to 2 mm after two treatments. These results were obtained with multiple passes to achieve vessel clearance. Hypopigmentation and mild hyperpigmentation, lasting 6 to 8 weeks, were noted in 20% of patients. No scarring was observed. Krause37 claimed similar results using a 2-mm diameter spot size. A 2-mm diameter spot size is claimed to produce a narrower band of either hypo- or hyperpigmentation.

A 532-nm KTP laser was also evaluated in a multipulse mode emission (three stacked pulses of 100 ms, 30 ms, 30 ms, and a delay between pulses of 250 ms), a fluence of 60 J/cm2, and a 0.75-mm collimated spot without cooling (Virdis Derma, Quantel Medical, France).38 On average, with one treatment, 53% of leg veins 0.5 to 1 mm in diameter were cleared, 78% with two treatments, 85% after three treatments, and 93% 6 weeks after a fourth treatment, all 6 weeks apart. It is suggested that the multipulse mode increases intravascular heating in a manner similar to the multipulse mode of IPL (see below) while allowing cooling of the epidermis. Hypopigmentation lasting ‘a few months’ was observed in 18% of patients and TM occurred in 7% of patients.

In a study by Woo et al,39 a 532-nm Nd:YAG at 20 J/cm2 delivered as a 50-ms pulse through a contact cooling and 5-mm diameter spot was compared with a 595-nm PDL at 25 J/cm2 with a pulse duration of 40 ms, cryogen spray cooling, and a 3- × 10-mm elliptical spot. After one treatment with the 532-nm Nd:YAG there was 50% to 75% improvement in 2 of 10 patients and more than 75% improvement in 3 of 10 patients. There was better improvement in the PDL-treated patients, with 6 of 10 having 50% to 75% improvement.

In another study, a 532-nm diode laser with a 1-mm diameter spot at fluences of 2 to 32 J/cm2 was compared with a 1064-nm Nd:YAG laser at 1- to 20-ms pulses through a 3-mm diameter spot at 130 to 160 J/cm2 in the treatment of TM vessels less than 0.3 mm in diameter that did not respond to sclerotherapy.40 Two to three passes were needed to close the vessels with each laser. Overall, 39% of vessels treated with the 532-nm laser and 55% of those treated with the 1064-nm laser had better than 50% lightening.

In short, the 532-nm, long-pulsed, cutaneous, chilled Nd:YAG laser is effective in treating leg telangiectasia. As summarized previously, efficacy is technique dependent, with excellent results achievable. Patients need to be informed of the possibility of prolonged pigmentation at an incidence similar to that with sclerotherapy, as well as temporary blistering and hypopigmentation that is predominantly caused by epidermal damage in pigmented skin (type III or above, especially when tanned).

Copper bromide 578 nm

Forty-six women with red leg telangiectasias less than 1.5 mm in diameter were treated with 1 minute of precooling to the skin followed by laser pulses at 50 to 55 J/cm2 through a 1.5-mm diameter spot size generated with a 300-ms pulse, with a 75-ms delay between pulses.41 Up to three treatments were given at 6-week intervals. An average of 1.7 treatments produced greater than 75% improvement in 72% of patients. Treatments were given through a circulating cooling window at 1 to 4°C. Problems with this new technology are the long warm-up time of the laser (15–20 minutes) and the long time required to treat the vessels with a 1.5-mm diameter spot size.

Flashlamp-pulsed dye laser, 585 or 595 nm

The PDL has been demonstrated to be highly effective in treating cutaneous vascular lesions consisting of very small vessels, including PWSs, hemangiomas, and facial telangiectasia.42 The depth of vascular damage is estimated to be 1.5 mm at 585 nm and 15 to 20 µm deeper at 595 nm. Therefore, penetration to the typical depth of superficial leg telangiectasia may be achieved.43 However, telangiectasia over the lower extremities has not responded as well, with less lightening and more post-therapy hyperpigmentation.44 This may be due to the larger diameter of leg telangiectasia as compared with dermal vessels in PWS and larger diameter feeding reticular veins, as described previously.

Vessels that should respond optimally to PDL treatment are predicted to be red telangiectasia less than 0.2 mm in diameter, particularly those vessels arising as post-sclerotherapy TM. This is based on the time of thermocoagulation produced by this relatively short pulse laser system (see Table 13.2). The PDL produces vascular injury in a histologic pattern that is different than that produced by sclerotherapy. In the rabbit ear vein, approximately 50% of vessels treated with an effective concentration of sclerosant demonstrated extravasated RBCs, whereas with PDL treatment, extravasated RBCs were apparent in only 30% of vessels treated (unpublished observations). Thus, the PDL may produce less post-therapy pigmentation because of a decreased incidence of extravasated RBCs (Figs 13.913.13).

The etiology of TM is unknown but has been thought to be related either to angiogenesis45 or to a dilatation of existing subclinical blood vessels by promoting collateral flow through arteriovenous anastomoses.46 One or both of these mechanisms may occur. Obstruction of outflow from a vessel (which is the end result of successful sclerotherapy) is one of the most important factors contributing to angiogenesis.47 In addition, endothelial damage leads to the release of histamine and other mast cell factors and vasokines, which promote both the dilatation of existing blood vessels and angiogenesis.48,49 Sclerotherapy by its mechanism of endothelial destruction provides the means for new blood vessel formation to occur. Indeed, it is remarkable that physicians do not see a higher incidence of post-treatment TM associated with sclerotherapy.

TM has not been reported to be a side effect of argon, PDL, or other laser treatment of any other vascular disorders. This may be due to the production of intravascular fibrin that occurs during laser treatment.5052 Fibrin develops through thermal alteration of fibrin complexes or proteolytic cleavage of fibrinogen. Fibrin deposition has been demonstrated to promote angiogenesis.48 Sclerotherapy-induced vascular injury has not been associated with the appearance of fibrin strands (unpublished observations). This is explained by limitation of angiogenesis by factors other than those associated with the absence of fibrin deposition, or by intravascular consumption of fibrin-promoting factors in laser treatment of cutaneous vascular disease.

Another possible mechanism for absence of TM in laser-treated blood vessels is a decrease in perivascular inflammation. Rabbit ear vein treatment with the PDL relatively decreases perivascular inflammation compared with vessels treated with sclerotherapy alone.52 Multiple factors associated with inflammation have been demonstrated to promote both a dilatation of existing blood vessels and angiogenesis.49

The pulse duration of the first generation of PDL was 450 µ seconds, optimal for the 50- to 100-µm diameter of PWS vessels. This pulse duration is most effective for treating leg telangiectasias that are less than 1 mm in diameter. Unfortunately, many studies failed to demonstrate satisfactory efficacy with the PDL at these parameters. We believe this is a result of failure to recognize the importance of high-pressure vascular flow from feeding reticular and varicose veins and treatment of these before treating the distal telangiectasia.

Polla et al44 treated 35 superficial leg telangiectasias with the PDL. The exact laser parameters were not given, except that vessels were treated an average of 2.1 times with a maximum of four separate treatments. These vessels were described as being either red–purple and raised, or blue and flat. No mention was made regarding the association of reticular or varicose veins or vessel diameter. Fifteen percent of treated vessels had greater than 75% clearing, with 73% of treated areas showing little response to treatment. The only lesions that responded at all were red–pink tiny telangiectasia. Almost 50% of the treated patients developed persistent hypopigmentation or hyperpigmentation.

Goldman and Fitzpatrick53 treated 30 female patients with red leg telangiectasias of less than 0.2 mm in diameter. Thirteen of 101 telangiectatic patches were noted to have an associated reticular ‘feeding’ vein between 2 and 3 mm in diameter that was not treated. Seven patients with 25 patches of TM after previous sclerotherapy were also treated.

PDL 5-mm diameter spots were overlapped slightly with every effort made to treat the entire vessel. After treatment, a chemical ice pack (Kwik Kold, American Pharmaseal Co., Valencia, Calif.) was applied to the treated area until the laser-induced sensation of heat resolved (5–15 minutes). Thirty-nine telangiectatic patches, chosen randomly, were treated with laser energies between 7.0 and 8.0 J/cm2 and compressed with a rubber ‘E’ compression pad (STD Vascular Products Ltd, Bristol, England) fixed in place with Microfoam 100-mm tape (3 M Medical-Surgical Division, St Paul, Minn.). A 30- to 40-mmHg graduated compression stocking was then worn over this dressing continuously for approximately 72 hours.

As hypothesized, TM and persistent pigmentation did not occur with PDL treatment of leg telangiectasia. Post-PDL hyperpigmentation completely resolved within 4 months. There were no episodes of cutaneous ulceration, thrombophlebitis, or other complications. However, hypopigmentation occurred in some patients with tanned skin (Fig. 13.14). The laser impact sites usually remained hypopigmented for years and in many cases were thought to be permanent. With PDL treatment, the most effective fluence appears to be between 7.0 and 8.0 J/cm2. With these parameters, approximately 67% of telangiectatic patches completely faded within 4 months (Figs 13.1513.18).

There appears to be no difference in the response to PDL treatment between linear leg telangiectasias and TM vessels. In the seven patients with 25 sites treated (mentioned earlier in this section), 72% of the treated sites completely faded at laser fluences between 6.5 and 7.5 J/cm2. Matted vessels did not respond to treatment in only one patient with four areas of TM. Less than 100% resolution occurred in 16% of treated areas (Fig. 13.19).

Like TM vessels, essential telangiectasia represents a network of fine red telangiectasia usually less than 0.2 mm in diameter. This condition responds well to the PDL at fluences of 7 to 7.25 J/cm2.54 Treatment, however, is tedious, with more than 2000 5-mm diameter pulses sometimes necessary to cover the entire affected area.

The reason for greater efficacy of treatment in Goldman and Fitzpatrick’s report in comparison with others44,55 may be due to the rigid criteria by which patients were selected for treatment. Patients who responded well to treatment had red telangiectasia less than 0.2 mm in diameter without associated ‘feeding’ reticular veins.

Many physicians have found that vessel location may affect treatment outcome, with vessels on the medial thigh being the most difficult to completely eradicate. However, with the PDL, vessel location appears to be unrelated to treatment outcome if telangiectatic patches with untreated associated reticular veins are excluded. In addition, there appears to be no obvious difference in efficacy between telangiectatic patches that are treated with compression and those that are not (Fig. 13.20). Sadick et al56 conducted a study which further supported the notion that graduated compression stocking use for 7 days starting immediately after treatment of class I-II venulectasia with PDL yielded no additional therapeutic efficacy.