Leg Veins
3.4.i SPIDER VEINS
Neil S. Sadick
BACKGROUND
Spider veins are the most frequently encountered manifestation of venous disease and most commonly treated cosmetic leg vein condition. In the United States, approximately 23% of adults suffer from a spectrum of chronic venous disease that includes spider telangiectasias, reticular veins, and true varicosities.1 Latest figures depict over 22 million woman and 11 million men between ages 40 and 80 years to have varicose veins, and when the definition of varicose veins is expanded to include cosmetic telangiectasias, they are present in 79% of men and 88% of women.2,3,4,5 Generally, they are more common in women and older adults, although studies have shown that, as opposed to being a mostly cosmetic concern in women, they are associated with a functional disorder twice as frequently in men than in women.6,7
PRESENTATION
Spider veins present as small, thin, pink-red to purple-blue arborizing or curvilinear threadlike structures close to the surface of the skin.
 FIGURE 3.4.I.1 Facial spider vein. |
DIAGNOSIS
Clinical Diagnosis
Spider veins, the most frequently encountered manifestation of venous disease result from mild venous dilation, leading a confluence of dilated intradermal venules near the surface of the skin or mucous membranes measuring between 0.5 and 1 mm in diameter (Figure 3.4.i.1). Also known as telangiectasias, hyphen webs, or thread veins, they belong to the C1 class of the CEAP classification system that has been created to define forms of venous disease.1 This system was based on stratifying venous disease characteristics including clinical manifestations (C), etiologic factors (E), anatomic distribution of disease (A), and underlying pathophysiologic findings (P) (Table 3.4.i.1).
Histopathology
Ultrastructurally, telangiectasias are not vascular proliferations but are caused by dilations of preexisting vessels, which include either capillaries or venules. Capillary telangiectasias appear red or pink and are usually less than 0.2 mm in diameter, whereas venous telangiectasias appear bluer in color and are greater than 0.2 mm in diameter.8 They are composed of a feeder vessel and ectatic venous sprouts in the reticular dermis with a depth between 180 µm and 1 mm in the skin and can develop anywhere on the body but are commonly seen on the face around the nose, cheeks, and chin and in the lower body in the upper thighs and below the knees and ankles. Presence of spider veins in the lower legs often signifies underlying venous reflux.9
TABLE 3.4.I.1 CEAP Classification of Chronic Venous Disease | ||||||||||||||||||||||||||||||||||||||||||||||||
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Subtypes
Goldman et al10 proposed that there are 4 pattern types of telangiectasia based on clinical appearance:
Sinus or simple (linear): A red, linear telangiectasia that occurs on the face, especially the nose, or legs. In addition, a blue linear anastomosing telangiectasia may be found often on the legs.
Arborizing: A treelike appearance of capillary vessels in inflamed condition.
Spider or star: A red, superficial telangiectasia arising from a central filling vessel of arteriolar origin. It
is a focal network of dilated capillaries seen chiefly in pregnancy and hepatic cirrhosis. These are characteristically 0.1 to 1.0 mm in diameter and red to cyanotic in color.
Punctiform (papular): Characterized by small circumscribed, superficial elevation of the skin and are the results of dilated vessels. These are generally less than 2 mm in diameter and frequently present in patients with collagen vascular disease.
Differential Diagnosis
Poikiloderma
Solar elastosis
Rosacea
Telangiectasia macularis eruptiva perstans
Discoid lupus erythematosus, systemic lupus erythematosus
Dermatomyositis
Systemic sclerosis/CREST syndrome
Pigmented purpuric eruption
Acroangiodermatitis
Erythema ab igne
Palmar erythema
Radiation dermatitis
Cutaneous collagenous vasculopathy
Generalized essential telangiectasia
PATHOGENESIS
Causative Factors
Telangiectasias arise from a number of causes, alone or more likely in combination with other etiologic factors, broadly categorized as genetic/congenital, acquired, and iatrogenic. The current body of research indicates that venous hypertension is a secondary event to the etiologic factors that render the vein wall pliable to dilation and affect the valves leading to the appearance of telangiectasia. Some of the congenital/genetic causes of telangiectasias include nevus flammeus (port-wine stains), nevus araneus (spider telangiectasia), hereditary hemorrhagic telangiectasia, and ataxia-telangiectasia. Genetic inheritance with variable penetrance may induce inherited weakness of the venous wall, predisposing vein valves and venous walls to incompetence.11,12 Acquired causes of telangiectasias can arise from a primary cutaneous disorder, such as varicose veins, or factors leading to venous abnormalities such as advanced age, gender, pregnancy, and lifestyle10 (Table 3.4.i.2). Pregnancy and the associated hormonal changes play a key role contributing to the formation of varicose and spider veins. In addition to circulating hormones that weaken vein walls, there is also a significant increase in the blood volume, which tends to distend veins, causing valve dysfunction and blood pooling in the veins. Among other acquired causative factors not related to other venous abnormalities, is acne, rosacea, environmental damage such as that caused by sun or cold exposure, or limited systemic sclerosis/scleroderma. Topical steroids, particularly at high doses, have also been identified as a possible causative factor.
TABLE 3.4.I.2 Causes of Spider Veins | ||||
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Molecular and Structural Mechanisms
The pathogenesis of each type of telangiectasia is somewhat different given the breadth of causative factors that may play a role in the development of new blood vessels or the dilation of existing blood vessels. Primary structural changes in the valves may make them “leaky,”
with progressive reflux causing secondary changes in the vein wall. Alternatively, or concurrently, the valves may become incompetent secondary to structural abnormalities and focal dilation in vein wall segments near the valve junctions, and the reflux ensues as a secondary event. Acquired telangiectasias are a consequence of the release or activation of vasoactive substances, such as hormones and other chemicals. Insights from histological evaluations have shown dilation of the valvular annulus, bulging valve leaflets, commissural dilation, leaflet stretching, shortening, tearing and perforation, and, ultimately, complete destruction of the valve, whereas the venous wall presents varied areas of either thickening or deterioration.13 Key ultrastructural findings include the infiltration of leukocytes and monocytes, suggesting activation of inflammatory cascades.14,15 The increase in venous pressure causes structural and functional changes in the vein wall that leads to further venous dilation and increases in vein wall tension that trigger the expression/activity of matrix metalloproteinases (MMPs). Engagement of this biochemical cascade induces degradation of the extracellular matrix proteins, thus affecting the structural integrity of the vein wall and engaging inflammatory pathways to scavenge the cellular debris. Recent evidence also suggests an effect of MMPs on the endothelium and smooth muscle components of the vein wall and thereby causing changes in the venous constriction/relaxation properties.16 Endothelial cell injury also triggers further leukocyte infiltration, activation, and inflammation, which leads to additional vein wall damage and release of several growth factors such as vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and platelet-derived growth factor (PDGF). Thus, in the underlying general pathogenesis, vein wall dilation and valve dysfunction, via MMP activation and superimposed inflammation and fibrosis, leads to the appearance of telangiectasias.17
with progressive reflux causing secondary changes in the vein wall. Alternatively, or concurrently, the valves may become incompetent secondary to structural abnormalities and focal dilation in vein wall segments near the valve junctions, and the reflux ensues as a secondary event. Acquired telangiectasias are a consequence of the release or activation of vasoactive substances, such as hormones and other chemicals. Insights from histological evaluations have shown dilation of the valvular annulus, bulging valve leaflets, commissural dilation, leaflet stretching, shortening, tearing and perforation, and, ultimately, complete destruction of the valve, whereas the venous wall presents varied areas of either thickening or deterioration.13 Key ultrastructural findings include the infiltration of leukocytes and monocytes, suggesting activation of inflammatory cascades.14,15 The increase in venous pressure causes structural and functional changes in the vein wall that leads to further venous dilation and increases in vein wall tension that trigger the expression/activity of matrix metalloproteinases (MMPs). Engagement of this biochemical cascade induces degradation of the extracellular matrix proteins, thus affecting the structural integrity of the vein wall and engaging inflammatory pathways to scavenge the cellular debris. Recent evidence also suggests an effect of MMPs on the endothelium and smooth muscle components of the vein wall and thereby causing changes in the venous constriction/relaxation properties.16 Endothelial cell injury also triggers further leukocyte infiltration, activation, and inflammation, which leads to additional vein wall damage and release of several growth factors such as vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and platelet-derived growth factor (PDGF). Thus, in the underlying general pathogenesis, vein wall dilation and valve dysfunction, via MMP activation and superimposed inflammation and fibrosis, leads to the appearance of telangiectasias.17
TREATMENT
Patient Selection
Patients with spider telangiectasias typically seek treatment for cosmetic reasons, but nevertheless a thorough assessment that includes not only an assessment of the person’s telangiectasia but also the medical history, family history, and the patient’s expectations relating to the treatment of the spider telangiectasias should be done. At times, the telangiectasia is the result of a more generalized, systemic problem such as venous insufficiency. In such instances, venous insufficiency must be treated before the treatment of the spider telangiectasia or the underlying venous hypertension is likely to thwart the desired treatment outcome. Finally, in assessing a patient as a potential candidate, high-flow spider arborizations such as those that refill rapidly upon slight pressure suggest damage to a deeper vessel, such as a perforator, and are a predictor for poor outcome. In these cases, the perforators must be treated first. Similarly, if on examination saphenous vein varicosities are noted, these must be treated before treating the downstream spider telangiectasia for optimal results.
Although there are no absolute contraindications to this treatment, people taking certain medications and/or patients with some chronic illnesses should be approached with extreme caution. Diabetes and peripheral arterial occlusive disease (ankle-brachial index <0.9) are contraindications because these conditions are associated with an increased risk of nonhealing wounds. Patients who have signs of acute thrombosis/phlebitis and pregnant patients should not be treated because of the increased risk of deep venous thrombosis. Some medications, such as minocycline or isotretinoin, can lead to adverse reactions if not discontinued before the treatment. Blood-thinning medications and supplements should also be stopped before treatment, or they render the treatment less effective.
After patient evaluation in terms of medical history, patient counseling and expectations need to be addressed. The patient should be educated on the scope of treatment, potential complications, and the fact that complete eradication is often not possible. Rather, spider veins will lighten and become less noticeable but may not completely disappear. Multiple treatments are typically required to achieve the desired effect, and alteration in skin pigmentation can occur. Hyperpigmentation, which is usually temporary but can last up to a year, and permanent hypopigmentation might occur especially in patients with Fitzpatrick skin types III, IV, V, and VI. Documenting veins photographically before each treatment and periodically reviewing with the patient is helpful to demonstrate treatment progression. Last, the patient must be informed that the treatment of spider
telangiectasias is not curative and that further development of telangiectatic areas is likely.18,19,20
telangiectasias is not curative and that further development of telangiectatic areas is likely.18,19,20
 ALGORITHM 3.4.I.1 Treatment algorithm for spider veins. KTP, potassium titanyl phosphate; Nd:YAG, neodymium-doped:yttrium aluminum; J/cm2, Joules per cm2; PDL, pulse dye laser; STS, sodium tetradecyl sulfate. (Courtesy of Macrene Alexiades, MD, PhD.) |
Algorithm 3.4.i.1 shows the treatment protocol for spider veins.
Medical
There are no routinely used medical treatments for spider veins. Although topical α-adrenergic agonists such as brimonidine gel and oxymetazoline cream are utilized to treat erythema and flushing in rosacea and other erythematous disorders, there is no evidence that telangiectasias are reduced by these agents. The use of compression stockings as a preventive tool is advised for those at risk, such as pregnant women, or for those who have developed early signs of spider veins.
Cosmetic
The most common treatments with proven efficacy in treating spider veins are laser/light energy devices and sclerotherapy. The choice of which treatment is more suitable is patient-dependent, because, for example, needle-phobic patients will likely prefer a cutaneous laser treatment, whereas patients of darker skin type are good candidates for sclerotherapy.
Sclerotherapy
Sclerotherapy is considered the gold standard to treat telangiectasia and reticular veins of various anatomical sites for cosmetic and therapeutic purposes. During sclerotherapy, specific sclerosing agents are injected in the unwanted veins causing the target vein to immediately shrink and then dissolve over a period of a week. Sclerotherapy is a noninvasive procedure taking only about 10 minutes to perform. The downtime is minimal, in comparison with an invasive varicose vein surgery.21
Sclerotherapy Protocol
In the absence of findings such as varicose veins, symptoms of varicose vein disease, or cutaneous sequelae such as stasis dermatitis, diagnostic ultrasound should be performed to define the anatomy and delineate any points of significant reflux.
Several sclerosants are available worldwide, and the treating physicians can choose from different solutions to treat small vessels like spider veins (Table 3.4.i.3). There has yet to be a gold-standard sclerosant established, and most investigators have experience in employing a single solution. Generally, the profile of an optimal sclerosant includes a low level of adverse reactions, minimal patient discomfort, and maximal clinical efficacy with the lowest number of treatment sessions necessary to yield the desired clinical end point.22
Sclerosing Agents
Detergents, hyperosmotic solutions, and chemical irritants have all been used successfully to treat telangiectasias (Table 3.4.i.3). The detergent polidocanol (Asclera, Merz Aesthetics, Frankfurt, Germany) is considered one of the most versatile and safest sclerotherapy agents, with very rare allergic reactions. The 0.5% solution is Food and Drug Administration (FDA) cleared for sclerosing vessels less than 1 mm. Risk for necrosis is low with extravasation, and intravascular injection tends to produce little discomfort.23 Sodium tetradecyl sulfate (STS) (Sotradecol, AngioDynamics, Latham, NY, USA) is also a commonly used agent. It is available commercially in 1% and 3% concentrations, which are often diluted to lower concentrations for smaller vessels, and presents a safe profile with allergic reactions being rare, but skin necrosis can occur with extravasation. Hyperosmotic solutions are also used off-label for sclerosing vessels as they cause cellular dehydration of both red blood cells and endothelial cells. They are some of the most popular agents in the United States primarily because of the low cost and ease of availability of hypertonic saline.
TABLE 3.4.I.3 Sclerosing Agents for Telangiectasia | ||||
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Their main advantage is the lack of allergenicity; however, they have several disadvantages such as losing concentration and efficacy over a short distance, irritating nerve endings, and causing intense burning sensations on injection. These agents, such as 11.7% sodium chloride, are used primarily on small telangiectasias. Chemical irritants with a wide range of potencies from glycerin to polyiodinated iodine have also been used as sclerosants with the aim of disrupting chemical bonds, leading to cellular death within the vessel structure. In terms of optimal volume, studies have shown that optimal outcomes result from using the lowest concentration of sclerosant and the least volume possible for the desired effect.24 Glycerin, 72% chromated glycerin solution in 1% lidocaine with dilute 1:200 000 epinephrine, has been used predominantly in Europe with excellent success and low risk of side effects or complications. However, this method of sterilization is challenging and not FDA approved in the United States, although it is used by experienced sclerotherapists owing to high efficacy and fewer adverse events.
Sclerotherapy Technique
The sclerotherapy treatment procedure for treating telangiectasias includes:
Inspection and palpation of veins, marking of the treatment area, photography
Skin preparation, cleansing with rubbing alcohol
Syringe preparation: 2.5-mL syringe, 30-gauge needle
Localization, puncture, and injection of telangiectasias
Use magnifying goggles, transillumination, or other visualization devices when needed. Multiple injections of low volumes are advocated and avoidance of blanching areas bigger than 2.5 × 2.5 cm from a single injection point.
After the procedure, injection sites are cleansed and cotton balls are applied, adhesive tape, compression stockings, and/or bandages if necessary. Some recommend wearing compression stockings for up to 3 days post procedure to improve outcomes.
The patient is advised to rest for 5 minutes. Application of nonsteroidal anti-inflammatory cream (ibuprofen ointment or equivalent) can be offered to limit bruising. Patients are advised to avoid hot tubs, hot showers, and hot wax depilation after sclerotherapy treatments because these are known to be responsible for vasodilatation, edema, swelling, and heaviness. Walking is encouraged but not engagement in heavy exercise.
Follow-up evaluation is required several days or weeks after the procedure to assess its outcome, to recognize potential side effects, and to carry out additional injections if necessary (Figure 3.4.i.2).
For spider veins, good lighting is necessary as well as magnifying goggles. Mohammed et al have reported dermatoscope-aided sclerotherapy for leg spider veins. The authors use a 3-mL syringe with a 0.5-inch, 30-gauge needle bent to a 45° angle to the syringe with the bevel up. The needle is positioned proximal to the desired entry point of the target vessel, and using the other hand, a dermatoscope set in the polarized mode is used to visualize the veins closely.25
Common sclerotherapy treatment side effects include but are not limited to transient hyperpigmentation, ulceration, allergic reaction, pain at the injection site, telangiectatic matting, thrombophlebitis, edema, bruising, and headache. Serious complications such as anaphylaxis or thromboembolic events are rare as are cerebrovascular accidents, transient ischemic attacks, as well as speech and visual disturbances.26
 FIGURE 3.4.I.2 A 30-year old woman before (A) and 3 weeks after (B) 1 treatment with 0.5% polidocanol. |
One final recommendation is that patients not be treated in seasons of exposed legs and to alert the patient that recovery from treatment, regardless of type, takes up to several weeks and that several treatments are necessary at 4-to 6-week intervals, and to plan accordingly.
Sclerotherapy Clinical Studies
Several peer-reviewed studies have documented the clinical efficacy of sclerotherapy in the treatment of spider veins in the legs, hands, face, and even chest. Bowes et al. treated 20 facial telangiectasias in 14 patients with either a hyperosmolar sclerosant or polidocanol 0.5% to 0.75%. At the 9-month follow-up period, results showed a mean improvement of 70%, with 11 of 20 sites showing a 90% to 100% improvement. Similarly, in the same study, telangiectasias of hands in 7 patients were treated with sclerotherapy using a detergent sclerosant (STS) at various concentrations (1%-3%). During the follow-up period ranging from 1 to 6.5 years, hand varicosities had a mean improvement of 97.8%, and all sites showed a 90% to 100% resolution of varicosities. Treating telangiectasias on the chest of 3 patients with
either STS 0.25% to 0.50% or polidocanol 0.75% with a follow-up of 2 to 9 years showed an improvement of 50% to 100%.27 In another study, Weiss et al compared the use of 0.5% polidocanol with 11.7% hypertonic saline (HS) for the treatment of leg telangiectasias. All patients completed 4 visits at 0, 1, 4, and 12 weeks and reported significantly greater pain during treatment with HS than with polidocanol. There were no significant differences in physician-assessed improvement of telangiectasias, but 2 subjects developed ulcerations with HS. Thus, both agents provided effective treatment, but HS caused more pain during injections and resulted in 2 episodes of tissue necrosis.28 In a clinical study by Rabe et al, 160 patients with telangiectasias were treated with 0.5% polidocanol, 1% STS, or placebo. Polidocanol demonstrated a statistically significant superiority versus placebo, and significantly more patients were satisfied with polidocanol at 12 or 26 weeks compared with STS and placebo.29
either STS 0.25% to 0.50% or polidocanol 0.75% with a follow-up of 2 to 9 years showed an improvement of 50% to 100%.27 In another study, Weiss et al compared the use of 0.5% polidocanol with 11.7% hypertonic saline (HS) for the treatment of leg telangiectasias. All patients completed 4 visits at 0, 1, 4, and 12 weeks and reported significantly greater pain during treatment with HS than with polidocanol. There were no significant differences in physician-assessed improvement of telangiectasias, but 2 subjects developed ulcerations with HS. Thus, both agents provided effective treatment, but HS caused more pain during injections and resulted in 2 episodes of tissue necrosis.28 In a clinical study by Rabe et al, 160 patients with telangiectasias were treated with 0.5% polidocanol, 1% STS, or placebo. Polidocanol demonstrated a statistically significant superiority versus placebo, and significantly more patients were satisfied with polidocanol at 12 or 26 weeks compared with STS and placebo.29
Laser/Light Devices
An alternative treatment approach to treating spider telangiectasias is the use of laser or light energy-based devices. Lasers emit a single, coherent wavelength of light, whereas intense pulsed light (IPL) sources emit white light from 515 to 1200 nm that is usually filtered to certain broad wavelengths. Laser therapy of venous structures is based on the concept of selective photothermolysis.30,31 Pulsed lasers and light sources heat the target tissue, inducing thermal injury with limited damage to the surrounding structures. The wavelength of light is chosen based on the chromophore of the target structure and the depth of the vessel. The oxyhemoglobin contained within red blood cells has three major absorption peaks at 418, 542, and 577 nm, with an additional infrared absorption around 1000 nm (Figure 3.4.i.3). The selected duration of the light pulse determines the size of the vessel that will respond to treatment. Shorter pulses selectively heat smaller vessels (<2 mm) and longer-pulse-duration light sources are effective for slightly larger vessels.32 Other parameters, such as fluence (energy density), spot size, and cooling are also important factors. No single laser type is used to treat the variety of vascular abnormalities seen in clinical practice. The specific laser selected for an individual patient depends on the size and depth of the vessels to be treated and patient skin phototype. The most commonly used lasers for the treatment of telangiectasias are pulse dye lasers (PDL), potassium titanyl phosphate (KTP), neodymium-doped:yttrium aluminum garnet (Nd:YAG) alexandrite laser, and IPL sources (Table 3.4.i.4).
 FIGURE 3.4.I.3 Chromophore absorption wavelengths. |
KTP Laser
KTP lasers emit light at 532 nm at pulse durations in the millisecond range, and the green wavelength matches the second oxyhemoglobin peak overlapping the absorption peak of melanin. Veins with diameters ranging from 0.5 to 1.5 mm can be effectively treated in light skin type patients (Figure 3.4.i.4). The main risk of this short superficially penetrating wavelength is crusting in tanned or more darkly pigmented skin. Refrain from conducting the treatment under these conditions to avoid crusting and transient hypopigmentation that may occur as a result.
Pulsed Dye Laser
PDLs emit light at 585 and 595 nm, matching the third oxyhemoglobin peak (Figure 3.4.i.3) at pulse durations of 0.45 to 40 ms. These lasers are most effective for treating small lower extremity veins less than 1.5 mm in diameter in light skin type patients. One should alert the patient that purpura may be observed and that the recovery from vascular treatment may take several weeks to manifest.
Nd:YAG 1064-nm Laser
Neodymium-doped:yttrium aluminum garnet (Nd:YAG) lasers emit light at a wavelength of 1064 nm, at pulse durations in the millisecond range. This longer
wavelength penetrates to deeper levels and, with long pulse durations, can be used to treat veins from 0.3 to 3 mm in diameter (Figure 3.4.i.5). Because of lower absorption in pigment, Nd:YAG lasers are less likely to cause pigmentary changes and are safer to use in darker skin types.
wavelength penetrates to deeper levels and, with long pulse durations, can be used to treat veins from 0.3 to 3 mm in diameter (Figure 3.4.i.5). Because of lower absorption in pigment, Nd:YAG lasers are less likely to cause pigmentary changes and are safer to use in darker skin types.
TABLE 3.4.I.4 Lasers Used to Treat Spider Veins | |||||||||||||||||||||||||||||||||||
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Alexandrite Laser
Alexandrite lasers with a pulse duration in the millisecond range emit light at a wavelength of 755 nm that corresponds to absorption by deoxygenated hemoglobin and also to absorption by melanin. Lower extremity veins may respond, but this laser should be limited to nontanned skin types I, II, and III.
Intense Pulsed Light
IPL sources emit white light from 515 to 1200 nm, but it is usually filtered to certain broad wavelengths. IPL sources are most effective for superficial, red telangiectasias <1 mm in diameter in fair-skinned individuals.
 FIGURE 3.4.I.4 A 36-year old woman before (A) and 4 weeks after (B) treatment with 532-nm KTP, 4 mm, 15 milliseconds, 10 J/cm2. |
 FIGURE 3.4.I.5 A 40-year-old before (A) and 2 months after (B) 2 treatments with 1064-nm Nd:YAG 140 to 150 J/cm2, 10 to 30 ms, 5°C to 8°C, 1 Tx/4 weeks. |
Laser Technique
Once the laser or light source and area to be treated have been selected, the patient is placed in a comfortable position and protective eyewear is given to the patient and all personnel in the room. The use of eye protection is essential, and when operating class 4 lasers (includes most medical lasers), it is required in the workplace by the United States Occupational Safety and Health Administration. The parameters for treatment are entered into the laser/light control panel. Most laser manufacturers currently provide set ranges of parameters either preset in the device or in a manual for initiating treatment. Start with conservative (low fluence) settings. The process proceeds by first cooling the skin over the vessels and then activating the laser/light over the target vessel. The patient will feel anything from a very mild sting to a strong pinching and burning sensation when the laser is activated; thus, application of a topical anesthetic agent can be used to lessen pain. A visible clearing of the vein should be seen, but if not, the vessel can be treated again or the laser parameters adjusted to improve the effect. Adjustments of parameters include increasing or decreasing the pulse duration to match the caliber of the vessel until blanching is achieved upon applying a pulse or, if necessary, increasing the fluence. To avoid burns, no more than 3 attempts should be tried over the same area of skin. Typically, no dressing or compression bandages are needed. Patients may return to their normal daily activities immediately after treatment, including work. Patients are advised to avoid sun exposure to the treated areas and apply sunscreen with a high sun protection factor (SPF 30). Vessels may need more than 1 treatment to achieve optimum results, and repeat therapy is generally performed within 4 to 8 weeks.
Common local reactions associated with laser therapy include pain, redness, swelling, bruising, and itching that are transient and usually resolve quickly. Purpura and ecchymosis are due to vessel wall rupture resulting in leakage of blood into the surrounding tissue and is most likely to occur with short-pulsed laser treatments (eg, PDL). More significant adverse reactions include telangiectatic matting, pigmentation changes, hyperpigmentation, hypopigmentation, ulceration, thrombophlebitis, and scarring. Hyperpigmentation and hypopigmentation are common in patients with skin type III, IV, V,
or VI, and usually develop within 3 weeks after treatment. Hyperpigmentation, which is due to hemosiderin deposition, is usually temporary but may last up to a year or can be permanent as can be hypopigmentation. Thrombosis has been reported in the superficial veins following laser therapy and may take up to 6 weeks to resolve, but it rarely has sequelae.
or VI, and usually develop within 3 weeks after treatment. Hyperpigmentation, which is due to hemosiderin deposition, is usually temporary but may last up to a year or can be permanent as can be hypopigmentation. Thrombosis has been reported in the superficial veins following laser therapy and may take up to 6 weeks to resolve, but it rarely has sequelae.
Laser Clinical Studies
Several clinical studies have evaluated the efficacy of laser modalities for the treatment of telangiectasias, and clinical trials have been conducted to compare different types of lasers and light sources for this indication.33 In observational studies, the long-pulsed Nd:YAG laser appears to be the best device as a single laser modality in the treatment of lower extremity telangiectasias.34 The value of the Nd:YAG laser was illustrated in a prospective study of 22 patients that evaluated vessel clearance rates of the Nd:YAG compared with either the alexandrite or diode laser in the treatment of vessels ranging from 0.3 to 3 mm.33 Thirty-six sets of comparable sites were treated, and greater than 75% improvement at 3 months of follow-up was observed at 88% of the Nd:YAG sites, compared with 29% of the diode sites and 33% of the alexandrite sites.
In a split-face study comparing the treatment efficacy of combined therapy versus separate delivery of IPL or 1064-nm Nd:YAG laser in facial telangiectasia, 24 patients were studied using monotherapy or sequential delivery of IPL followed by Nd:YAG laser. Subject evaluation at the 4-week follow-up showed higher efficacy scores in combined therapy sides than in separate therapy sides. Patients were satisfied in both treatments but experienced less pain from separated treatment than from combined treatment. There were no reports of scarring, dyspigmentation, telangiectatic matting, crusting, blistering, or textural changes in any subjects.35
A recent prospective, single-center split-face study with 20 participants assessing the safety and efficacy of a novel single-band IPL handpiece versus dual-band IPL handpiece in the treatment of photodamage showed that subjects who received treatments with the single-band handpiece showed a statistically superior level of improvement in telangiectasia and pigmentation at 20-week follow-up than those treated with the dual-band handpiece.35,36
Finally, a pivotal study by Bernstein et al investigating the efficacy of a novel, high-power, 532-nm frequency-doubled Nd:YAG, KTP laser with contact cooling for the treatment of spider veins of the lower extremities in 20 female subjects with Fitzpatrick skin types I to III demonstrated it to be safe and effective, with minimal discomfort and adverse effects. Subjects received 2 treatments 12 weeks apart (5 mm, 15 J/cm2, 40 ms) and at the follow-up, both subjects and the treating physician reported “significant” to “very significant” (˜51%-100%) improvement in 75% and 69% of subjects, respectively.37
Surgical
Historically, electrodessication methods have been used to treat very small facial telangiectasias using low amperage current (1-2 A), in a pulsed technique every 2 to 3 mm length of vessel. However, this technique is less consistent and leads to higher complications such as scarring, keloid formation, and dyspigmentation than do the newer preferred methods described earlier in this chapter.38
SUMMARY
Telangiectasias on the face or body can be safely and effectively treated with either sclerotherapy or laser/light modalities. The treatment choice is most commonly case dependent and relies on both the patient preferences and physician recommendations. Often and especially if they arise in conjunction with other features such as photodamage, crepey skin, and dyschromias, telangiectasias may also be eradicated with other noninvasive aesthetic treatment modalities such as fractional lasers or nanofractional radiofrequency.39,40 Few innovations or superior alternatives to sclerotherapy/lasers have emerged for spider veins. A novel approach for the treatment of spider veins was recently described, whereby an insulated microneedle with beveled tip harnessed low current through the skin to obliterate the vein while minimizing adjacent tissue damage.41 Currently for spider veins needing treatment
for cosmetic reasons, both sclerotherapy, which is the gold standard, and lasers, which are an appropriate alternative, are excellent options that are effective in a few treatment sessions and can provide long-term results.
for cosmetic reasons, both sclerotherapy, which is the gold standard, and lasers, which are an appropriate alternative, are excellent options that are effective in a few treatment sessions and can provide long-term results.
REFERENCES
1. Eklof B, Rutherford RB, Bergan JJ, et al. Revision of the CEAP classification for chronic venous disorders: consensus statement. J Vasc Surg. 2004;40(6):1248-1252.
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3. Callam MJ. Epidemiology of varicose veins. Br J Surg. 1994;81(2):167-173.
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3.4.ii RETICULAR VEINS
NEIL S. SADICK
CHRISTIAN R. HALVORSON
ROBERT A. WEISS
BACKGROUND
Reticular veins are dilated blue veins, typically found in the legs, that are a subtype of leg varicosity. According to the clinical, etiological, anatomical, and pathological classification (CEAP) definition, reticular veins are included in the C1 class and affect almost 25% of the adult population in the Western world. Treatment is sought mainly for aesthetic reasons, although reticulate eruptions of vascular origin may represent an underlying arterial, venous, microvascular, or combined pathology.
If a reticular vein permits both antegrade and retrograde blood flow depending on vein position in relation to gravitational force, it is termed an “incompetent reticular vein” and is associated with nonfunctioning valves and a more serious venous condition.1
PRESENTATION
Patients present with visible narrow blue veins in a reticulated pattern, usually on the legs. Translucent skin may allow normal veins to be visible as bluish subdermal reticular pattern, but reticular blue veins due to venous dilatation are more prominent, darker blue, and wider.
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