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other plasma components in vitro , Eur J Vasc Endovasc Surg . 2008 .
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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 , etal. 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 , etal. 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 ( Suppl1 ): 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
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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 , etal. 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
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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 1mm 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
RETICULARVEINS
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. Atypical network is shown in Figure13.1. 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 ARBORIZINGWEBS
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 rapidlyrecur.
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 TREATMENTTEST
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).
109

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Figure13.1 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
thechart.
TREATMENTPLAN
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
Figure13.2). 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
Figure13.2 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 toarrow.
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 varicoseveins.
e patient is recumbent in a position that allows convenient access to the reticular veins to be treated. A3-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 Figure13.3). 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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Figure13.3 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 isseen.
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 in1994.
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 Figure13.4). 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
•
Protectivegloves
•
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 orpaper)
•
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
Figure13.4 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 2mm 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 THEVESSEL
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
0.1mm. 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 Table13.1). 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 2cm
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.
Table13.1 SCLEROSANT CONCENTRATIONS FOR TELANGIECTASIA AND RETICULARVEINS
SIZE OF VESSEL MINIMUM EFFECTIVE
Reticular 1–3mm 0.1% 0.25% Yes Sodium tetradecyl sulfate (STS)
Reticular 1–3mm 0.25% 0.5% Yes Polidocanol (Laureth-9)
Telangiectasias 0.2–1mm 0.2% 0.5% No Polidocanol (Laureth-9)
Telangiectasias 0.2–1mm 0.1% 0.2% No STS
Telangiectasias 0.2–1mm 72% in water Same No Glycerine 72%
Telangiectasias 0.2–1mm 10% hypertonic saline and
CONCENTRATION
MAX CONCENTRATION FOAMED SCLEROSANT
Same No SclerodexTM
25%dextrose
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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.
Arandomized 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
6months 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
(15–20mm Hg) placed over cotton balls secured with tape
at the sites of injection. If larger reticular veins (>3mm)
are treated at the same session, then compression consists
of ClassI 20–30mm Hg compression. Some authorities
recommend that continuous compression be applied for as
long as the patient will tolerate it (usually 1–3days). 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:Apersonal 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. Apersonal and/or family history of deep
venous thrombosis and spontaneous thrombophlebitis
may indicate a hypercoagulable predisposition. Ahistory
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 1mm,
(2)venulectasias (1–2mm), (3)reticular veins (2–4mm) and
(4)presence of varicose veins (greater than 3mm).
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 Figure14.1). 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
Figure14.2 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 Figure14.3). ey appear as blanching
small blood vessels with a blemish-like appearance measuring less than 0.2mm 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
Figure14.1 Reticular or feeder veins can be visualized with the use of a
light source such as near-infrared imaging as demonstrated in this gure.
Figure14.3 Blemish-like appearance of ne vessels attributed to TM
following treatment of reticular veins. Duplex ultrasound evaluation
revealed underlying insu ciency of theGSV.
116 • PRIMARY SUPERFICIAL VENOUS INSUFFICIENCY

A
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Figure14.4 (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 3months. (C)Macular HP persisting for several months a er sclerotherapy with 0.5%POL.
B C
patients undergoing sclerotherapy,
spontaneously in 3 to 12months.
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 Figure14.4, A–C). e general incidence of hyperpigmentation ranges from 10% to
30%, although persistent pigmentation lasting greater than
1year 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 thanPOL.
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 etal., 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 posttreatmentcare.
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
Figure14.5 represents a patient who demonstrated extensive
Figure14.5 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
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