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other plasma components in vitro , Eur J Vasc Endovasc Surg . 2008 .
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36 : 216–223 .
69. Cavezzi A , Carigi V , Buresta P , Di Paolo S , Sigismondi G . Flebectomía de las várices + espuma esclerosante del tronco safé­nico:Una propuesta terapéutica innovadora , Flebologia y Linfologia. 2008 . 8 : 426–427.
70. Partsch B , Partsch H . Which pressure do we need to compress the great saphenous vein on the thigh?, Dermatol Surg. 2008 . 34 ( 12 ): 1726–1728.
71. Feied C . Sclerosing solutions. In: Bergan J , ed.  e vein book . Boston: Elsevier . 2007 . 125–131.
72.  ibault P . Sclerotherapy and ultrasound-guided sclerotherapy. In: Bergan J , ed.  e vein book . Boston: Elsevier . 2007 . 189–199.
73. Cavezzi A , Carigi V , Collura M , etal. Phlebectomy of varicose tribu­taries combined with transcatheter foam sclerotherapy of the saphe­nous vein , Int Angiol. 2009 . 28 (Suppl 1 ): 78.
74. Hamel-Desnos C , Desnos P , Wollmann JC , etal. Evaluation of the e cacy of Polidocanol in the form of foam compared with liquid form in sclerotherapy of the long saphenous vein: Initial results . Dermatol Surg. 2003 . 29 : 1170–1175 .
75. Kern P , Ramelet AA , Wutschert R , Bounameaux H , Hayoz D . Single-blind, randomized study comparing chromated glycerin, poli­docanol solution, and polidocanol foam for treatment of telangiectatic leg veins , Dermatol Surg . 2004 . 30 ( 3 ): 367–372 ; discussion 372; com- ment Dermatol Surg . 2004 . 30 ( 9 ): 1272 ; author reply, 1272–1273 .
76. Capurro S . La phlébothérapie régénératrice tridimensionnelle ambulatoire (TRAP):Concept innovant de traitement de la vari­cose , Phlebologie. 2010 . 63 : 1–5.
77. Mariani F , Izzo M , Trapassi S , Mancini S . Sclerotherapy of reticu­lar varices and teleangiectasias: erapeutic strategy and result , Acta Phlebol. 2001 . 2 : 71–76 .
78. Izzo M , Amitrano M , Bacci PA , Mancini S , Mariani F . Pigmentation post-sclérothérapie: Physiopathologie et traitement , Phlebologie. 2001 . 54 : 273–277 .
79. Izzo M , Mariani F , Bianchi V , Bacci PA , Di Stefano R . A new scleros­ing agent:Potassium salicylate , Int Angiol. 2001 . 20 ( Suppl1 ): 2 .
80. Parsi K . Catheter-directed sclerotherapy, Phlebology. 2009 . 24 : 98–107.
81. Cavezzi A , Parsi K . Complications of foam sclerotherapy , Phlebology. 2012 . 27 ( Suppl 1) : 46–51.
82. Morrison N , Neuhardt DL , Rogers CR , et al. Incidence of side e ects using carbon dioxide oxygen foam for chemical ablation of super
cial veins of the lower extremity , Eur J Vasc Endovasc Surg.
2010 . 40 : 407–413.
83. Watkins MR . Deactivation of sodium tetradecyl sulphate injection by blood proteins, Eur J Vasc Endovasc Surg . 2011. 41 ( 4 ): 521–525.
84. Peterson JD , Goldman MP , Weiss RA , etal. Treatment of reticular and telangiectatic leg veins:Double-blind, prospective comparative trial of polidocanol and hypertonic saline , Dermatol Surg. 2012 . 38 : 1–9.
85. Schuller-Petrović S , Brunner F , Neuhold N , Pavlović MD , Wölkart G . Subcutaneous injection of liquid and foamed polidoca­nol:Extravasation is not responsible for skin necrosis during reticu­lar and spider vein sclerotherapy , JEADV. 2011 . 25 : 983–986.
86. Ramelet AA . Sclerotherapy in tumescent anesthesia of reticular veins and telangiectasias, Dermatol Surg . 2012 . 38 ( 5 ): 748–751.
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SCLEOTHERAPY TREATMENT OF TELANGIECTASIAS
Robert A. Weiss and Margaret A.  Weiss
INTRODUCTION
Isolated small reticular veins and telangiectasias o en cause severe symptoms that are worsened by prolonged standing or sitting and may be relieved by wearing support hose or
1
by elevation of the legs.
Vein size alone does not predict
the presence of symptoms. Vessels causing symptoms may
2
be as small as 1mm in diameter or less.
Besides symptoms of pain, burning, and fatigue, women typically curtail their activities and modify their lifestyles to avoid situations in which their legs are easily seen. Sclerotherapy not only o ers the possibility of remarkably good cosmetic results, but also has been reported to yield an 85% reduction in symptoms.
1
Prior experience with venipuncture helps very little with treatment of larger veins and is completely irrelevant in the treatment of the smallest veins. Successful treatment requires the correct technique, the correct diagnosis, and the correct treatment plan for the type and size of vein to be treated.
TELANGIECTASIA FROM
RETICULARVEINS
Telangiectasia can develop as a result of re ux from reticular veins, thin-walled blue super cial venules that are part of an extensive network of the lateral subdermic venous system; a system that is separate from the saphenous system. Atypi­cal network is shown in Figure13.1. Reticular veins associ­ated with telangiectasia are commonly called “feeder” veins. Both handheld Doppler and duplex ultrasound have been used to map the path of transmission of venous hyperten-
3,4
sion from small reticular veins into telangiectasia.
ISOLATED ARBORIZINGWEBS
High-pressure re ux through failed valves is at the root of nearly all telangiectatic webs, although there are some excep­tions due to arteriovenous malformations or shunts.  is has been estimated to occur approximately one in twenty
5
times, although this may be a high estimate.
Typically, localized valve failure will produce arborizing networks of dilated cutaneous venules that are direct tributaries of underlying larger veins. Arborization occurs through a recruitment phenomenon in which high pressure causes dilatation of a venule, failure of its valves, and transmission of the high pressure across the failed valves into an adjacent vein. Treatment of an arborizing system must be directed at the entire system, because if the point source of re ux is not ablated, the web will rapidlyrecur.
PRETREATMENT INSTRUCTIONS
Patients are told to wear shorts and not to use moisturiz­ers or shave their legs on the day of treatment. Shaving the leg may cause erythematous streaks, making it di cult to visualize patterns of reticular and telangiectatic veins. Use of moisturizers causes poor adhesion of tape used to secure compression following injections and causes slower evapo­ration of alcohol used to prep the leg. Patients are encour­aged to eat at least a small meal beforehand in order to minimize vasovagal reactions.
FIRST TREATMENTTEST
 e  rst treatment session usually is limited to a small num­ber of sites in order to observe the patient for any allergic reactions and the ability to tolerate the burning or cramp­ing of a hypertonic solution, to judge the e ectiveness of a particular concentration and class of sclerosing agent, and to observe the ability to comply with compression. It also serves to familiarize the patient with the treatment, treating physician, clinic surroundings, and the sensation of the  ne needle.  is allows more extensive treatment on the second visit with the patient being familiar with the technique and surroundings.  e test site also complies with the sugges­tion in the package insert of sodium tetradecyl sulfate (STS; Sotradecol, Bioniche Pharma, Belleville, Ontario).
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Figure13.1 Typical telangiectatic web–reticular vein complex of the lateral subdermic venous system.
When the patient returns in 4 to 8 weeks, the test site or limited treatment area is compared with pretreatment pho­tographs. Any side e ects such as matting and pigmentation can be explained to the patient. Reasonable time intervals for clearance of treated vessels can be reinforced. At each session, all sites treated are noted in anatomic diagrams in thechart.
TREATMENTPLAN
With increasing experience and recognition of common patterns, injection sites are based on known patterns of re ux. For example, reticular veins usually feed a group of telangiectasias on the lateral thigh from a varicose lateral subdermic venous system. During the treatment session, treatment would begin with reticular veins from which re ux is suspected to arise and would proceed along the course of the reticular vein, with injections every 3–4 cm along the feeder.
Our typical treatment regimen is to foam or agitate STS at 0.1 to 0.2% using a ratio of one part sclerosant to four parts air.  is foam mixture is injected into reticular veins that are directly connected to visible telangiectasias (see Figure13.2). It is not advisable to treat every reticular vein of the thigh; only those reticular veins visibly connected to a telangiectatic web should be targeted.
As sclerosing solution/foam  ows away from the point of injection, it is clearly seen for a distance of several cen­timeters before it is diluted by blood and becomes less potent.
When injecting a reticular vein, the sclerosing foam is sometimes seen  owing into the telangiectasia. When this is observed, the telangiectasias do not need to be injected directly. Similarly, sclerosing solution injected into a telan­giectasia may be seen  owing into the feeder vein, but retic­ular veins usually still need to be injected directly, because it
Figure13.2 Foam mixture of STS 0.1% comprising liquid sclerosant agitated with air at a ratio of one part liquid to four parts air. Here the foam is seen injected into a reticular vein. Foam is visualized in the vein up toarrow.
is di cult to deliver an e ective volume and concentration of sclerosant foam to the reticular vein indirectly.
TECHNIQUE
 e technique used for injection of small reticular feeder veins is the direct cannulation technique used for the injec­tion of larger, deeper reticular veins and varicoseveins.
 e patient is recumbent in a position that allows con­venient access to the reticular veins to be treated. A3-cc syringe with a 27 or 30 gauge is used, and the needle is bent to an angle of 10 to 30 degrees to facilitate cannula­tion of the vein (see Figure13.3).  e syringe is held in the dominant hand, which rests on the patient’s leg, and the needle is advanced at a shallow angle through the skin and into the reticular vein. When the physician feels the typical “pop-through” sensation of piercing the vein, the plunger is pulled back gently until blood return is seen in the transpar­ent plastic hub. Typically one injects up to 2 cc of foamed sclerosant and then massages the solution toward any associ­ated telangiectasias. Injection must stop immediately if any signs of leakage occur or if a bleb or bruising is noted. As the needle is withdrawn, pressure is applied immediately either with cotton ball then tape, or compression bandaging.
 e cannulation of a reticular vein can be quite di ­cult at times, because reticular veins can go into spasm, and may virtually disappear during an attempt at cannulation. It is best to avoid applying alcohol to the skin just prior to treatment as the evaporative cooling may cause venospasm of the reticular vein. Any resistance to injection means the needle tip is not inside the vein. When this happens, the injection should be terminated immediately and the needle withdrawn. Failed cannulation will rapidly produce a bruise at the site of injection.
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Figure13.3  e position of the syringe with needle bend in the hands of the injecting physician for injecting reticular and telangiectatic veins.  is shows the injection of 72% glycerine into telangiectasias. Some blanching isseen.
E Q U I P M E N T
•
Cotton balls soaked with 70% isopropyl alcohol
syringes. We have not yet seen allergic reactions to STS in over 500,000 injections since switching to latex-free syringes in1994.
PATIENT PREPARATION
 e patient is recumbent in a position that allows conve­nient access to the telangiectasias to be treated. If available, a motorized table with height adjustment will facilitate easy access to all regions of the leg. Use of double polarized lighting (InVu Vantage, Syris Scienti c, Grey, ME) has also proven to be helpful (see Figure13.4).  e neck and back position of the treating physician must be optimal to avoid injury over the long term to the physician. Indirect lighting is best, as harsh halogen surgical lights bleach out reticular veins and some telangiectasias.
A
•
Protectivegloves
•
1-cc or 3-cc disposable syringes
•
3-way intravenous stopcock for agitation/foaming
•
30-gauge 1/2-inch disposable transparent hub needles
•
Cotton balls or foam pads for compression
•
Hypoallergenic tape (synthetic silk orpaper)
•
Topical nitroglycerine ointment(2%)
•
Sclerosing solutions (stored separately from other
injectables in the clinic)
•
Magnifying loupes or lenses(2–3×)
The choice of syringe is a personal one. Some phle­bologists believe that a 3-cc syringe allows optimal control. Others hold that a 1-cc syringe is preferable because the smaller plunger offers reduced plunger fric­tion and allows smoother control with less jerkiness, but higher pressures may induce quicker vessel rupture. It is worth the effort to try a variety of syringes, as there is a marked difference in plunger friction among differ­ent types of syringes and among syringes from different manufacturers.
With use of STS, it is recommended to use latex-free syringes. In high enough concentration, STS (0.5% and greater) will dissolve the rubber from the plunger, thereby releasing rubber and rubber products into solution.  ere is a relatively high and increasing incidence of latex allergy
6
in the general population.
 eoretically the risk of a severe
allergic reaction may be increased with latex-containing
B
Figure13.4 Use of cross-polarized lighting to increase visualization of telangiectasias. A)  igh telangiectasias as seen with conventional light. B) Group of telangiectasias in center of thigh as visualized using cross-polarized light (InVu Vantage, Syris Scienti c, Grey,ME).
SCLEOTHERAPY TREATMENT OF TELANGIECTASIAS • 111
HAND POSITION
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INJECTION OF SCLEROSANTS
A syringe of sclerosant is prepared with a 30-gauge needle that has been bent to an angle of 10 to 30 degrees with the bevel up.  e needle is placed  at on the skin so that the needle is parallel to the skin surface.  e nondominant hand plays an important role in stabilization of the syringe.  e injecting hand rests on the patient’s leg with the fourth and   h  nger providing stabilization in a  xed position to facilitate controlled penetration of the vessel.  e non­dominant hand is used to stretch the skin around the needle and may o er additional support for the syringe.  e  rmly supported needle is then moved slowly 1 to 2mm forward, piercing the top of the tiny vein just su ciently to allow infusion of solution with the most minimal pressure on the plunger.
CANNULATION OF THEVESSEL
 e technique requires a gentle, precise touch, but with practice the beveled tip of the 30-gauge (0.3-mm diam­eter) needle may be used to cannulate vessels as small as
0.1mm.  e bevel of the needle usually can be seen within the lumen of the telangiectasias with use of 1.75 to 2× magni cation. Needles smaller than 30 gauge or longer than ½ inch are di cult to use because they tend to veer o course when advanced through the skin. Depending on the patient’s skin type, needles can become dull rather quickly, and should be replaced whenever resistance to skin puncture is noted.  is typically occurs within three to 10 punctures. In the United States, one must follow OSHA blood-borne pathogen guidelines when changing needles.
Once the needle tip is seen in the lumen of the ves­sel, a tiny bolus of air (<0.05 cc) may be injected to help demonstrate that the needle is within the vein. With the use of glycerine as a sclerosant we o en utilize an air block technique, in which a small bolus of air (0.1 cc) is used to clear the arborizing vessels of blood before the sclerosing solution is infused.  is is much smaller than previously
7
described.
Concentrations of sclerosants used for telangiectasias are less than those used for reticular veins. Typically the solu­tions are not foamed. We now prefer to use 72% glycerine for the telangiectasias of a telangiectatic web–reticular vein complex (see Table13.1). When sclerosing solutions are injected into telangiectasia, blood usually is flushed out of the vessel ahead of the solution, thus the sclerosant usually is not diluted at all. For this reason, the initial treatment of telangiectatic webs begins with the mini-
8
mal effective concentration of sclerosant.
At the next visit, the same concentration is used if sclerosis was effec­tive, and a higher concentration is used if sclerosis was ineffective.
 e injection of telangiectasias is performed very slowly, with minimal pressure on the syringe. A few drops of sclerosant are su cient to  ll the vein and maintain con­tact with the vessel wall for 10 to 15 seconds.  e amount infused is approximately 0.1 cc to 0.2 cc per site, and this o en is su cient to produce blanching in a radius of 2cm from the site of injection. Rapid  ushing of the vessels with larger volumes of sclerosant or with higher pressures leads to problems with extravasation, tissue necrosis, and ulceration, as well as an increased incidence of telangiectatic matting
9,10
and of hyperpigmentation.
For glycerine injection, the telangiectasias are  lled with solution and the injection is stopped. Glycerine has the least
11
risk of causing subsequent matting or pigmentation.
When detergent sclerosants are used, small volumes and small areas of short-duration blanching are still important to minimize side e ects such as telangiectatic matting. Sometimes there is no blanching at the site of injection, but the sclerosing solution  ows easily through the telangiectasia or can even be seen  owing through adjacent telangiectasias or reticu­lar veins several centimeters away from the injection site. In this case the injection is stopped a er no more than 0.5 cc of sclerosant has been injected. Immediately a er injection, the treated area is gently massaged in the desired direction of further spread of sclerosant. We strongly recommend against the use of hypertonic saline as it is painful and highly ulcerogenic.
Table13.1 SCLEROSANT CONCENTRATIONS FOR TELANGIECTASIA AND RETICULARVEINS
SIZE OF VESSEL MINIMUM EFFECTIVE
Reticular 1–3mm 0.1% 0.25% Yes Sodium tetradecyl sulfate (STS)
Reticular 1–3mm 0.25% 0.5% Yes Polidocanol (Laureth-9)
Telangiectasias 0.2–1mm 0.2% 0.5% No Polidocanol (Laureth-9)
Telangiectasias 0.2–1mm 0.1% 0.2% No STS
Telangiectasias 0.2–1mm 72% in water Same No Glycerine 72%
Telangiectasias 0.2–1mm 10% hypertonic saline and
CONCENTRATION
MAX CONCENTRATION FOAMED SCLEROSANT
Same No SclerodexTM
25%dextrose
112 • PRIMARY SUPERFICIAL VENOUS INSUFFICIENCY
To minimize skin necrosis, extravasation must be
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avoided, although the risks are minimized with glycerine or
12
very low doses of liquid 0.1% STS.
If there is resistance to the  ow of sclerosant, or if a bleb begins to form at the injection site, the injection must be stopped immediately. Extravasation of low concentrations of polidocanol does not cause tissue necrosis, but signi cant extravasation of higher concentration (>0.1%) STS or of hypertonic saline
13
will cause necrosis and ulceration.
Arandomized study in animals found the incidence of ulceration to be greater when attempts were made to dilute the extravasated sclerosant by
14
the injection of normal saline into the area.
Vigorous mas­sage of any blebs is recommended to minimize the chance of necrosis. Application of 2% nitroglycerine paste if bone white blanching is observed is used to cause immediate vasodilatation and minimize risks of small areas of necrosis.
COMPRESSION
 e number of treatments needed depends on the extent of the problem and the extent of areas treated at each ses­sion. Some patients are highly responsive to treatment and can be treated with weak sclerosants in only a few sessions. Others are highly resistant and may require more sessions and stronger sclerosants.  e younger the patient the better and faster the response.
A er the initial series of treatments, a rest period of 4 to 6months will allow time for pigmentation and matting to clear, and for any remaining reticular veins to establish new routes of re ux or drainage. Approximately 80% of patients will clear to their satisfaction during the  rst course of treat­ment. Any remaining telangiectatic webs or new telangiec­tasias are then reassessed to determine the best approach for another round of treatment.
POOR RESPONSE TO
TREATMENT
Compression will speed vessel clearance and reduce stain­ing from any vessel that protrudes above the surface of the skin. A er treatment of telangiectasias, compression is provided by ready-to-wear gradient compression hose (15–20mm Hg) placed over cotton balls secured with tape at the sites of injection. If larger reticular veins (>3mm) are treated at the same session, then compression consists of ClassI 20–30mm Hg compression. Some authorities recommend that continuous compression be applied for as long as the patient will tolerate it (usually 1–3days).  en the stockings are removed and the cotton balls discarded; the patient bathes and reapplies his or her stockings, wear­ing them for the next two weeks except when bathing and sleeping. We have the patient remove both stockings and cot­ton balls at bedtime of the day of treatment. Compression hose are then worn daily for 2 weeks except when bathing and sleeping. Patients are encouraged to walk, and the only restrictions on activity are those such as heavy weightli ing that result in sustained forceful muscular contraction and venous pressure elevation.
TREATMENT INTERVALS
Physician and patient preferences play a large role in deter­mining treatment intervals. New areas may be treated at any time, but retreatment of the same areas should be deferred for several weeks, because the immediate post­treatment appearance of telangiectasias is either bruising, matting, or pigmentation; this will ultimately clear a er 2 to 4 weeks. Patients o en are anxious to speed their course of treatment, but allowing a longer time between treatment sessions may minimize the number of sessions needed. We strongly recommend waiting as long as 4 to 8 weeks between treatments.
When patients have had a poor response to the initial series of treatments, the original diagnosis must always be called into question. Unsuspected sources of re ux can include truncal varices, incompetent perforating veins, and unrecognized reticular vessels. If no untreated source of re ux can be identi ed, the patient must be carefully questioned about proper compliance with compression. Many patients abandon compression immediately a er sclerotherapy, and this can lead to treatment failures.  e concentration and volume of sclerosant used should also be reexamined. It is not uncommon to  nd that the con­centrations selected were ine ective for the size and type of vessel being treated.
S U M M A R Y
When based on a correct diagnosis and an appropriate treatment plan, sclerotherapy is a highly e ective method of treatment for telangiectasias. Formulating an e ective treat­ment plan requires a detailed knowledge of venous anatomy, a thorough understanding of the principles and patterns of re ux, and intimate familiarity with a range of volumes and concentrations of sclerosing solutions.  e results obtained depend greatly on the experience of the clinician, but with care and with attention to detail, clearing rates of 90% can be achieved in most patients. Su cient time must be allowed between treatments.
Patient satisfaction is enhanced through education and informed consent, photographic documentation, and a measured approach to treatment. When the basic prin­ciples of diagnosis and treatment are followed meticulously, a successful outcome is highly likely. It is important to educate the patient that telangiectasias may be a lifelong problem. Development of new veins within a few years
SCLEOTHERAPY TREATMENT OF TELANGIECTASIAS • 113
a er successful treatment does not constitute treatment
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failure; rather, it demonstrates the chronicity of venous insu ciency.
REFERENCES
1. Weiss RA , Weiss MA . Resolution of pain associated with varicose and telangiectatic leg veins a er compression sclerotherapy , J Dermatol Surg Onc . 1990 . 16 : 333–336 .
2 . W e i s s R A , H e a g l e C R , R a y m o n d -M a r t i m b e a u P .  e Bulletin of
the North American Society of Phlebology: Insurance Advisory Committee Report , J Dermatol Surg Onc . 1992 . 18 : 609–616 .
3. Weiss RA , Weiss MA . Doppler ultrasound  ndings in reticular veins of the thigh subdermic lateral venous system and implications for sclerotherapy , J Dermatol Surg Onc . 1993 . 19 ( 10 ): 947–951 .
4. Somjen GM , Ziegenbein R , Johnston AH , Royle JP . Anatomical examination of leg telangiectases with duplex scanning [see com­ments], J Dermatol Surg Onc . 1993 . 19 ( 10 ): 940–945 .
5. Bihari I , Muranyi A , Bihari P . Laser-doppler examination shows high  ow in some common telangiectasias of the lower limb , Dermatol Surg . 2005 . 31 ( 4 ): 388–390 .
6. Cheng L , Lee D . Review of latex allergy , J Am Board Fam Pract . 1999 . 12 ( 4 ): 285–292 .
7. Bodian EL . Sclerotherapy:Apersonal appraisal , J Derm Surg Onc . 1989 . 15 : 156–161 .
8. Sadick NS . Sclerotherapy of varicose and telangiectatic leg veins: Minimal sclerosant concentration of hypertonic saline and its relationship to vessel diameter [see comments] , J Derm Surg Onc . 1991 . 17 ( 1 ): 65–70 .
9. Weiss MA , Weiss RA . E cacy and side e ects of 0.1% sodium tetradecyl sulfate in compression sclerotherapy of telangiecta­sias:Comparison to 1% polidocanol and hypertonic saline , J Derm Surg Onc . 1991 . 17 : 90–91 .
10. Weiss RA , Weiss MA . Incidence of side e ects in the treatment of telangiectasias by compression sclerotherapy:Hypertonic saline vs. polidocanol , J Derm Surg Onc . 1990 . 16 : 800–804 .
11. Georgiev M . Postsclerotherapy hyperpigmentations: Chromated glycerin as a screen for patients at risk (a retrospective study), J Derm Surg Onc . 1993 . 19 : 649–652 .
12. Martin DE , Goldman MP . A comparison of sclerosing agents:Clinical and histologic e ects of intravascular sodium tetra­decyl sulfate and chromated glycerine in the dorsal rabbit ear vein , J Derm Surg Onc . 1990 . 16 : 18–22 .
13. Du y DM . Small vessel sclerotherapy:An overview , Adv Dermatol . 1988 . 3 : 221–242 .
14. Zimmet SE .  e prevention of cutaneous necrosis following extrava­sation of hypertonic saline and sodium tetradecyl sulfate , J Derm
Surg Onc
. 1993 . 19
: 641–646 .
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COMPLICATIONS OF LIQUID SCLEROTHERAPY
Nisha Bunke-Paquette
INTRODUCTION
Sclerotherapy remains the gold standard of treatment for lower limb telangiectasia and reticular veins. Sclerotherapy, by de nition, is the injection of a chemical irritant into a vein to produce in ammation, eventual  brosis, and oblit­eration of the lumen.  e cellular mechanisms that occur in vein sclerosis involve endothelial swelling with desqua­mation, deposition of a mixed thrombus, connective orga-
1
nization, and  brosis.
While endothelial cell injury and in ammation are necessary to e ectuate sclerosis, these responses can also be causation for undesirable side e ects. Most adverse events are minor and inconsequential, such as local injection site pain, urticaria, itching, erythema,
2,3
and bruising.
Other common but usually self-limiting responses include cutaneous hyperpigmentation (HP) and telangiectatic matting (TM). Cutaneous necrosis is infrequent but can be severe and extensive. Systemic life-threatening reactions and fatal anaphylaxis have been reported. As with the use of any medication, other compli­cations such as cardiotoxicity have been attributed to the
4
use of sclerosants but are rare and unlikely.
 rombotic complications are more common with foam sclerotherapy.  e use of a sclerosant in foam form, where the sclerosing power is increased and there is the added ability to migrate, carries its own set of unique complications, which are described elsewhere in this text.  is chapter describes the common and signi cant adverse events pertaining to liquid sclerotherapy.
GENERAL CONSIDERATIONS
 ere are two basic principles that the phlebologist should consider in the approach to sclerotherapy of leg veins.  ese were described by Ouvry in 1982 and con­tinue to be a rmed by various authors:(1)treat the most proximal source of venous re ux  rst, and (2)use the low-
5
est e ective concentration of the sclerosant.
 e use of
higher sclerosant concentrations is associated with more
side e ects.
6
Additionally, failure to recognize and treat underlying venous insu ciency can result in suboptimal results.
As a result, sclerotherapy should be performed by trained clinicians who have a knowledge of the pharmacol­ogy and side e ects of sclerosing medications and the ability to recognize the presence of underlying venous insu ciency and the need for further ultrasound evaluation.
P R E T R E A T M E N T A S S E S S M E N T
P A T I E N T H I S T O R Y
A thorough medical history and clinical examination will help to identify patients who require further evaluation with ultrasonography, and risk strati cation for adverse events.
A detailed history should be obtained from each patient with particular attention to potential risk factors for adverse events such as their vascular history, allergy pro le, medication list, history of prior vein treatment, and treatment failures. Apersonal and/or family history of deep venous thrombosis and spontaneous thrombophlebitis may indicate a hypercoagulable predisposition. Ahistory of poor response to prior treatment, or varicose vein sur­gery may suggest the need for ultrasonographic evaluation. Atopic individuals may be identi ed by a history of mul­tiple allergies, asthma, allergies to detergents (if a detergent sclerosant is being considered) or iodine (if polyiodides
7
are used), and repeated exposure to sclerosants.
Risks for
complications such as pigmentation may be greater in those
8
taking tetracycline or minocycline.
With sclerotherapy, aspirin, nonsteroidal anti-in ammatory drugs, and other blood-thinning medications can cause increased capillary
9
leakage and subsequent pigmentation.
Hormonal medi­cations that increase the risk of thrombotic events such as ovulatory agents, oral contraceptives, estrogens, and selec­tive estrogen receptor modulators (SERMs) should be addressed.
115
Clinical Examination
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 e clinical assessment should be done with the patient standing so as to maximally dilate leg veins. Documentation should be made of the type and location of telangiectatic and reticular veins. Since sclerosant selection and concentration is dependent on vessel size, the type of abnormal veins should be noted:(1)telangiectatic matting or telangiectasias up to 1mm, (2)venulectasias (1–2mm), (3)reticular veins (2–4mm) and (4)presence of varicose veins (greater than 3mm). vein-imaging devices such as a  ber optic vein transilluminator or near-infrared imaging device may help identify reticular or “feeder veins” that are not readily visible with the naked eye (see Figure14.1). Particular note should be made of the ana­tomical location and distribution of telangiectasias and retic­ular veins, because anatomical location may be suggestive of underlying venous insu ciency. Telangiectasias in the lateral thighs are o en accompanied by reticular veins from the lateral plexus. Fan-shaped intradermal telangiectases on the medial or lateral malleoli, known as corona phlebectasia, can be associ­ated with underlying saphenous or perforator insu ciency. Other identi ers to indicate saphenous vein insu ciency may be lacking. Engelhorn reported that 46% of women (125 out of 269)with spider veins had underlying venous insu ciency of either the great or small saphenous veins.
INJECTION SITE REACTIONS
Local injection site reactions are common to all sclerosants and tend to be mild, transient, and somewhat expected.  ey include localized injection site pain, hematoma, urti­caria, pruritis, erythema, and warmth (see Figure 14.2). Polidocanol (POL), which has an anesthetic property, is
13–15
generally described as well tolerated.
However, urticaria
10
 e use of
11
12
3
Figure14.2  is  gure demonstrates the appearance of injection-site urticaria immediately following intravenous injection of 0.5% POL. It was associated with localized pruritis.
may be more prevalent with POL. Urticaria is a result of local histamine release occurring with vascular injury.  is is transient, and associated itching is usually relieved within 30 minutes. POL analogues have been studied for e ects on skin irritation and sensitization and found to produce only
16–18
negligible skin irritation.
TELANGIECTATIC MATTING
Telangiectatic matting (TM) refers to the appearance of new clusters of  ne vessels within super cial layers of the dermis that typically appear 4 to 6 weeks a er sclerother­apy treatment (see Figure14.3).  ey appear as blanching small blood vessels with a blemish-like appearance measur­ing less than 0.2mm in diameter.  e most common loca­tion for TM to appear is on the inner and outer thighs, near
19
the knees and calves.
TM may a ect up to one-third of
Figure14.1 Reticular or feeder veins can be visualized with the use of a light source such as near-infrared imaging as demonstrated in this  gure.
Figure14.3 Blemish-like appearance of  ne vessels attributed to TM following treatment of reticular veins. Duplex ultrasound evaluation revealed underlying insu ciency of theGSV.
116 • PRIMARY SUPERFICIAL VENOUS INSUFFICIENCY
A
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Figure14.4 (A) Telangiectasias before sclerotherapy. (B)Mild linear HP overlying veins of larger diameter, 6 weeks following sclerotherapy with 0.5% POL. It resolved a er 3months. (C)Macular HP persisting for several months a er sclerotherapy with 0.5%POL.
B C
patients undergoing sclerotherapy, spontaneously in 3 to 12months.
20–22
and usually resolves
21
 e development of TM is attributed to reactive in am-
matory or angiogenic mechanisms and is more prevalent with
22
high concentrations of sclerosing solution.
Other risk factors that have been associated with the development of TM include being overweight, female, or of a high estrogen state during
20
treatment, and a longer duration of spider veins.
Weiss and
Weiss found a relative risk of 3.17 (p > 0.003) for development
20
of TM while patients were receiving exogenous estrogen.
In the authors’ experience, TM can be observed when underlying venous insu ciency is present; for example, TM on the inner knees can indicate underlying saphenous vein incompetence.  erefore, further investigation with duplex evaluation may be indicated in TM. O en self-resolving, TM can also be treated with lower concentration sclero­therapy or certain lasers.
SKIN HYPERPIGMENTATION
Skin hyperpigmentation (HP) refers to the brown staining of the skin following sclerotherapy that can occur as linear or macular pigmentation (see Figure14.4, A–C).  e gen­eral incidence of hyperpigmentation ranges from 10% to 30%, although persistent pigmentation lasting greater than 1year occurs in approximately 1% of patients.  e incidence of hyperpigmentation is related to both vessel size and to
22–24
the sclerosing agent.
For example, hypertonic saline has
higher rates of HP thanPOL.
Two explanations permeate medical literature regard­ing the pathological mechanisms of HP. HP is attributed to either direct hemosiderin deposition or post-in ammatory processes or a combination of the two. Hemosiderin depos­its from hemoglobin degradation of red blood cells, enter the
2
dermis by extravasation a er rupture of treated vessels
9
perivenulitis.
Histologic evidence of hemosiderin deposition,
or
presented by Goldman etal., supports the theory of extravasa­tion of red blood cells into the dermis following rupture of
9
fragile vessels.
 erefore, vessel fragility, increased concentra­tions, type of solution (the pH levels of sclerosants cause vary­ing degrees of endothelial damage), vessel size, and injection
pressure have been implicated as factors for HP, which thus may be initiated by high sclerosant concentrations in super ­cial and dermal veins as well as sclerosant-dependent.
Postsclerotherapy HP tends to be more common when greater amounts of intravascular coagula are present. Persistent thrombi are thought to produce a subacute “peri­venulitis,” which favors extravasation of red blood cells.  e presence of intravascular coagulum that is persistent can cause tenderness to the patient. In our experience, extrac­tion almost immediately relieves discomfort and expedites the resolution of hyperpigmentation. Compression stock­ings minimize the amount of intravascular coagulum and therefore are an important part of posttreatmentcare.
Additionally, untreated re uxing veins that connect to the a ected area should be soug ht and treated. Gravitational pres­sure is a generally accepted risk for increased HP.  erefore, veins should be treated in a proximal to distal direction and, in cases of persistent HP, a proximal source of venous insuf­ ciency should be investigated with duplex ultrasonography.
 ere is no general agreement on whether certain skin types are prone to HP. Munavalli and Weiss report more frequent HP in patients with dark skin and dark hair.
2
Figure14.5 represents a patient who demonstrated extensive
Figure14.5 HP in a patient prior to vein treatment.  e HP is not related to sclerotherapy treatment, but is likely a result of chronic in ammation from venous insu ciency.
COMPLICATIONS OF LIQUID SCLEROTHERAPY • 117