The new appearance of previously unnoticed, fine red telangiectasia occurs in a number of patients. The reported incidence varies from 5% to 75%.
Reasons for the development of TM are multiple. Recovery from an ischemic injury such as closing blood vessels with sclerotherapy may produce a hypoxia-induced neovascularization. In addition, injury to endothelial cells may stimulate the release of a variety of growth factors. These responses are probably a fundamental feedback response, acting to satisfy tissue needs for oxygenation. For example, this response commonly is seen in myocardial collateraliza-tion. Given these protective factors, it is curious that the incidence of TM after sclerotherapy is not higher; therefore other innate factors must predispose to the development of TM.
Although most authors do not comment on a sexual predisposition, we have seen the development of TM in only one male patient with leg telangiectasia. Because fewer men seek treatment for leg telangiectasia than women, an accurate appraisal of the sexual incidence of TM cannot be stated.
TM may appear anywhere on the leg and we have never seen it to occur on the face, hand, or chest after sclerotherapy treatment. Duffy has reported that in 80% of his patients TM developed within 10 inches of the knees (personal communication, Oct 1994). Our experience is similar to Duffy's. Duffy postulates that relative ischemia occurs in this area from tissue hypoxia that results from the thighs and knees pressing on each other during sleep when one lies on his or her side. Hypoxia has been found both in the retina and around compressive tumors to promote vascular endothelial growth.
Probable risk factors for the development of TM in patients with leg telangiectasia include obesity, use of estrogen-containing hormones, pregnancy, and a family history of telangiectatic veins. Excessive postsclerotherapy inflammation also may predispose toward development of TM.
After sclerotherapy, the development of TM occurs rapidly, often patients report the development over a few days three to six weeks after treatment. Normally, the more than one trillion endothelial cells that line blood vessels have a turnover time of more than 1000 days.20 However, under appropriate conditions new vessels can develop in two to three days. Observations of mammalian systems have demonstrated the development of a vein from a capillary, an artery from a vein, a vein from an artery, or from either back to a capillary. In coronary vessels the number of arterioles and capillaries increases within one week after injury.
A study comparing different times of postsclerotherapy compression in treating leg telangiectasia also demonstrated a decrease in TM when compression was maintained for one to three weeks (5%) versus three days (30%) or no compression (40%).21 This is most likely a reflection of a decrease in intravascular thrombosis with prolonged graduated compression, which results in a decreased phlebitic effect with decreased inflammation.
Estrogen may play a role in the development of TM. It appears that the incidence of persistent TM may be increased in patients taking systemic estrogen preparations. Weiss and Weiss22 found a relative risk of 3.17 (p > 0.003) for development of TM while patients were receiving exogenous estrogen. The mechanism for promotion of TM by estrogen is speculative but may be the result of its effect on modulating mast cell responses.
In addition, Davis and Duffy23 have reported on the virtual disappearance of leg telangiectasia and TM in a 51-year-old woman with estrogen-receptor-positive breast carcinoma after initiation of antiestrogen therapy with tamoxifen citrate (Nolvadex). This may be due to the inhibition of angiogenesis by tamoxifen.
Regardless of the cause of TM, since patients seek treatment to eliminate leg telangiectasia, it is disconcerting for the sclerotherapist to produce new areas of telangiectasia. Unfortunately, despite one's best efforts, TM occurs in a significant percentage of patients. Fortunately, TM usually resolves spontaneously over three to 12 months. Our experience is that less than 1% of patients will have TM persisting for one year (see Figure 15.6).
Treatment methods for TM are limited. Reinjection with hypertonic solutions or glycerin may be helpful. Because of the extremely small diameter of these vessels, use of a 31-33-gauge needle is helpful. Injection of any feeding reticular veins or venulectases into the TM area also should occur.
Various vascular-specific lasers and intense pulsed light (IPL) sources may be useful in treating these vessels.24 In our practice, at least 75% of patients with persistent TM partially or completely improve after laser or IPL treatment. Interestingly, individual TM lesions may respond better to one laser or IPL than another. Reasons for the variable response are speculative. The 532-nm long-pulse
Nd:YAG laser set at the highest fluence and pulse durations available has been found to be most effective on the most recalcitrant lesions. However, persistent and rarely permanent hypopigmentation may occur. The use of the PDL may also be effective but result in long-term hyperpig-mentation. Unfortunately, even with all these therapeutic approaches, rare TM may be resistant to treatment, possibly because these resistant TM lesions may have a feeding arteriolar network that prevents persistent vessel elimination.
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