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Chapter
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8
A
Figure 8.18 Folliculitis apparent 7 days after sclerotherapy; compression of
the treated area was produced with STD foam pads overlaid with
Microfoam tape.
Complications and Adverse Sequelae of Sclerotherapy
B
Figure 8.17 A, Superficial blister that developed 1 week after sclerotherapy
treatment; compression of the treated area was produced with an STD
pad overlaid with Microfoam tape and a 30- to 40-mmHg graduated
thigh-length compression stocking (seen pulled down below the knee).
B, Complete resolution 3 weeks later.
addition, Microfoam tape usually is placed over the foam
dressing with a slight amount of tension, thus increasing the
tension on either end of the tape. Blistering is also more
common in the summer months, when the weather is hotter,
and in elderly patients with thinner, more fragile skin.
The only problem with blistering is that it must be distinguished from early cutaneous necrosis, cutaneous infection, or an allergic reaction. Early cutaneous necrosis may
appear as a superficial blister. In this situation, the underlying and adjacent tissue usually is indurated and erythematous. Bullous impetigo can also have a similar physical
appearance. With it, the blister usually is overlying warm,
erythematous skin. If not warned beforehand, patients may
think that the blister is the result of an allergy to the sclerosing solution. A detailed explanation of the cause of the blister
is usually required before treatment can continue. Thick tape
with adhesive is not a recommended method of compression.
Prevention
If compression pads will be used under graduated stockings
in a patient susceptible to blistering, a tubular support bandage
194
can be used over the pad to hold it in place while the stocking
is being applied. Although somewhat costly, this dressing
(similar to a net dressing used in burn patients) helps prevent
blister formation. (It also can be used in patients with allergies
to tape.)
Treatment
Resolution of the blister occurs within 1 or 2 weeks without
any adverse sequelae. To aid healing and prevent infection of
the denuded skin, the use of an occlusive hydroactive dressing
is helpful. Occlusive dressings may also help alleviate any pain
associated with the blister.
Tape compression folliculitis
Occlusion of any hairy area can promote the development of
folliculitis (Fig. 8.18). If patients do not have secondary alopecia associated with chronic venous insufficiency, men
seeking treatment for varicose veins usually have hairy legs. If
a tape dressing is placed over foam or cotton ball pads under
a graduated compression stocking, a follicular inflammation
or infection may occur. Folliculitis is more likely to occur in
the summer months or when patients are active and perspire
under the dressing.
Treatment
Treatment consists of removal of the occlusive dressing and
application of topical treatment with an antibacterial soap
such as chlorhexidine gluconate or a topical antibiotic gel such
as erythromycin 2% or clindamycin phosphate topical solution 1%. The folliculitis usually resolves within a few days.
Systemic antibiotics are rarely necessary.
Other skin disorders
More benign than blisters is skin suntan fading (Fig. 8.19),
which is due to the removal of more superficial skin layers
of tanned skin. Although completely harmless, these little
inconveniences can be misinterpreted by certain patients; fortunately, their duration is limited to a couple of weeks.
In some cases, the tape can cause a dehydration of superficial skin layers and be responsible for an allergic-like reaction
(Fig. 8.20).
Morpheas
Presenting like morphea observed in scleroderma, this can
appear after injection of subcutaneous varicose veins. The etiology is unknown and the incidence is rare. Some patients
suffering from scleroderma have been treated by sclerotherapy
Figure 8.19 Skin tan fading after removal of adhesive tape and
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consecutive removal of superficial skin layers. Skin color gradient will
disappear when suntan fades.
Adverse Sequelae
Figure 8.21 Morpheas: subcutaneous and cutaneous retraction following
sclerotherapy of subcutaneous varices. The patient (a 67-year-old female)
was not suffering from scleroderma (neither clinical nor biological). A type
of localized scleroderma can be suspected.
Figure 8.20 Epidermal dehydration by adhesive tape. Not to be considered
as an allergy.
without presenting morphea; conversely, patients without
scleroderma have developed morphea (Fig. 8.21).
Recurrence
Although we believe that recurrence is really the formation of
new vessels in the same region that was previously treated,
recurrence of sclerotherapy-treated vessels has been estimated
to occur in 3% to nearly 100% of leg telangiectasias at 5-year
follow-up (Figs 8.22–8.24).
196,197
Recanalization of initially
thrombosed leg veins is procedure dependent. The larger the
extent of intravascular thrombosis, the greater the likelihood
of recanalization of the thrombosis during organization.
198,199
The recanalization of injected varices without subsequent
compression or with inadequate compression is caused by the
following:
• clot contraction and the formation of sinuses that may
become lined with endothelium
• central clot liquefaction and the formation of vascular
tunnels through the thrombosis
• formation of vascular organization of the thrombosis
and collateral vessel formation of the newly formed
capillaries
• formation of peripheral sinuses filled with sludged blood
(Figs 8.25–8.27).
199,200
Therefore, the most important factor in preventing recur-
rence is the limiting of intravascular thrombosis.
Treatment
Tournay
postinjection removal of blood clots, in 1938. The importance
of draining these postsclerotherapy thrombi has since been
emphasized by Sigg,
biopsy study of six patients with ‘recurrence’ of previously
treated veins demonstrated that the veins thought to have
recurred were in reality new varicose veins.
Martimbeau and Dupuis
rate with 2-year follow-up of 884 sites of telangiectasia in 525
201
was the first physician to stress the importance of
202
Pratt,
203
Hobbs,
204
and Orbach.
198
With proper technique, varicose veins only rarely recur. A
205
197
have reported a 3.6% recurrence
Raymond-
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8
Complications and Adverse Sequelae of Sclerotherapy
A
Figure 8.22 A, Original photo of reticular and telangiectatic veins treated with sodium tetradecyl sulfate 0.25% with complete resolution. B, 53-year-old
woman 12 years after treatment of reticular and telangiectatic leg veins on the right posterior thigh. Note persistent resolution of originally treated veins with
development of new reticular and telangiectatic leg veins bilateral posterior legs.
A
B
B
Figure 8.23 A, Marked telangiectasia and reticular veins left lateral thigh. B, 17 years after sclerotherapy treatment with sodium tetradecyl sulfate 0.25%;
note complete resolution of the treated veins with appearance of some new reticular veins.
patients. When high recurrence rates are reported, the patients
have usually been treated with minimal compression.
example, in one recent study of 310 patients, 83% required
reinjection of a treated varicosity. These patients received only
48 hours of compression with elastic bandages.
Unlike recanalization through a varicose vein cord, recanalization is not common through a sclerosed telangiectasia.
Post-treatment histologic studies have demonstrated only
fibrosis in an area treated with sclerotherapy.
telangiectasia found a ‘recurrence rate’ of 56% when patients
were evaluated 5 years after sclerotherapy. In 48% of patients
affected by a recurrence, the additional telangiectasias were of
minimal extent, requiring little if any treatment.
tion of telangiectasia present 1 year after treatment most likely
196
198
For
192
7
One study of
206
Examina-
indicated either untreated telangiectasia or new telangiectasia,
and not recurrent veins. Our experience in observing before
and after images on thousands of patients with multiple treatments over two decades confirms that telangiectasias are typically not recurrent but new.
Stress-related symptoms
Vasovagal reflex
The vasovagal reflex (neurocardiogenic syncope) is a common
adverse sequela of any surgical or invasive procedure. A survey
conducted in an ambulatory care center revealed an incidence
of 10.6% during vein cannulation in 1500 patients.
has been estimated to occur in 1% of patients during
207
It
Adverse Sequelae
Ideal compression
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A
Figure 8.24 A, 48-year-old woman with multiple reticular and telangiectatic leg veins right lateral knee treated with sodium tetradecyl sulfate 0.25%.
B, 12 years after sclerotherapy; note total resolution of the treated veins with some new telangiectasia in other locations.
Skin
Endothelium
Inadequate compression
Skin
Endothelium
Thrombosis
B
Figure 8.25 Diagrammatic representation
of recanalization of a varicose vein through a
sclerotherapy-induced thrombosis.
Wenner L: Vasa 15:180, 1986.)
Endosclerosis
Recanalization
(Redrawn from
sclerotherapy
nique of Fegan or Sigg, which requires patients to stand on
208
and is more frequent when using the tech-
insertion of needles.
with 30-gauge needles in reclining patients, estimates the incidence of vasovagal reactions as 0.001%. Interestingly, the percentage of men who have this response far exceeds the
percentage of women. We (MPG, RAW) have seen a patient
with a vasovagal reaction only twice in over 20 years of performing sclerotherapy in reclining patients, and, interestingly,
have seen vasovagal reactions many times in male patients just
being examined with duplex ultrasound or hearing the
Doppler flow sound.
Vasovagal reactions have typical clinical findings. The usual
symptoms include light-headedness, nausea, and sweating.
The patient also may have shortness of breath and palpitations.
Syncope may occur and usually provokes the most concern in
the physician and staff. With progression of the reaction, a
209
Duffy,8 who performs sclerotherapy
seizure may occur, as well as cardiac arrhythmia with a rapid
decrease in cardiac output and even cardiac arrest.
210
Vasovagal
reactions most often are preceded by painful injection but may
even occur from the patient seeing the needle or smelling the
topical isopropyl alcohol or sclerosing solution.
Prevention
The main concern with a vasovagal reaction is that the patient
will fall and be injured. Therefore, both the nurse and physician should watch the patient closely for signs of restlessness,
paleness, and excessive perspiration. All patients should be
warned to sit down if they become dizzy. It is also helpful
when needle placement is performed on a standing patient for
the patient to hold onto an arm rail or other support, although
treatment while the patient is standing is not a technique
we advocate. All such reactions are easily reversible when
the patient assumes the supine or Trendelenburg position.
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Complications and Adverse Sequelae of Sclerotherapy
Preventive measures consist of recommending that the patient
eat a light meal before the appointment, maintaining good
ventilation in the treatment room, and maintaining constant
communication with the patient during the procedure.
The physician must recognize the vasovagal response in a
patient and not assume that an anaphylactic reaction is occurring. If subcutaneous epinephrine (adrenaline) is given in the
mistaken belief that an anaphylactic reaction is occurring, the
symptoms will become both exaggerated and obscured. This
only further confuses the clinical situation and adds to patient
apprehension about further treatment sessions.
Treatment
The patient should be placed in the Trendelenburg position
and observed. If the reaction persists or intensifies, consider a
subcutaneous injection of 1 mL atropine 0.4 mg/mL.
safe and effective treatment rapidly reverses the vasovagal reaction and prevents its progression. Although a medical workup
Liquification
Retracted clot
A
Small clot adherent to intima,
invaded by histiocytes
Thickened vein wall
B
Figure 8.26 Diagrammatic representation of a histologic study from
Fegan, demonstrating the appearance of a varicose vein after sclerotherapy
treatment. A, Without compression. B, With continuous compression for
6 weeks.
(From Orbach EJ: Vasa 3:475, 1974.)
211
This
is rarely necessary, the reader is referred to an excellent review
article on this subject.
212
Underlying medical disease
More serious stress-induced problems include exacerbation of
certain underlying medical diseases. Patients with a history of
asthma may start wheezing, which can be treated with bronchodilator therapy such as metaproterenol sulfate (Alupent,
Proventil) or over-the-counter epinephrine bitartrate or
metered-dose inhalers (Primatene).
Angina may develop in patients with cardiovascular disease
and can be treated with sublingual nitroglycerin (NTG) tablets.
As discussed in detail later, POL is a negative inotropic agent
and slows cardiac contractility in a dose-dependent manner.
Chest pain has also been reported with the use of STS, but this
is not cardiac in nature. In our practice, one 65-year-old
patient without a history of cardiac disease and treated with
STS had acute chest pain on two separate occasions when
using 2–4 mL of 0.5% STS. An electrocardiogram taken immediately while the patient was having chest pain was normal,
and sublingual NTG was ineffective in resolving the pain,
which lasted approximately 5 minutes. This may have been
an idiosyncratic reaction.
Urticaria
Urticaria is easily treated with an oral antihistamine but
may be a sign of systemic allergy. Therefore, the use of the
sclerosing agent in future treatment sessions should be
carefully evaluated. The incidence of urticaria with various
sclerosing agents is detailed later. Urticaria has occurred in
only one of our patients treated with STS, in over 20 years. It
lasted less than 1 hour and resolved with oral diphenhydramine. Subsequent treatment with POL was unremarkable.
RAW had one patient who developed urticaria secondary to a
latex-containing syringe with injection of 3 mL of STS 0.5%
liquid. It also lasted 1 hour, was not accompanied by respiratory symptoms and resolved with intramuscular (IM) epi and
oral diphenhydramine.
It is intriguing that urticaria and periorbital edema have
occurred even with injection of unadulterated HS solution
(Duffy DM, personal communication, 1989). This may
be related to histamine release from irritated perivascular
mast cells.
Rarely, an urticarial reaction has been noted with use of
graduated compression stockings. In one patient, a diffuse
urticarial eruption occurred under the compression stocking
only on the leg treated with sclerotherapy that was compressed
A
Figure 8.27 A 50-year-old man with a varicose great saphenous vein (GSV) fed by an incompetent midthigh perforator vein without evidence of
saphenofemoral junction reflux. The vein recurred 1 year after successful closure with 2 mL of sodium tetradecyl sulfate 3% and was subsequently removed
with ambulatory phlebectomy. A, Appearance of recanalized sclerosed vein (hematoxylin–eosin; ×10). B, At ×400 magnification, endothelial slits are lining a
newly recanalized channel.
198
B
Figure 8.28 One day after sclerotherapy treatment of telangiectasia with
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application of a 30- to 40-mmHg graduated compression stocking. Note
generalized urticarial reaction on the leg treated with the compression
stocking. The nontreated leg appears normal.
Complications
A
B
with the stocking (Fig. 8.28). This ruled out a systemic reaction
from the sclerosing solution, making the most probable cause
the compression stocking itself. In another patient, a dermatopathic urticarial reaction was observed in the skin under
contact with the silicone band of the compression stocking
(Fig. 8.29). Both of these patients did well when a different
brand of compression stocking was used. Detailed communication with the stocking company whose product caused the
reaction failed to disclose a definite etiologic factor.
Localized hypertrichosis
Localized hypertrichosis developing after sclerotherapy with
the use of multiple sclerosing agents has been described. The
cause may be multifactorial. The most logical explanation of
increased hair growth appears to be improved cutaneous
oxygen content. Other factors may also stimulate increased
hair growth. A longstanding low-grade inflammatory reaction
may increase vascularity, as well as release various cytokines
and growth factors. Vascular endothelial growth factor serves
as a growth factor for hair follicle dermal papilla cells.
cell histamine release is associated with the release of various
neuropeptides that may also have a direct effect on the isthmus
and bulge region of the hair follicle.
chronic venous insufficiency have been reported to develop
localized hair growth after surgical treatment.
214
Clinically, patients with
215
Localized hair growth has been reported from a variety of
sclerosing solutions. Hair growth at the site of injection has
been described in three patients treated with STS.
patients were given injections of 1 to 6 mL of STS over 5 to
10 sessions. Localized hair growth developed 4 to 7 months
after the last injection. The site of hair growth was related to
the area of skin most damaged by venous incompetence.
Another report of localized hypertrichosis occurring 9 months
following a patient’s (second) STS sclerotherapy session was
213
Mast
216
All
Figure 8.29 A, Localized linear erythematous urticarial reaction in similar
pattern as silicone banding on the compression stocking 1 day after
application. B, 48 hours after application; note urticarial pattern of silicone
beads on the thigh secondary to the compression stocking.
notable in that it is the first published case to our knowledge
of this phenomenon occurring after use of the foam technique.
217
Weissberg
218
also has reported the development of
localized hypertrichosis in 1 of 62 patients treated with STS.
The hair growth occurred at the site of injection 1 month after
treatment. It lasted for 4 months and then subsided. A 44-yearold Korean woman also developed localized hypertrichosis on
the shin 1 month after sclerotherapy with 3% STS for recurrent
varicose veins.
also been associated with hypertrichosis at the injection site
in three cases.
after sclerotherapy with POL.
of the SFJ, as well as sclerotherapy of the posterior arch vein,
has also produced temporary hypertrichosis in two patients.
219
Sclerotherapy with polyiodinated iodine has
205
Two cases of hypertrichosis have been noted
220
Duplex-guided sclerotherapy
221
Therefore, the sclerosing solution itself is most likely not the
cause of localized hypertrichosis; its stimulation of the surrounding microcirculation and/or induction of inflammation
produces this effect. Although there are multiple case reports
of hypertrichosis, this effect must be very rare, since we have
seen it in only two patients despite having performed thousands of sclerotherapy treatments over the past 25 years.
Complications
Complications have been observed and described since the
very beginning of the technique but their precise incidence
remained unclear until recently.
222–224,
The actual number of
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Complications and Adverse Sequelae of Sclerotherapy
200
Table 8.2 Complications observed in a prospective French registry of
12,173 sclerotherapy sessions*
IMMEDIATE COMPLICATIONS
Liquid (T = 12) Foam (T = 28)
Anaphylactic shock – –
Intra-arterial injections – –
Vasovagal fainting (VVF) alone 4 6
Headaches alone – –
Paresthesias alone 2 1
Nausea, vomiting alone 1 0
Visual disturbances alone 4 8
Visual disturbances associated with
one or more of: headache nausea,
VVF
Others 1 5
DELAYED COMPLICATIONS
Deep vein thrombosis – 1
Muscular vein thrombosis – 1
Muscular vein extension – 1
Perforating vein thrombosis – 3
Intense superficial thrombophlebitis – 3
Skin necrosis – –
*5434 (44.6%) with liquid, 6395 (52.5%) with foam, and 344 (2.8%) using both.
T, total number of complications per type of agent form (liq or foam)
Adapted from Guex J-J, Allaert F-A, Gillet J-L, Chleir F: Dermatol Surg 31:123, 2005.
– 8
Liquid (T = 0) Foam (T = 9)
complications in a collective of sessions including all types of
sclerotherapy (liquid, foam, with ultrasound guidance or not;
varicose, reticular and spider veins) is presented in Table 8.2.
Interestingly, certain complications previously presented as
frequent, such as allergy or skin necrosis, have not been
observed in this study. This might demonstrate the progress
of the technique: improvement in quality of sclerosing agents,
improvement in phlebologists’ training and subsequent skill,
impact of ultrasound guidance and foam sclerosants, better
knowledge of indications, etc. Regardless, analysis and knowledge of complications is an important part of sclerotherapy.
Cutaneous necrosis
Etiology
Cutaneous necrosis may occur with the injection of any sclerosing agent, even under ideal circumstances, and does not
necessarily represent physician error (Fig. 8.30) Fortunately, its
occurrence is both rare and usually of limited sequelae. Its
cause may be the result of:
1. extravasation of a sclerosing solution into the
perivascular tissues
2. injection into a dermal arteriole or an arteriole feeding
into a telangiectatic or varicose vein
3. a reactive vasospasm of the vessel, or
4. excessive cutaneous pressure created by compression
techniques.
Extravasation
Extravasation of caustic sclerosing solutions may directly
destroy tissue. The extent of tissue injury is directly related to
both the concentration of the sclerosing solution and the
quantity extravasated. As discussed below, different sclerosing
solutions have a greater or lesser ability to destroy tissue. Since
the final clinical appearance of the skin may not be apparent
for several days, therapeutic intervention must be undertaken
as soon as possible in all cases.
Clinically, bright erythema is present in the skin overlying
the extravasated solution (Fig. 8.31). With certain extravasation injuries, the formation of epidermal blistering may occur
but does not predict a partial-thickness injury, although it may
precede eventual full-thickness necrosis.
225
During injection of an abnormal vein or telangiectasia,
even the most adept physician may inadvertently inject a
small quantity of sclerosing solution into the perivascular
tissue (Fig. 8.32). A tiny amount of sclerosing solution may
be left in the tissue when the needle is withdrawn, and sclerosing solution may leak out of the injected vessel, which has
been traumatized by multiple or through-and-through needle
punctures. Rarely, the injection of a strong sclerosing solution into a fragile vessel may lead to endothelial necrosis
and rupture producing a ‘blow-out’ of the vessel and perivascular extravasation of sclerosing solution (Fig. 8.33). Therefore, injection technique is an important but not foolproof
factor in avoiding this complication, even under optimal
circumstances.
Sclerosing solutions vary in the degree of cellular necrosis
they produce. If minimal tissue necrosis is caused by a sclerosing agent, it may perhaps be suitable for perivascular injection
in the treatment of telangiectatic mats whose vessels cannot
be cannulated even with a 33-gauge needle.
With an osmolality greater than that of serum (281–
289 mOsm/L), hyperosmotic agents can cause tissue damage
as a result of the osmotic gradient. Epidermal necrosis has
even occurred from extravasation of solutions containing 10%
dextrose.
226
Hypertonic saline 23.4% is a caustic sclerosing
agent, as demonstrated in intradermal injection experiments.
Clinically, small punctate spots of superficial epidermal
damage occur at points of injection, especially when a small
bleb of the solution escapes from the vein. However, subcutaneous injection of up to 1 mL of HS 23.4% (by mistake) in
lieu of lidocaine into the neck or cheek has been reported to
result in no adverse sequelae.
227
In this situation, cutaneous
necrosis was most likely avoided by rapid physiologic dilution
of the HS. Alternatively, dermal tissue may be more resistant
to the caustic effects of hypertonic solutions. However, the
increasing frequency of cutaneous necrosis occurring after
extravasation of inadvertent subcutaneous injection of HS has
moved the US Department of Health and Human Services and
the product manufacturer (American Regent Laboratories,
Inc.) to recommend that HS be stored only in pharmacies
where all dilutions would be performed before dispensing.
This would eliminate the possibility of an iatrogenic medication error outside the pharmacy (Mary Helenek, American
Regent Laboratories, Inc., written communication, May 1990).
It is recommended that HS be stored in a location separate
from other injectable solutions to prevent this potential
complication.
Experimentally, POL apparently is minimally toxic to sub-
cutaneous tissue. Duffy
228,229
has reported injecting 0.5 mL of
a 3% solution of POL directly into his own forearm skin
without the development of an ulceration. Although some
physicians advocate the use of intradermal POL 0.5% to treat
tiny telangiectatic leg veins,
230,231
POL in sufficient concentration causes cutaneous necrosis. Solutions of POL greater
than 1.0% may produce superficial necrosis with intradermal injection.
230
This unfortunately occurred with the mistaken injection of 0.1 mL POL 5% solution into a leg
telangiectasia 0.2 mm in diameter in our practice. This injection resulted in extensive overlying cutaneous necrosis that
took 8 weeks to heal. Therefore, POL is not without the risk
Complications
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A
B
Figure 8.30 Cutaneous necrosis after injection with polidocanol 0.5% into telangiectasia. A, Preinjection. B, Early atrophie blanche 10 days after injection.
C, Superficial ulceration is present 5 weeks after injection. D, Clinical appearance 24 weeks after injection; complete resolution had occurred in 12 weeks.
C D
the Eighth Annual Meeting of the North American Society of
Phlebology, Fort Lauderdale, Fla., February 28, 1995.) As discussed below, this probably represents injection into an
arteriole.
Of note, several cases of Nicolau’s livedoid dermatitis
(NLD) following sclerotherapy have been reported.
232–235
Although most commonly seen after intramuscular injections,
NLD manifests as pain at the injection site followed by the
development of a livedoid plaque, often progressing to cutaneous necrosis. One case of delayed NLD following ultrasoundguided sclerotherapy with POL 2% foam was described
recently.
235
This particular case was unique in that, not only
did it follow an intravenous injection but it also did not manifest until 4 days after the procedure, when the patient first
experienced acute pain followed by subsequent cutaneous
ischemia. Interestingly, in each reported case of NLD follow-
Figure 8.31 Erythema overlying an area of extravasation from injection of a
telangiectasia with sodium tetradecyl sulfate 0.25%.
ing sclerotherapy, duplex scans failed to show evidence of
thromboses in major arteries or deep veins. The author
hypothesized that NLD most likely occurred via perivascular
spreading of the sclerosant, after leakage from a site of intravenous injection. Subsequently, POL probably acted as a local
of cutaneous necrosis if a strong enough concentration is
injected.
Although STS is more toxic to tissue than is POL, with
extravasation, concentrations above 0.25% usually are necessary to produce ulceration. Banning reported on the development of ulcerations in 5 of 4860 consecutive patients after
telangiectasias were injected with STS 0.1%. (Presentation at
irritant, inducing arterial or arteriolar vasospasm. Concentrations of POL associated with sclerotherapy-induced NLD
ranged from 0.5% to 3%, disfavoring a concentrationdependent phenomenon. One unifying theme among these
isolated cases of NLD is that each occurred after injection into
veins known to be in close proximity to rich arterial or arteriolar networks. Examples of these at-risk sites include the
201
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SkinVein SkinVein SkinVein SkinVein SkinVein
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Complications and Adverse Sequelae of Sclerotherapy
A B C D E
Figure 8.32 Mechanism for extravasation of sclerosing solution. A, Extravasation through multiple needle puncture holes. B, Extravasation from injection of
sclerosing solution after slight withdrawal of the needle. C, Extravasation of sclerosing solution along needle shaft. D, Extravasation from injection with
needle bevel partially in the vein. E, Extravasation through excessive destruction of the vein wall.
sclerotherapy: a guide for practitioners, Montreal, 1984, Eden Press.)
(Redrawn from Biegeleisen HI: Varicose veins, related diseases, and
A
Figure 8.33 Cutaneous necrosis after injection of sodium tetradecyl sulfate 0.5%. A, Immediately after injection. Note ‘hyperemic burn reaction’. B, Necrotic
epidermis 2 weeks after injection.
B
inguinal fold, medial knee, and medial ankle. Although the
limited number of cases of NLD following sclerotherapy
reflects its rarity, the clinician is encouraged to remain aware
of this potential complication.
Glycerin or CG solutions have not been reported to produce
cutaneous necrosis with extravasation. Duffy (personal communication, 1992) has shown that injection of ‘full-strength’
CG will not produce cutaneous necrosis when it is injected
into the mid-dermis. Histologic examination of his patient
showed no evidence of dermal or epidermal damage.
Even when sclerotherapy is performed with expert technique,
using the safest sclerosing solutions and concentrations, cutaneous ulceration may occur (Figs 8.30, 8.34, and 8.35). Therefore, it appears that extravasation of caustic sclerosing solutions
alone is not totally responsible for this complication.
Arteriolar Injection
De Faria and Moraes
angiectasias is associated with a dermal arteriole. Bihari and
237
Magyar
have found pulsatile flow in 68.9% of patients in
16 of 18 biopsies (2.5 ×
telangiectasia in patients demonstrating arteriovenous (AV)
microshunts. This gives a 61% incidence of AV microshunts
in patients with leg telangiectasia. An expanded study of 155
patients with leg telangiectasia by the same group demonstrated a 72.2% incidence of pulsatile flow.
the incidence seen in our patients is considerably lower and
may represent only 10% or less and might be attributed to a
different age or subset of patients, or perhaps to the more
physiologic conditions seen with Duplex ultrasound rather
202
236
have observed that 1 in 26 leg tel-
1.5 cm) taken from the pulse-positive
238
We believe that
Figure 8.34 Cutaneous necrosis 6 weeks after sclerotherapy with
polidocanol 0.25%. Note that 2 mL of solution was injected into a feeder
vein approximately 10 cm distal to the necrotic area.
than biopsy. The higher incidence found in the later two
studies is probably caused by the larger biopsy specimens
taken. Of the 22 Doppler-positive telangiectasias, 19 demonstrated AV microshunts on biopsy. Thus, it is likely that rapid
injection or large-volume injection into leg telangiectasias that
are associated with microshunts will force the sclerosing solu-
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tion into the arterial circulation. It is our opinion that inadvertent injection into or near this communication is the most
common cause of cutaneous ulcerations.
It has been shown by Duffy and by our experience that
when POL is injected intradermally to effect sclerosis of TM,
cutaneous ulceration does not occur, even with the injection
of 0.5 mL of a 0.75% solution. However, we have noted the
development of 3- to 6-mm diameter ulcerations in approximately 0.0001% of injections with POL 0.5%. Five consecutive ulcerations that appeared over the course of 12 months
were excised. In these patients, each cutaneous ulceration
developed as the result of the occlusion of the feeding dermal
arteriole. This produced a classic wedge-shaped arterial ulceration (Fig. 8.36). The Australian Polidocanol Open Clinical
Trial at 2 years reported 43 ulcers on 32 legs after sclerotherapy
treatment of varicose and telangiectatic leg veins on 12,544
legs, for an incidence of 0.23%.
239
Therefore, it appears that
rare cases of small ulcerations may be unavoidable to some
extent, especially in the pretibial and malleolar areas.
Figure 8.35 A 38-year-old woman who had undergone numerous
sclerotherapy treatments with and without ultrasound guidance. The last
ultrasound-guided sclerotherapy treatment with sodium tetradecyl sulfate
2% into a perforating vein resulted in immediate blanching of the overlying
skin. Nitroglycerin paste was rubbed into the affected area. A 7 × 5cm dusky
blue patch developed 1 week later when the compression stocking was
removed, with 2 ×
instance the injection was clearly intravenous even though the effects were
those of arterial ischemia.
26:535, 2000.)
5 mm diameter areas of superficial skin necrosis. In this
(From Bergan JJ, Weiss RA, Goldman MP: Dermatol Surg
Interestingly, since we have been using glycerin solution in
a 72% concentration mixed 2 : 1 with lidocaine 1% with or
without epinephrine 1 : 100,000 we have not seen ulcerations
at all. The safety of glycerin may be its high viscosity, which
prevents the solution from flowing into arteriole connections.
Alternatively, the epinephrine mixed into the solution may
put the arteriolar portion of the AV anastomosis into spasm
and/or the lidocaine portion may vasodilate and protect the
arteriolar portion of the AV anastomosis. Or the actual incidence of AV anastomosis is much lower than previously
estimated.
Vasospasm
Rarely, after injection of the sclerosing solution, an immediate
porcelain-white appearance is noted at the site of injection
(Fig. 8.37). A hemorrhagic bulla usually forms over this area
within 2 to 48 hours (Fig. 8.38) and progresses to an ulcer.
cutaneous reaction might represent an arterial spasm. Duffy
reported this effect when injecting facial telangiectasia.
Vasospastic reactions of arteries occur in predisposed
individuals for unknown reasons.
with puncture of the artery without injection of sclerosing
solution.
242
Thus, small vessels, when irritated in susceptible
240–242
This may occur even
patients, may spasm.
In an attempt to reverse the spasm, vigorous massage when
the white macule appears usually prevents the development
of ulceration. However, prevention of the ulceration with
massage alone is not always successful. Massaging in a nitroglycerin ointment 2% is more likely to prevent the development of ulcerations in this setting.
The major systemic action of nitrates is a direct reduction
in venous smooth muscle tone.
243
Nitrates also relieve spasm
of angiographically normal and diseased arteries.
nitroglycerin ointment has been reported as beneficial in
treating both dopamine extravasation and vasoconstriction
necrosis.
245,246
Although more experience from other investigators needs to be reported, it seems prudent to use this
technique.
Another technique that may help in reversing vasospasm is
the topical application of nitric-oxide-generating gel. This gel
has been found to increase baseline blood flow in the fingers
of patients with Raynaud’s syndrome.
247
Since patients with
Raynaud’s syndrome have abnormal digital vasoconstriction,
the improvement found in application of this gel may crossover to potential improvement in sclerotherapy-induced
vasospasm. The gel is prepared by mixing a solution of KY jelly
and sodium nitrate (5% weight per volume (w/v)) with a
solution of KY jelly and ascorbic acid (55% w/v).
87
244
Topical
This
229
Complications
A
Figure 8.36 A, Low-power view showing skin ulceration and focal inflammation extending into the subcutaneous fat. A thrombosed vessel, most likely an
artery, is present directly under the area of necrosis (hematoxylin–eosin; ×25). B, Higher magnification of the same area as in A, showing a thrombosed artery
that caused the infarct. The arterial lumen is completely occluded by fresh thrombus (hematoxylin–eosin; ×200).
B
203
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