Treatment of telangiectasia: A review

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Continuing medical education (Derma/ologic surgery) Treatment of telangiectasia: A review Mitchel P. Goldman, M.D., and Richard G. Bennett, M.D. Los Angeles, CA Telangiectasias are thought to occur through the release or activation of vasoactive substances under a multitude of conditions. Patients seek therapy for telangiectasias principally because of the unsightly visual appearance. This paper discusses the etiology, histology, and treatment of telangiectasias, emphasizing microsclerotherapy. Specifically, the indication for sclerotherapy, mechanism of action of the various sclerosing agents, microinjection technic, and the advantages and disadvantages of the most commonly used sclerosants, sodium morrhuate, sodium tetradecyl sulfate (Sotradecol), hypertonic saline, hydroxypolyethoxydodecane (polidocanol; Aethoxysklerol), and, Sclerodex (a mixture of dextrose and sodium chloride) are reviewed. (J AM ACAD DERMATOL 1987;17:167-82.) The term telangiectasia was first coined in 1807 by Von Graf to describe a superficial vessel of the skin visible to the human eye.* Individually, telangiectasias measure 0.1 to 1 mm in diameter and represent either an expanded venule, capillary, or arteriole. Telangiectasias that originate from arterioles or the arterial side of a capillary loop tend to be small, bright red, and do not protrude above the skin surface. Telangiectasias that originate from venules on the venous side of a capillary loop, on the other hand, are blue, wider, and often protrude above the skin surface. Sometimes telan-

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The CME articles are made possible through an educational grant from Syntex Laboratories, Inc. From the Division of Dermatology, Department of Medicine, University of California, Los Angeles. Presented in part at the 45th Annual Meeting of the American Academy of Dermatology, New Orleans, LA, Dec. 6-11, 1986. Reprint requests to: Dr. Mitchel P. Goldman, 850 Prospect St., Suite 2, La Jolla, CA 92037. *Merlen JF. Red telangiectasias, blue telangiectasias. Soe Franc Phlebol 1970;22:167-74.

giectasias, especially those arising at the capillary loop, are at first red, but with time become blue, probably because of an increasing hydrostatic pressure and backflow from the venous side. Varicose veins are dilated veins arising in vessels larger than venules, measuring more than 1 mm in diameter. Redisch and Pelzer ~ classified telangiectasias into four types: (1) sinus or simple (linear), (2) arborizing, (3) spider or star, and (4) punctiform (papular) based on clinical appearance (Fig. 1). Papular telangiectasias are frequently part of genetic syndromes, such as Rendu-Osler-Weber disease or collagen vascular disease. Spider telangiectasias are red and arise from a central filling vessel of arteriolar origin. If one puts pressure on the feeding vessel, the branching "arms of the spider" blanch. Red linear telangiectasias occur on the face (especially the nose) or legs. Blue linear or anastomosing telangiectasias are found most often on the legs. These are commonly seen for treatment. Because their pathogenesis is somewhat 167

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Table I. Causes of cutaneous telangiectasia I. Genetic

Vascular nevi Nevus flammeus Nevus araneus Congenital neuroangiopathies Ataxia telangiectasia Sturge-Weber syndrome Maffucci's syndrome Klippel-Trtnaun ay-Weber syndrome Congenital poikiloderma (Rothmund and Thomson syndromes) Bloom's syndrome Cockayne's syndrome Hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber disease) Essential progressive telangiectasia Generalized essential telangiectasia Familial (autosomal dominant) Acquired (hormonal or infectious stimulation) Unilateral nevoid telangiectatic syndrome Diffuse neonatal hemangiomatosis II. Acquired disease with a secondary cutaneous component

Collagen vascular diseases Lupus erythematosus (especially periungual) Dermatomyositis Progressive systemic sclerosis (especially periunguaI, and with the calcinosis, Raynaud's, esophageal dysmotility, sclerodactyly, and telangiectasia [CREST] syndrome)

different, this must be appreciated so that the choice for therapy is more rational. All forms of telangiectasias are thought to occur through the release or activation of vasoactive substances under a multitude of conditions, including anoxia, hormones, chemicals, infection, and/or physical factors, with resulting capillary or venular neogenesis. 2.3.* Table I (which is an extension of the observations of Shelley 4 and Anderson and Smith 5) lists the major causes and diseases associated with telangiectasias. Telangiectasias of the face are probably due to persistent active arteriolar vasodilation resulting from weakness in the vessel wall, with elastic changes or weakness in the surrounding connective tissue from chronic sun exposure. These telan*MerlenJF. Red telangieetasias,bluetelangiectasias.SoeFrancPhlebol 1970;22:167-74.

II. Acquired disease with a secondary cutaneous component--cont' d

Other Telangiectasia macularis eruptiva perstans (mastocytosis) Carcinoma telangiectasia (metastatic tumors) III. Component of a primary cutaneous disease Rosacea Varicose veins Basal cell carcinoma Necrobiosis lipoidica diabeticorum Poikiloderma atrophicans vasculare Capillaritis (purpura annularis telangiectodes) Xeroderma pigmentosum Pseudoxanthoma elasticum Degos' disease IV. Hormonal

Pregnancy Corticoid-induced Cushing's syndrome/disease Iatrogenic (frdm systemic, topical, or intralesional use) Estrogen therapy (usually with high dose) V. Physical damage

Actinic dermatitis Radiodermatitis Postsurgical Especially in suture lines under tension and after rhinoplasty Physical trauma

giectasias arise primarily from arterioles and are seen frequently in individuals with fair complexions, often on the nose, especially the ala nasi and nasolabial crease. Rosacea may be present along with the telangiectasias. Telangiectasias on the legs are usually different from those on the face, both in pathogenesis and vessel type. These telangiectasias arise primarily in venules and are due to persistent passive venous dilatation (from increased hydrostatic pressure), as well as an increased distensibility of the vessel wall. Although they may appear at first as erythematous streaks, with time they turn blue. Often they are directly associated with underlying varicose veins, so that the distinction between telangiectasias and varicose veins becomes blurred. ~ Such telangiectasias are c o m m o n in w o m e n between the ages of 30 and 50, many of w h o m have been pregnant or who have taken birth control

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pills.* Interestingly, pregnant women often develop telangiectasias on the legs within a few weeks of conception, even before the uterus has enlarged to compress venous return to the pelvis. 7,s In addition, pregnant women and those taking birth control pills have been shown to have an increase in the distensibility of vein walls. 9 Thus, a primary hormonal influence is involved in the development of varicose veins and their associated telangiectasias in this group of patients. The hormonal influence in telangiectasia neogenesis has also been noted in ten of fifteen cases of unilateral nevoid telangiectasia syndrome that occurred during pregnancy or puberty and was related to high serum estrogen levels. Four of the remaining five cases were associated with alcoholic cirrhosis and one was congenital.Z~ Two common patterns of telangiectasias on the legs of women, besides red or blue streaks, are the parallel linear pattern, especially found on the medial aspect of the thigh, and the arborizing or radiating cartwheel pattern, especially seen on the lateral aspect of the thigh. '~ These two subsets of telangiectasias seem to run in families and may form anastomosing complexes that may be as large as 15 cm in diameter. These complexes have been termed "venous stars," "sunburst stars," "sunburst venous blemishes," and "telangiectatic mats" by various authors. Varicose veins of the lower legs are thought to be due to incompetent perforating veins ~2 and/or small arteriovenous communications.~3'~4'l These veins and/or communications connect the deep venous system to the superficial veins in the lower extremities. When the muscles in the legs relax, pressure in the deep veins falls below that in the superficial veins. Blood then flows from the superficial to the deep venous system. With muscle contraction, one-way valves in the deep and perforator veins help keep the blood from being pushed into the superficial veins. If these valves are incompetent, venous backflow occurs, resulting in venous hypertension and chronic venous insufficiency: Incompetent valves may occur because of local trauma, thrombophlebitis, familial *Merlen JF. Red telangicctasias, blue telangiectasias. Soc Franc Phlebol 1970;22:167-74. tSchroth R, Venose sanerstoffsattigung bei Varicen. Arch Kiln Chir 1962;300:419,

Treatment of telangiectasia

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Fig. 1. Four types of telangiectasias. A, Simple. B, Arborized. C, Spider. D, Papular. (From Redisch W, Pelzer RH. Am Heart J 1949;37:106-14.) weakness in vein structure, increased blood volume, or hormonal influences. When associated with varicose veins, telangiectasias are more common on the dorsum of the foot, on the leg below the knee, and/or on the medial aspect of the thigh. Telangiectasias of the face are usually asymptomatic, but on the legs they may cause a buming discomfort noted chiefly during warm weather.* Superficial or fine varicosities on the anterior and external aspects of the thighs may also become painful preceding or during menses. ~5..~Larger varicose veins are more symptomatic, being associated with a feeling of muscle fatigue in the legs and throbbing pain. ~2 In addition, pruritus, dermatitis, nocturnal cramping, and ulceration with bleeding may also occur, t6-~s HISTOLOGY Histologic examination of simple telangiectasias demonstrates dilated blood channels in a normal dermal stroma with a single endothelial cell lining, no muscularis, and no adventitia. 1 Therefore, such vessels probably evolve from capillaries. Vascular spiders arise from a terminal arteriole.:~ Bluish

*Pierce HE, Management of unsightly micro-varicositles, Am J Cosmet Surg 1984;1:45-7, tTournay PR. Sclerosing treatment of very fine intra or subdermal varicosities. Soe Franc Phlebol 1966;19:235-41.

~:Merlen JF. Red telangiectasias, blue telangiectasias. Soc Franc Phlebol 1970;22:167-74.

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Table H. Methods for treating telangiectasias I. Electrosurgery Electrodesiccation Timed diathermocoagulation II. Laser Argon Carbon dioxide Tunable dye HI. Dermabrasion IV. Medical Tetracycline For generalized essential telangiectasia Estrogen For hereditary hemorrhagic telaniectasia V. Sclerotherapy Intradermal Intravascular

arborizing telangiectasias of the lower extremities are probably dilated venules, possibly with intimate and direct connections to underlying larger veins from which they are direct tributaries: Both Bodian 19 and Faria and Moraes2~ have found on biopsy examination that such "telangiectasias" are actually ectatic veins. TREATMENT

Patients seek therapy for telangiectasias or varicose veins principally because of the unsightly visual appearance. However, treatment is frequently difficult to obtain because, except for surgical venous stripping, other forms of therapy are largely untaught in medical schools or residency programs. For smaller telangiectasias of the legs patients are told they must live with their problem. Forms of therapy, such as sclerotherapy, are either not discussed or are mentioned disparagingly. However, the available evidence would indicate that safe, effective forms of treatment (other than surgery) are possible and mostly successful. The following discussion will confine itself to the treatment of telangiectasias, emphasizing sclerotherapy. Electrosurgery

Numerous methods have been used to treat telangiectasias (Table II). Riviere~ first described electrotherapy of cutaneous disease in the early 1900s. Electrodesiccation was used to treat telan-

Journal of the American Academy of Dermatology giectatic vessels and is still used today, especially on the face. Very low amperage current is employed, as is used in electrolysis. 22 Electrodesiccation is a dehydration process that creates heat in the tissue immediately adjacent to the needle point. The heat results from resistance offered by the body tissues to passage of a highly damped current radiated through a monoterminal electrode. Cellular fluids are thus evaporated, resulting in tissue destruction. Recoules-Archez3 noted that with electrodesiccation the vessel must be penetrated in depth 1.0 to 1.5 mm with an electrode every 2 to 3 mm with a 1- to 2-A current. Histologic examination demonstrates a bursting of tissue with cellular elongation. ~3 Some degree of superficial necrosis always occurs, and thus treatments can be performed only every 5 to 6 weeks to allow for interval cutaneous healing. Three to four sessions are usually needed for blue telangiectasias and five or more treatments sessions for red telangiectasias. ~3Multiple punctiform, whitish, or pigmented scars may occur.~S Visible scarring may be more common in fair-skinned blondes and redheads. Keloids may also form in blacks: 3 Bolliger and Holzer24 believe that tissue coagulation in circumscribed subcutaneous regions is necessary to produce vascular sclerosis.. They describe a modified electrocoagulation device that passes electrical current into the vessel until coagulation is produced, thereby utilizing the least amount of electrical current. They believe that this technic avoids the pain and scarring associated with other electrical treatments. A more refined technic of electrocautery, "timed diathermocoagulation," was recently reported by Capurro. zs With this technic, microbums, 5/100 second at 28 watts, are used to sclerose the vessel. Capurro does not note scarring with the treatment of facial telangiectasia. Most recently, Kobayashi 26 reported the use of insulated needles to treat telangiectasias. His electrosurgical needle is insulated on the upper half of the tip as well as on the l-ram base. He utilizes an IME HR 5000 electrosurgical apparatus set at 30-40 W, with 0.5- to 1-second pulses. He inserts the needle directly over the vessel, under and parallel to the skin surface at about 5-mm intervals. He reports "very satisfying" results without scarring. Temporary postoperative hyperpigmentation occurs in most o f his cases as the only adverse effect of note. Thus,

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until further studies with diathermocoagulation and insulated needles are reported, electrosurgery is best reserved for the smallest of telangiectasias. Laser therapy Argon and carbon dioxide (CO2) lasers have also been used for the obliteration of venules and telangiectatic vessels. 27 The CO2 laser emits light energy at 10,600 nm in the infrared portion of the electromagnetic spectrum. Tissue destruction is nonselective and occurs by vaporizing water within cells. Thus, the skin surface, as well as the dermis, is destroyed. Because of this nonselective action, the CO2 laser is of no advantage over the electrodesiccation needle and has not been utilized successfully in treating telangiectasias. The argon laser is theoretically better suited for treating telangiectasias. The blue-green light (488 and 514 nm) that is emitted from this machine is, for the most part, selectively absorbed by the red-purple oxygenated hemoglobin located in the superficial dermal ectatic blood vessels, and it passes relatively unabsorbed through the skin surface for a distance of about 1 m m in Caucasian skin. 28 Light energy is transformed into heat and dermal damage ensues. Vessels thrombose and the lesions lighten. However, the argon laser light is not entirely hemoglobin-specific. Epidermal melanin also absorbs a variable portion of argon laser light. This may result in hypopigmentation of the treated areas. In addition, argon laser exposures with pulse durations of 50-200 milliseconds allow time for extensive radial diffusion and dissipation of heat generated in the exposed blood vessels, thereby resulting in a relatively nonselective thermal destruction. 29 Thus, there is a risk of hypertrophic or atrophic scarring secondary to nonspecific epidermal and upper dermal necrosis and subsequent fibrosis. This is noted clinically by epidermal sloughing postoperatively, followed by crusting and gradual reepithelialization over 1 to 2 weeks.3~ Apfelberg et a131"33 and Landthaler et a134 have reported on the use of the argon laser in patients with facial telangiectasias. They utilized laser parameters of between 0.8 and 1.5 W power with exposure times of 0.2 to 0.3 second and spot sizes between 0.2 and 1.0 ram. They reported subjectively good results in 90% to 99% of patients. However, Lyons et al, 35 Remington, 36 Gold-

Treatment of telangiectasia 171

man,* Arndt, 37 and Ratz et al3s have noted pitted and depressed scars, frequent hypopigmentation (which in most cases slowly resolves over 1 year), and hyperpigmentation (in 5%-10% of patients, especially around the lips and mouth, trunk, and extremities,) with these laser parameters. In addition, Dolsky 39 noted a high rate of recurrence of the dilated veins in the ala nasi crease, with frequent formation of a depressed groove where the vessel was treated when elimination of the vessel occurred. In contrast to the relatively good results obtained when treating facial telangiectasias, telangiectasias or superficial varicosities of the lower extremities are not responsive to laser treatment. Apfelberg and McBumey 33caution that the treated areas in this location usually appear purple or depressed, often leaving a worse cosmetic appearance than the untreated condition. In treating vessels of the lower extremities, Dixon et al4~ 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. 4t Thus, argon laser therapy appears to be a satisfactory method for treating selected facial telangiectasias and is much less effective in treating leg telangiectasias. In the future, the tunable dye laser, with its ability to be tuned to produce highly selective vascular damage, may become the laser of choice for treating vascular lesions. When tuned to 577 nm (corresponding to the alpha band of oxyhemoglobin), the laser energy penetrates to the depth of dermal blood vessels with little interfering absorption by melanin. Thus, highly specific vessel damage occurs. Dermabrasion Recently, Lapins42 described a patient with telangiectasias on the nose secondary to x-ray therapy and solar damage. He utilized a dermabrader with a diamond fraise and a light freeze to "flick the ectasia from the skin," with an excellent postoperative result. Such telangiectasias, however, are usually secondary to an underlying etiology, such as solar damage, rosacea, and corticosteroid treat*Goldmaa L. Application of laser therapy. Paper given at the Noah Worcester Dermatologie Society, Hilton Head, SC, April 1984.

172 Goldman and Bennett

ment. Thus, recurrences will be common. In addition, complications common in facial dermabrasion (hypo- and hyperpigrnentation and hypertrophic scarfing) make this procedure tenable only when treating anatomic units. Nevertheless, this modality of therapy will remove many telangiectasias at one time. Medical therapy Medical therapy has also been reported to be successful in patients with acquired and congenital diffuse telangiectasias. Generalized essential telangiectasia has been reported to resolve after treatment with tetracycline, thus, postulating an underlying infection for its e t i o l o g y . 4'43 Hereditary hemorrhagic telangiectasia has also been reported to be treated or improved successfully with oral estrogen therapy. 44The rationale in treating hereditary hemorrhagic telangieetasia with oral estrogens is to produce metaplasia of the normal nasal mucosa, which thickens layers of keratinizing squamous epithelium to protect the abnormal fragile vessels from local traumal. 45 In addition, estrogen may restore the continuity of the endothelium to these abnormal vessels. 46 However, medical therapy with these two agents has not been noted to be helpful with other acquired telangiectasias, and, as noted previously, increased serum estrogen has been associated with an increased number of telangiectasias.6

Sclerotherapy Sclerotherapy with a wide variety of substances has become a popular method for obliterating both varicose veins and telangiectasias and is widely practiced in Europe. Sclerotherapy refers to the introduction of a foreign substance into the lumen of a vessel, causing thrombosis and subsequent fibrosis. This procedure, when performed on telangiectasias, is referred to as microsclerotherapy.47 Injection treatment of varicose veins was probably initiated by Hippocrates, who traumatized varices with "a slender instrument of iron," thus causing thrombosis.~ Intravascular sclerotherapy of varicose veins was first performed shortly after the introduction to the medical world of the hypodermic syringe by Rynd,49,5~either by Monteggio and Leroy D'Etiolles in 1840 with a solution

Journal of the American Academy of Dermatology

of absolute alcohol* or by Charles-Gabriel Pravaz, of the Lyonnaise School of Medicine, in 1851 with a solution of ferric chloride: ~,Sz Clinical results were good but the procedure produced many complications, including mortality from both sepsis and embolism. The procedure was abandoned. It was not until the early 1900s that a revival of sclerotherapy occurred, after it was noted that intravenous injections for antisyphilitic treatment at times resulted in the obliteration of elbow veins.5~ Physicians then began searching for the ideal sclerosing agent (Table III) and utilized many different compounds, including the following: 50% grape sugar, ~4mercury biniodide, t 20% and 30% sodium salicylate: 5:6 sodium citrate, s7 20%-30% sodium chloride: 7 1% bichloride of mercury, 5~ 50%-60% calorose (75% invert sugar with 5% saccharose), 59 and 12% quinine sulfate with 6% urethane.59 These substances were widely used but resulted in unacceptable levels of allergic reactions, necrosis, pain, and even fatalities, 6~ With the advent of modem surgical technics, surgical treatment of varicose veins gained wide acceptance by the medical community, and sclerotherapy, especially in this country, fell into disrepute. It was not until the 1930s and 1940s, with the introduction of sodium morrhuate and sodium tetradecyl sulfate (Sotradecol), that sclerotherapy of varicose veins began its second revival. Sclerosing treatment for telangiectasias was ignored until the 1930s, when Biegeleisen63 injected sclerosing agents intradermally and/or subcutaneously into the area of capillary enlargement. However, this resulted in severe necrosis and/or lack of effect on the telangiectases. ~3Biegeleisen, in 1934, 6~ developed and popularized a method of "microinjection" of telangiectasias with sclerosing agents through the use of an "extremely fine metal needle" (later described as a handmade 32- or 33-gauge needle). 64 He utilized sodium morrhuate, which was popularized by Higgins and Kitte165 in 1930 for treating varicose veins.

*Schneider W. Contribution to the history of the sclerosing treatment of vadees and to its anatomo-pathologie study. Soe Franc Phlebol 1965;18:117-30. tBazelis R. Thesis de doctorate. Pads, 1924. (Cited in Reference 51.)

Volume 17 Number 2, Part 1 August 1987 Indication The indication for microsclerotherapy is theoretically any small telangiectatic vessel or venule on the cutaneous surface. Best results are obtained on superficial linear or radiating vessels of the lower extremities. Telangiectasias on the face are less reliably responsive to microsclerotherapy, although they may still be injected successfully. This is because telangiectasias in this location probably have more of an arteriolar component and are due to active vasodilatation. Some sclerosants affect arteries in a different manner than veins. Although thrombosis occurs, intimal damage may not. 66 MacGowen et a166 studied the local effects of intra-arterial injections of sodium tetradecyl sulfate. They injected sodium tetradecyl sulfate 3.0% into the central auricular artery at the base of the rabbit ear and visualized the resulting chain of events through a Perspex ear chamber with high-power and oil immersion lenses. Spasm was not noted in any vessel, but within minutes the erythrocytes appeared distorted and broken, with formation of a central homogeneous thrombus that moved down the arteriole and lodged into a capillary. Intimal damage did not occur. Thus, the major effect of sodium tetradecyl sulfate was on the blood cell mass, which it destroyed and converted into an intravascular embolus. Subsequent biopsy of the ears at 1 hour and at 5 days demonstrated thrombus only without evidence of intimal damage. These results are distinctly contrary to effects of sclerosis of veins. The reason for this different mechanism of action is unknown but may relate to the difference in velocity of blood flow between arteries and veins. Specifically, sodium tetradecyl sulfate injected intra-arterially may not have enough time to react with endothelium, being inactivated by serum factors and/or diluted to a "safe" concentration by the more rapid m e d a l flow. "Safe" is a relative term because inadvertent intra-arterial injections of sodium tetradecyl sulfate have produced gangrene through thrombosis of vessels downstream from the area of injection. 66'67 In addition, prolonged compression cannot be placed easily on facial vessels after microsclerotherapy to minimize thrombus formation. Therefore, complications common to sclerotherapy (pigmentation

Treatment of telangiectasia 173

Table HI. Historical introduction of sclerosing agents 1840 1851-3 1855 1880 1904 1906 1910 1917 1919 1919 1920 1922 1922 1926 1927 1929 1929 1930 1933 1946 1949 1959 1966 1969

Absolute alcohol (Monteggio, Leroy D'Etiolles) Ferric chloride (Pravaz) Iodo-tannic liquer (Desgranges) "Chloral" (Negretti) 5% phenol solution (Tavel) Potassium iodo-iodine (Tavel) "Sublime" (Scharf) Hypertonic glucose (Calorose) (Kausch) Sodium salicylate (Sicard and Gaugier) Sodium bicarbonate (Sicard and Gaugier) Bichloride of mercury (Wolf) 12% quinine sulfate with 6% urethane (Geneurier) Biiodine of mercury (Lacroix, Bazelis) Hypertonic saline with procaine (Linser) 50% grape sugar (Doerffel) Sodium citrate (Kern and Angel) 20%-30% hypertonic saline (Kern and Angel) Sodium morrhuate (Higgins and Kittel) Chromated glycerin (Jausion) Sodium tetradecyl sulfate (Sotradecol) (Reiner) Phenolated mercury and ammonium (Toumay and Wallois) Stabilized polyiodated ions (Imhoff and Sigg) Hydroxypolyethoxydodecane (Aethoxysklerol) (Henschel and Eichenberg) Hypertonic saline/dextrose (Sclerodex)

and necrosis), as well as revascularization of the injected vessel, are probably more common than when injections are performed elsewhere. Mechanism of action The mechanism of action for sclerosants appears to be one of activation or release of thromboplastic activity by unknown mechanisms, which initiates the extrinsic pathway of blood coagulation. Alternatively, endothelial damage may result in exposure of subendothelial collagen fibers, which causes platelet adherence, release, and aggregation, thereby initiating the intrinsic pathway of blood coagulation by activating factor XII. Either or both of these mechanisms result in thrombus formation, with subsequent organization, and fibrosis.

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Factors predisposing to thrombus formation include decreased velocity of blood flow, hypercoagulability, and endothelial cell damage. 68The velocity of blood flow is unaffected by the sclerosing agent itself but flow is usually slower in varicose veins and/or telangiectases in general. Wuppermann69 studied fibrinolysis in subjects injected with 3% polidocanol (Aethoxysklerol). A slight, statistically insignificant hyperfibrinolysis appeared in blood drawn from the antecubita] vein. Thus, thrombus formation gradually occurs only at the injection site and does not result in systemic hypercoagulability. Indeed, polidocanol, when utilized in patients on systemic anticoagulants, has no decrease in its sclerosing action. 7~Earlier work had also demonstrated the lack of effect of polidocanol on coagulation parameters in rabbits. 7t MacGowen et a166combined sodium tetradecyl sulfate with whole normal blood, resulting in a homogeneous red lysate without the formation of thrombin. Thus it appears that the mechanism of action ofpolidocanol and sodium tetradecyl sulfate is to produce endothelial damage* with resultant thrombus formation, but not thrombus formation associated with platelet aggregation. This mode of action is also seen with other sclerosing agents. Lindemayr and SantlerSt studied the sclerosing effect of 4% stabilized polyiodated ions (variglobin) with standard and immunofluorescent microscopy and demonstrated fibrin deposition on the sclerosed veins only. Platelets fixed only to elastin, collagen, basement membrane, and the amorphous material of the subendothelial layer, not to intact endothelial cells. Thus, the sclerosant produces its end result of vascular fibrosis through the irreversible destruction of endothelial cells, with resultant thrombus formation on the subendothelial layer. Scanning electron microscopy of sclerosed rabbit veins (agent not noted) by Merlen et a172demonstrated intimal cracks and fissures that left intirdal connective tissue fibers and elastic lamina exposed. Ultrastructural damage occurred in 5 minutes in the dorsal rabbit ear vein, with stasis of blood and platelet aggregation on intact endothelial intima. A review of the mechanism of action for specific *Klein-FeinL What happens during the injection of sclerosant. Ph[el)ologie 1977130:165-6.

sclerosants appears elsewhere. 73 In short, detergent-sclerosants like sodium morrhuate, sodium tetradecyl sulfate, and polidocanol produce endothelial damage through interference with the cell surface lipids. Hypertonic saline and hypertonic glucose solutions probably cause dehydration of endothelial cells through an osmosis, resulting in endothelial destruction.* Whether altered vessels (which may be dilated) are more susceptible to the action of sclerosants than normal vessels is unknown. Manufacturers of polidocanol believe that this agent acts selectively on damaged vessels, t'~: However, experimental injection of sclerosants in normal dorsal rabbit ear veins yields effective vessel sclerosis. 73 Human varicose and telangiectatic vessels are noted to sclerose focally at times after the injection of various sclerosants. The focal nature of endothelial necrosis and thrombus formation may be related to toxic effects of sclerosant on the surrounding media. Venograms of varicose veins injected with sodium tetradecyl sulfate demonstrate segmental, intense, and diffuse spasm, both proximally and distally, at time of injection and 6 minutes after injection. TM Thus, maximal sclerosis probably occurs at points of vessel spasm where the entire endothelium is adherent. This agrees with the clinical impression that total compression of the sclerosed vessel is necessary for ideal, longlasting, and complication-free sclerosis.75.76 Goldman et a173demonstrated that effective sclerosis with one detergent, polidocanol is dependent on the concentration. Thus, there may be a concentration that is ideal for effective sclerosis of other sclerosants. Other factors, including vessel diameter, rate of blood flow, and anatomic site of the vessel, may also be important. Available sderosing agents The only sclerosing agents approved for use in this country by the Food and Drug Administration are sodium morrhuate and sodium tetradecyl sulfate. Hypertonic saline is available in a 23.4% *Klein-Fein J. What happens during the injection of sclerosant. Phlebologie 1977;30:165-6. tDexo Labs (Nanterre, France), Product description on hydroxypolyethoxydodeeane. Received with correspondence, May 1985. :~Kreussler & Co. (Wiesbaden-Biebdch, West Germany). GMbH: Product insert for Aethoxysklerol. Chemisehe Fabrik, D-6200 Wiesbaden Biebrich, 1985.

Volume 17 Number 2, Part 1 August 1987

concentration for use as an abortifacient, but it is commonly used in various concentrations with and without the addition of heparin and procaine or lidocaine for sclerosis of telangiectasias and superficial varicosities. Polidocanol has recently been popularized by D. Duffy and P. Goldman at the annual American Academy of Dermatology meetings (Washington, DC, 1984, and Las Vegas, NV, 1985) and at the annual meeting of the Society for Dermatologic Surgery and Oncology (Lake Buena Vista, FL, 1985) and is widely used. Sclerodex, a solution of dextrose 25% and sodium chloride 10%, is commonly used in Canada for sclerosis of superficial varicosities and telangiectasias. Therefore, the remainder of this paper will discuss the pros and cons of these commonly used and readily available agents. Sodium m o r r h u a t e . Sodium morrhuate (a mixture of sodium salts of the saturated and unsaturated fatty acids present in cod liver oil) was first prepared for injection by Ghosh 77 and Cutting. 7s This sclerosant met with much enthusiasm in the United States by Biegeleisen 79 and others. The disadvantages consisted primarily of its lack of standardized composition, instability in solution, inability to be prepared aseptically, and extensive cutaneous necrosis when inadvertently injected perivascularly. Many cases of anaphylactic reactions have been reported and rarely have resulted in fatalities. 8o An attempt was then made to isolate a pure fatty acid salt from psyllium seeds, castor oil, olive oil, and synthetic oleates. However, allergic reactions secondary to protein contamination still occurred at an unacceptable rate. 8~ Thus, this agent is rarely used as a sclerosant for telangiectasias. Sodium tetradeeyl sulfate. Sodium tetradecyl sulfate (Sotradecol; sodium 1-isobutyl-4-ethyloctyl sulfate plus benzoyl alcohol 2% [as an anesthetic agent], also called Trombovar outside of the United States), a synthetic surface-active substance, was first described by Reiner in 1946. 82 It is a long-chain fatty acid salt of an alkali metal and has properties of a soap. Tretbar, '2 in 1978, first reported the injection of a 1% solution into spider angiomas. He noted excellent results in virtually all 144 patients treated. He also noted an unspecified number of episodes of epidermal necrosis, without significant sequelae, and a 30% incidence of postsclerosis pigmentation that re-

Treatment of telangiectasia 175

solved within a few months. Shields and Jansen, 83 in 1982, were first to describe microsclerosis of telangiectases with sodium tetradecyl sulfate in the dermatologic literature. They injected 1% sodium tetradecyl sulfate in 105 patients and reported only one episode of necrosis in over 600 treatments in vessels less than 5 mm in diameter. There were no systemic reactions and the majority of postsclerosis pigmentary changes resolved i n 3 to 4 months. Mantse, 84however, reported a near universal incidence of superficial necrosis when a 1% solution of sodium tetradecyl sulfate is used to sclerose telangiectasias, even when extravasation does not occur. In this regard, experimental intradermal injection of sodium tetradecyl sulfate in rabbit skin has also been found to produce epidermal and dermal necrosis both clinically and histologically, sS,* Occasionally, anaphylactic shock and, more commonly, generalized urticaria and edema or diffuse maculopapular eruptions have been noted86ag,t (Table IV). In order to prevent allergic manifestations from sodium tetradecyl sulfate, French sclerotherapists advocate a 3-day pre- and posttreatment course with an antihistamine. P. Flude noted no episodes of allergic reactions in 500 patients who were treated in this manner.t Thus, a measurable, and perhaps preventable, number of allergic reactions have been noted with sodium tetradecyl sulfate. Temporary postsclerosis pigmentation has been noted by Toumay:l: to occur in up to one third of patients. Thus, sodium tetradecyl sulfate has a measurable but small incidence of allergic reactions, a real risk for epidermal and dermal necrosis with inadvertent extravasation, and postsclerosis pigmentation occurring in a significant percentage of patients. Hypertonie saline. Hypertonic saline was first used to sclerose varicose veins by Linser in 1926w *Miyake H, Kauffman P, de Arruda Behmer O, WoloskerM, Lean LEP. Mechanisms of cutaneous necrosis provoked by sclerosing injections in the treatment of microvarices and telangieetaslas: experimental study. Rev Ass Brasil 1976;22:115-20. tPassas H. One case of tetradecyl-sodlumsulfate allergy with general symptoms. Soc Franc Phlebol 1972;25:19-26. :~Tournay PR. Sclerosing treatment of very fine intra or subdermal varicosities. Soc Franc Phlebol 1966;19:235-41. w E, Stemmer R. Classification and mechanism of action of selerosing agents. Soc Franc Phlehol 1969;22:143-8.

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and by Kern and Angle in 1929.57 In 1975 Foley9~ described the microinjection of "venous blemishes" with a 30-gauge needle utilizing 20% hypertonic saline, 100 U/ml of heparin, and 1% procaine, which he termed Heparsal. He reported no allergic or anaphylactic reactions and only rare pigmentary problems in over 1,000 treatments to more than 100 patients. He believed that addition of heparin helped to prevent thrombi in larger vessels and addition of procaine helped alleviate pain on injection. No mention was made concerning necrosis caused by extravasated solution. Alderman9t reported on 150 patients with telangiectasias treated over 8 years with 18% to 30% hypertonic saline--18% to 20% hypertonic saline most commonly for "venous telangiectasias" (blue telangiectasias), 22% to 25% hypertonic saline for "arterial lesions" (red telangiectasias), and 30% hypertonic saline for rare, large arterial lesions. He diluted the saline with lidocaine to achieve a 0.4% concentration of lidocaine. Tissue necrosis was not noted, and the only adverse side effects reported were mild, temporary burning with injection, and residual brownish pigmentation, which occurred in up to one third of patients. The pigmentation usually resolved, for the most part, over 1 year. Bodian 19recently described his experience with hypertonic saline (23.4%) in the sclerosing treatment of telangiectases (superficial "sunburst venous blemishes"). He compared hypertonic saline with and without heparin clinically and does not believe that the addition of heparin is necessary for effective sclerosis. The only complication mentioned by Bodian was muscle cramps at the site of injection, which lasted 3 to 5 minutes before relief with gentle massage and walking. He injects 0.5 to 1 ml of hypertonic saline after a small amount of air bolus to ensure undiluted contact of the hypertonic saline with the intima to produce maximal irritation of the vessel. He believes that hemolysis of blood by the sclerosant occurs and may lead to, or exacerbate, hemosiderin staining; thus, it should be lessened by the prior injection of air, which washes out the red blood cells from the vessel.* Sodium chloride, 0.2 gm, in*Bodian E. $clerotherapy. Webster S, ed. Dialogues in dermatology. 1983;13(3), December~ (Tape produced and distributed by the American Academy of Dermatology, Evanston, IL.)

Journal of the American Academy of Dermatology

jected during a long treatment session is well tolerated. C h r i s m a n 92 believes that wrapping of the leg and injection of air are not necessary for effective sclerosis of small vessels. The only adverse effects in his patients are slight discomfort with hypertonic saline from the needle prick, a burning sensation, and rarely muscle cramping in the injected areas. He believes that small brownish spots result from extravasation of red blood cells. In his experience, these spots fade over months and are never permanent. Experimentally, intradermal injection of 0.5 ml of hypertonic saline 20% in rabbit skin produces significant epidermal and dermal necrosis. * Goldman et a185have confirmed this with the injection of 0.1 ml of hypertonic saline 23.4% intradermally in rabbit skin. Thus, besides the pain on injection, the significant but limited postsclerosis pigmentation, and the low incidence but real risk of superficial skin necrosis from extravasation, hypertonic saline with or without heparin and/or lidocaine or procaine is a relatively safe and effective sclerosant. Polidocanol. Polidocanol (Aethoxysklerol; hydroxypolyethoxydodecane) was developed in the early 1950s under the trade name Sch 600 as a local and topical anesthetic. Unlike the two main groups of local anesthetics, esters (procaine, benzocaine, and tetracaine) and the amides (lidocaine, prilocaine, mepivacaine, procainamide, and dibucaine), polidocanol is a urethane (compound with an - NHCO2 linkage). Polidocanol is unique among local anesthetics in its lack of an aromatic ring. The actual active substance is the topical anesthetic agent hydroxypolyethoxydodecane, an aliphatic molecule composed of a hydrophilic chain of polyethylene glycol ether and a lipidsoluble radical of dodecyl alcohol. It was used as a topical anesthetic agent in ointments and lotions for mucous membranes. 93 It was also used as a local anesthetic94 and an epidural anesthetic. 95 The subcutaneous anesthetic effect of a 0.4% solution is equal to a 2% solution of procaine hydrochloride (Novocaine). 94 The LDs0 in rabbits at 2 hours is *Miyake H, Kauffman P, de Arruda Behrner O, Wo|osker M, Leao LEP. Mechanisms of cutaneous necrosis provoked by sclerosing injections in the treatment of microvarices and telangiectasias: experimental study. Rev Ass Brasil 1976;22:115-20.

Volume 17 Number 2, Part 1 August 1987

0.2 gm/kg, which is three to six times greater than the LDso for procaine hydrochloride. 9~ The LDso in mice is 1.2 gm/kg. 94 The systemic toxicity is similar to lidocaine and procaine. 9~ Thus, polidocanol was considered an ideal local anesthetic. However, it soon became apparent that intravascular and intradermal instillation produced sclerosis of small-diameter blood vessels and compound Sch 600 was shelved as an anesthetic. Polidocanol was first used as a sclerosant in the late 1960s by Eichenberger in Germany,97 followed a few years later by Ouvry and others in France, 98 Cacciatore in Italy, 99 Jacobsen in Denmark, '~176 and Hofer in Austria. 1~ Telangiectasias were treated in concentrations of 0.4% to 0.7%. Varicose veins were treated in concentrations from 1% to 3%. Small vessels and telangiectasias respond well, with decreased efficacy in treating large or medium-sized varicose veins. Polidocanol has been reported to be almost free of toxicity, pain, necrosis, or pigmentation problems.'~176 Amblard 1~ reported no allergic reactions in over 250 patients, even in two patients who were intolerant to sodium tetradecyl sulfate. Hofer t~ reported no allergic reactions nor necrosis in over 19,000 patients. In addition, patients who are allergic to sodium tetradecyl sulfate or iodine do well with injections of polidocanol.1"'~: However, further use demonstrated rare allergic reactions97'l~176167 (Table IV), including a case of nonfatal anaphylactic shock to 1 ml of 2% polidocanol injected into a varicose vein during the fourth treatment session, t03 Jaquier and Loretan? believe that the decrease in antigenicity is secondary to the absence of a benzene nucleus and a para-amine group and to the presence of a lonely free alcohol group. Dexo Labs., the product manufacturer in Nanterre, France, recommends that this substance not be used in subjects with an allergic diathesis

*Wesener G. Morphology and modem therapy of small varicose dilatations of cutaneous veins and essential telangiectasias. Berufsderhatosen 1969;17:273-81. "l'Jaquier ,]7, Loretan RM. Clinical trials of a new selerosing agent, Aethoxysklerol. Soc Franc Phlebol 1969;22:383-5. ~Hiirtel S. Complications and side effects of sclerotherapy. Z Arztl Fortbfld 1984;78:331-2. w HE. Management of unsightly micro-varicosities. Am J Cosmet Surg 1984;1:45-7.

Treatment of telangiectasia

177

Table IV. Allergic reactions to sclerosants*

Clinical study

Number of reactions

Number without reactions

Sodium tetradecyl sulfate Eichenbergets7 Hoffer t~ Feuerstein'~ Jacobsen~~176 Heberovat Amblard '~ Ouvry et al 9s Cacciatore99 Havlik:]: Total Percent of reactions (less case reports)

1 0 1 (case report) 1 0 0 1 0 0 4

160 19,000 316 140 103 2,000 458 631 22,798

0.01

Polidocanol Berangerw 1 (case report) Marmassew 1 (case report) Avramw I (case report) Reid and Rothnies9 5 Pattisson and Tretbarl] 0 Walloisss 32 Passasw 2 (case reports) Boespflug'~ 1 (case report) Perchuk '~ 0 Aldermant~ 2 Tretbar'2 0 Weissberg'~~ 0 Shields and Jansen s3 0 Sladen11~ 0 Mantaseses4 2 Total 47 Percent of reactions 0.27 (less case reports)

---974 264 4,440 -84 7,000 144 62 103 533 1,000 14,404

*Allergic reactions are defined as anaphylactie reactions, urticaria, and/or bronchospasm. tHeberova V. Treatment of telangieetasias of the lower extremities by sclerotization. Results and evaluation. Cs Dermatol 1976;51: 232-5. :~Havlik P, The significance of deep cmral thrombosis and pulmonary embolism in the sclerotherapy of varices (practical experience). Cs Dermatol 1982;57:182-5. w H. One case of tetradecyl-sodium sulfate allergy with general symptoms. Soc Franc Phlebol 1972;25:19-26. [IPattisson PH, Tretbar LL. The injection treatment of varicose veins: a follow-up study of 264 patients. Vas Surg 1971;5:1-5.

such as asthma.* Kreussler & Co., the product manufacturer in Germany, however, states that *Dexo Labs. (Nanterre, France). Product description on hydroxypolyethoxydodecane. Received with correspondence, May 1985.

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there are no contraindications that arise from the product itself.* Thus, allergic reactions to polidocanol have been much rarer than those reported with sodium tetradecyl sulfate (Table IV). Very rarely superficial necrosis has been rep o r t e d . 9;',99,]m,* Jaquier and Loretant and Hofer ~~ extensively use and advocate the use of intraderreal polidocanol 0.5% to treat vessels that cannot be injected intravascularly and report no evidence of cutaneous necrosis. However, solutions over 1% may produce superficial necrosis with intradermal injection.l" Experimentally, cutaneous necrosis does not occur,:l: or occurs to a very limited degree with intradermal injection of O. 1 ml of polidocanol in 1% concentrations.85 Duffy (personal communication, 1986) notes a similar incidence of postsclerosis pigmentation with all sclerosing agents, including polidocanol. However, Cacciatore 99 has reported a 10.7% incidence of postsclerosis pigmentation with polidocanoI. Thus, postsclerotic pigmentation may be less than, or similar to, hypertonic saline and sodium tetradecyl sulfate. In addition, superficial necrosis occurs less frequently (with concentrations of polidocanol used for telangiectasias [< 1%]) than with hypertonic saline and/or sodium tetradecyl sulfate. Goldman et al. 73 clearly demonstrated that the concentration of polidocanol injected is critical as to the final outcome of vein sclerosis. Thus, polidocanol is probably a weaker detergent type of sclerosant than sodium tetradecyl sulfate, and higher concentrations are necessary to produce complete vascular sclerosis. Sclerodex. Sclerodex, a mixture of dextrose 250 mg/ml, sodium chloride 100 mg/ml, and phenethyl alcohol 8 mg/ml (as a local anesthetic/preservative), is mainly used in Canada for sclerosis of telangiectasias and superficial varicosities, s4 It is essentially a hypertonic solution

*Kreussler & Co. (Wiesbaden-Biebrich, West Germany). GMbH: Product insert for Aethoxysklerol. Chemische Fabrik, D-6200 Wiesbaden Biebrich, 1985. tJaquier JJ, Loretan RM. Clinical trials of a new sclerosing agent, Aethoxysklerol. Soe Franc Phlebol 1969;22:383-5. ~Miyake H, Kauffman P, de Arruda Behmer O, Wolosker M, Leao LEP. Mechanisms of cutaneous necrosis provoked by sclerosing injections in the treatment of microvarices and telangieetasias: experimental study. Rev Ass Brasil 1976;22:115-20.

with a mechanism of action similar to hypertonic saline. Mantse 84 noted one allergic reaction in 500 patients treated with Sclerodex, or an incidence of 0.2%. Like hypertonic saline, it is slightly painful on injection* and has an occasional incidence of superficial necrosis (probably less than hypertonic saline)) ~'1~ Postsclerosis pigmentation is also noted to occur with a frequency similar to all of the other sclerosing agents, by us, although Mantse TM noted a decreased incidence of complications with Sclerodex compared with polidocanol and sodium tetradecyl sulfate.

Injection technic Regardless of the sclerosant used, microsclerotherapy is performed using a standard technic. The patient is placed in a supine position. Gravitational dilatation of telangiectasias is usually unnecessary. The skin is then wiped with alcohol to make the telangiectasias more visible by indirect lighting. The glistening effect of alcohol also renders the skin more transparent, changes the refraction coefficient of the skin to increase the contrast between vessel and skin, and helps to clean the injection site. A loupe for magnification may also be helpful to aid visualization. The goal of microsclerotherapy is ideally to cannulate the vessel so that the sclerosant will be deposited within and not outside the vessel wall. Usually a 30-gauge needle is sufficient, although some physicians97't believe that a 32-gauge needle is less likely to result in inadvertent perivenular injection. It is helpful if the needle is bent at a 145 ~ angle with the bevel side up so that one may enter the vascular lumen at a less acute angle. This may lessen the likelihood of transection of the vessel. One enters the vessel by feel. In this regard the use of a glass syringe will best reflect an impedance to flow that occurs when the vessel is not properly cannulated. Vessel appearance is also important in guiding the needle placement. Most sclerotherapists (specialists in phlebology) use magnifiers between 21/4 and 5 x magnification to facilitate vessel cannulation. Bodian, 19 Alderman, 9t artd Foley9~ recommend *Nguyen VB. Scl6roth~rapie des varices des membres inf6rieurs 6tude de 522 cas, Le Saguenay MEdical 1976;23:134-45. tlmhoff E, Stemmer R. Classification and mechanism of action of sclerosing agents. Soc Franc Phlebol 1969;22:143-8.

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Treatment of telangiectasia

179

Table V. Sclerosing agents for telangiectasias Agent

Active ingredient

I Allergic reaction

Necrosis

Sodium morrhuate* Sodium tetradecyl sulfate* Hypertonic saline Polidocanol:~ Sclerodex:~

Fatty acids in cod liver oil Sodium tetradecyl sulfate Hypertonic saline 15%-30% Hydroxypolyethoxydodecane 10% saline, 25% dextrose

Occasional Occasional None Rare Rare

Frequentt Occasionalt Occasionalt Raret Occasional

1

Pain

Moderate Mild Moderate None Mild

*Approved for use by the Food and Drug Administration. t Concentration-dependent. :~Not approved for use in this country.

injecting with a small amount of air to clear the vessel prior to injection. This minimizes the risk of inadvertent intradermal injection of the sclerosing agent. If the vessel is cleared of blood by first injecting air, the risk of extravasation of red blood cells may also be minimized. This is thought to limit the degree and/or incidence of postsclerotherapy pigmentation. However, antegrade and retrograde filling of the treated vessel occurs after the injection. Thus, the air-bolus technic may not prevent or lessen the incidence of postsclerosis pigmentation. Another variant of the air-bolus technic to visualize clearing of the vessels is to create a foamy solution prior to injection. This is done with sodium tetradecyl sulfate or polidocanol by shaking the solution, which creates bubbles because both agents are detergents. Another method described by Green and Morgan 47 is to add Haemacel to sodium tetradecyl sulfate to accentuate the bubble formation. Ouvry and Davy t~ have summarized the general procedure for sclerosis of telangiectasias. Basically, sclerotherapy should progress from largest to smallest vessels. The quantity of solution to be injected should be enough to produce an obliteration 1 to 2 cm in diameter around the point of injection, and never more than 0.5 ml to avoid the risk of initiating the formation of new telangiectasias around the edge of the treated area. Injections should be performed every 3 to 4 weeks. Compression of the sclerosed vessel with 30 to 40 m m Hg should be maintained for 24 to 72 hours. This may be accomplished with individually measured graded stockings, such as Sigvaris, Jobst, or Medi-Strumpf. The patient is instructed to walk immediately after the injection session to help minimize significant thrombosis. If thrombosis of the

injected vessel occurs, the thrombus should be evacuated with incisional expression. Postsclerosis compression serves a number of purposes. First, the provided pressure helps to seal the irritated vascular lumina. Second, the pressure will help decrease the likelihood of recanalization of the sclerosed vessel, especially if compression is maintained for 1 to 2 weeks. Third, the possibility of clinical and symptomatic thrombosis will be minimized, thus, minimizing postsclerosis hyperpigmentation. Although some physicians 19'83'92'97'1~ do not advocate postsclerosis compression, the procedure is so simple and the benefits theoretically so great that its routine use is recommended. The agent of choice should demonstrate few adverse reactions and should be clinically efficacious and relatively comfortable for patients (Table V). In this regard, all agents except sodium morrhuate are fairly similar. Sodium tetradecyl sulfate is slightly painful upon injection, has the highest incidence of allergic reactions, and may produce necrosis with inadvertent extravasation. Hypertonic saline is virtually reaction-free but will produce necrosis even without noticeable extravasation, and it is relatively painful when injected. Polidocanol has the least tendency to produce superficial necrosis when inadvertently extravasated, 93'* is painless upon injection, and has an extremely low incidence of allergic reactions. Sclerodex is basically identical to hypertonic saline but may have a decreased incidence of superficial necrosis because of its lower tonicity. Clinical *Miyake H, Kauffman P, de Arruda Behrner O, WoloskerM, Leao LEP. Mechanisms of cutaneous necrosis provoked by sclerosing injections in the treatment of microvaricesand telangiectasias:experimental study. Rev Ass Brasil 1976;22:115-20.

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trials u n d e r w a y will better distinguish the relative e f f i c a c y b e t w e e n these agents.

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Journal of the American Academy of Dermatology

23. Recoules-Arche J. Electrocoagulation. Phlebologie 1966;33:885-92. 24. Bolliger A, Holzer J. Theproblem of electrocoagulation of the smallest telangiectasias. Zentralbl Phlebol 1966; 5:185-8, 25. Capurro S. Timed diathermocoagulation for the treatment of microtelangiectasias of the face: first impressions. Minerva Chit 1983;38:947-9. 26. Kobayashi T. Electrosurgery using insulated needles: treatment of telangiectasias. 2 Dermatol Surg Oncol 1986;12:936-42. 27. Kaplan I, Peled I. The carbon dioxide laser in the treatment of superficial telangiectasias. Br J Plast Surg 1975;28:214-5. 28. Wheeland RG, Kantor GR, Bailin PL, Bergfeld WF. Role of the argon laser in treatment of lymphocytoma cuffs. J AM ACADDERMATOL1986;14:267-72. 29. Greenwald J, Rosen S, Anderson RR, et al. Comparative histological studies of the tunable dye (577 nrn) laser and argon laser: the specific vascular effects of the dye laser. J Invest Dermatol 1981;77:305-10. 30. Finley JL, Amdt KA, Noe JM, Rosen S. Argon laser port-wine stain interaction. Immediate effects. Arch Dermatol 1984;120:613-9. 31. Apfelberg DB, Maser MR, Lash H. Argon laser management of cutaneous vascular deformities--a preliminary report. West J Med 1976;124:99-101. 32. Apfelberg DB, Maser MR, Lash H. Treatment of nevi aranei by means of an argon laser. I Dermatol Surg Oncol 1978;4:172-4. 33. Apfelberg DB, McBurney E. Use of the argon laser in dermatologic surgery. In: Ratz JL, ed. Lasers in cutaneous medicine and surgery. Chicago: Year Book, 1986:31-71. 34, Landthaler M, Haina D, Waidelich W, Brown-Falco O. Laser therapy of venous lakes (Bean-Walsh) and telangiectasias. Plast Reconstr Surg 1984;73:78-83. 35. Lyons GD, Owens RE, Mouney DF. Argon laser destruction of cutaneous telangiectatic lesions. Laryngoscope 1981;91:1322-5. 36. Remington BK. Argon laser therapy--rosacea, telangiectasia [letter]. J Dermatol Surg Oncol 1'983; 9:424. 37. Arndt KA. Argon laser theJrapy of small cutaneous vascular lesions. Arch Dermatol 1982;118:219-20. 38. Ratz JL, Goldman L, Bauman WE. Post treatment complications of the argon laser. Arch Dermatol 1985; 121:714. 39. Dolsky RL. Argon laser skin surgery. Surg Clin North Am 1984;64:861-70. 40. Dixon JA, Rotering RH, Huether SE. Patient's evaluation of argon laser therapy of port wine stain, decorative tattoo and essential telangiectasia. Lasers Surg Med 1984;4:181-90. 41. Dixon JA, Gilbertson JJ. Cutaneous laser therapy. In: High-tech medicine [special issue]. West J Med 1985; 143:758-63. 42. Lapins NA. Dermabrasion for telangiectasia. J Dermatol Surg Oncol 1983;9:470-2. 43. McGrae JE Jr, Winkelmann RK. Generalized essential telangiectasia: report of a clinical and histochemicat study of 13 patients with acquired cutaneous lesions. JAMA 1963;185:909-13. 44. Harrison DFN. Use of estrogen in treatment of famil-

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45. 46; 47. 48. 49. 50. 51. 52. 53. 54. 55. 56. 57. 58. 59. 60. 61. 62. 63. 64. 65. 66.

67. 68. 69.

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72. 73.

74. 75. 76. 77. 78. 79. 80. 81. 82. 83. 84. 85.

86. 87. 88. 89. 90.

181

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Answers for CME examination* July 1987 issue of the

Identification No. 887-107

JOURNALOF THE AMERICANACADEMYOF DERMATOLOGY

Questions 1-33, Modlin RC, Rea TH. J AM ACAD DERMATOL 1987;17:1-13. 1. c ( p l , c2, pa2) 2. c (p3, c l , pa2) 3. a ( p l , Abs;p2, c l , p a l ; p 2 , c2, p a 6 - - p 3 , el, pal) 4. c (p5, c l , pa2) 5. c (p7, c2, pa2) 6. b (p7, c l , pa4) 7. e (p7, c2, pa3) 8. d (p7, c 2 , pa4) 9. a (p9, c l , pa3) I0. d (p5, c l , p a 4 ; p 6 , c l , p a l )

18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28.

I1. a b a c b a b

29. d 30. c 31. None of the choices is correct 32. b , c , d 33. a , b , c , d , e

12. 13. 14. 15. 16. 17.

(p2, (p2, (p2, (p 2, (p2, (p2, (p2,

cl, pal;pa2) c l , pa3) cl, pal;pa2) e 1, pa 3) cl, pal) c2, p a 2 ; p a 3 ) c2, p a 2 ; p a 3 )

*p: page;c: column;pa: paragraph;Abs: abstract.

a b b b a b a a a c d

(p 2, (p 2, (p 2, (p2, (p 2, (p 2, (p 2, (p 2, (p5, (p5, (p 4, (p 4, (p5, (p 1,

c 2, c 2, c 2, c2, c 2, c 2, c 2, c 2, c 1, cl, c 2, c 2, c 1, c2,

pa 2; pa 3) pa 2; pa 3) pa 2; pa 3) p a 6 - - p 3 , c l , pa 1) pa 6---p 3, c 1, pa 1) pa 5) pa 5) pa 5) pal) pal) pa 2) pa 2) pal) pa2)

(p 2, c 2, pa 4) (p3, c 2 , p a 4 - - p 4 ,

c 2 , pa 1)