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A B
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Figure14.6 (A) Resolution 2months a er the second of two treatments
with the Q-switched ruby laser at 8.0 J/cm
sclerotherapy lasting over 1year.
RA, Bergan JJ, eds. Varicose veins and telangiectasias:Diagnosis and treatment . St Louis. MO:uality
Medical Publishing.1999.)
(Courtesy David Du y, MD; from Goldman MP, Weiss
2
. (B)Pigmentation from
linear HP along reticularveins in the absence of any type of
vein treatment.
e majority of HP will resolve spontaneously in 1year.
Exfoliation by trichloroacetic acid, phenolic peeling agents,
and pumice stone have been described with variable results.
Treatment with intense pulsed light (IPL) has shown good
24
results (Figure14.6).
CUTANEOUS NECROSIS
Cutaneous necrosis most commonly presents as an ulceration but can result in extensive loss of tissue (Figures14.7).
It can occur as far out as weeks a er the initial insult, and
may be associated with pain, localized in ammation, and
edema. Etiologic explanations include (1)extravasation of
the sclerosant into perivascular tissue, (2)injection into a
dermal arteriole or an arteriole feeding into a telangiectatic
25
or varicose veins, or (3)reactive vasospasm of the vessel.
Evidence tends to favor theories of nonextravasation,
because in many cases intravenous injection was veri ed.
Miyake etal. showed that vessel size, sclerosant viscosity and
strength not extravasation, play a role in cutaneous ulceration.
26
Bergan etal. proposed a theory of distribution of the
27
sclerosant into the arterial arborization.
Based on this theory, the distribution of sclerosant into the arterial tree could
result in extensive tissue necrosis (Figure14.8).
Additionally, Du y intentionally extravasated 3% POL
into a human volunteer’s arm, which did not cause ulcer-
18
Schuller-Petrovic demonstrated that subcutanous
ation.
injections of POL strengths 0.5%–3% into a rabbit ear did
28
not result in extravasation necrosis.
MICROTHROMBI
“Microthrombi” refers to the common occurrence of palpable intravascular coagulum in a treated vessel appearing
A
B D
Figure14.7 is patient documented the natural history of a necrotic skin ulcer over several months, as a result of 1% POL liquid injections on her
medial malleolus. (A)3 weeks a er sclerotherapy, (B)6 weeks, (C)12 weeks, (D)16weeks.
C
118 • PRIMARY SUPERFICIAL VENOUS INSUFFICIENCY
A
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Figure14.8 (A) Skin pigmentation and atrophie blanche in a patient with chronic venous insu ciency. (B)Cutaneous necrosis developed 3 weeks
a er treatment of a varicose vein with intravenous injection of 0.5% POL sclerofoam. e feeding varix was located several centimeters proximal to
the a ected area. e sclerofoam traveled into distal veins and lled small capillary vessels of this already compromised skin. (C)At 3months.
B C
1 to 6 weeks a er sclerotherapy (Figure14.9). e larger
the vessel size, the more frequently intravascular coagulum
occurs. e intravascular thrombus tends to remain lique ed. Persistent microthrombi can be a source of tenderness
for the patient and result in SH. Persistent microthrombi
should prompt evaluation for a proximal source of re ux.
Evacuation of microthrombi is indicated to reduce tenderness and decrease risk of residualHP.
Microthrombi and larger volumes of intravascular coagulum can be evacuated by puncture with a 16- or 18-gauge
needle (depending on the vessel size) and manually
expressed. e coagulum remains highly viscous liquid and
can be extracted by applying manual pressure and “milking”
the vein (Figure14.10).
In the author’s experience, evacuation of intravascular coagula almost immediately reduces tenderness and
in ammation. Continued use of compression is recommended, and evaluation for an underlying source of venous
insu ciency may be indicated for persistent or recurrent
intravascular coagulum. Microthrombi can be minimized
with external compression following sclerotherapy. In the
author’s experience and others, microthrombi are less prevalent when patients are compliant with the use of posttreat-
29
ment compression stockings.
HYPERSENSITIVITY REACTIONS
ANAPHYLAXIS AND
ANAPHYLACTOID RESPONSES
Most reported allergic reactions a er sodium tetradecyl
sulfate (STS) administration showed mild intensity.
30,31
e incidence of nonfatal allergic reactions such as hives,
asthma, and anaphylactic shock are estimated at 0.3% with
32
Both anaphylaxis and anaphylactoid reactions have
STS.
been reported following injection of a sclerosant. ey can
occur at the rst exposure to the sclerosant or a er several
innocuous treatments. As a result, the utility of a test site as
the sclerosant package inserts suggest, is not practical nor
will it necessarily predict an allergic reaction. In one case,
a nonfatal anaphylactic reaction occurred on the second
sclerotherapy treatment with STS 6months following the
initial uneventful session. e patient showed initial signs
of reaction, such as tongue and lip swelling, within 20 min-
33
utes of the injection.
Since the risk of anaphylaxis increases
with repeated exposures to the antigen, one should always
be prepared for this reaction in every patient.
Figure14.9 Microthrombi in treated venules and reticularveins.
Figure14.10 Manual evacuation of intravascular coagulum following
puncture with a 16-gauge needle. e intravascular coagulum has a
highly viscous, “molasses-like” appearance.
COMPLICATIONS OF LIQUID SCLEROTHERAPY • 119
Anaphylaxis is an immunoglobulin E (IgE)-mediated
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mast cell–activated reaction that usually occurs within
minutes of antigen exposure. Asystemic reaction is caused
by antigen-speci c cross-linking of IgE molecules on the
surface of tissue mast cells and peripheral blood basophils,
which results in immediate release of potent mediators.
On occasion, this complication may occur hours to
weeks a er treatment.
ANAPHYLACTOID REACTION
e same chemical mediators that cause the physical manifestations of anaphylaxis produce anaphylactoid reactions.
Anaphylactoid reactions are not IgE mediated and do
not require previous exposure to an antigen. In one case,
a 49-year-old woman developed anaphylactoid reaction
34
a er the administration of STS for varicose veins.
In this
case report, the patient developed a generalized itch with
rash and nausea prior to cardiovascular symptoms. She was
promptly treated and had a full recovery.
35
Benzoyl alcohol
and carbitol 36 have been implicated
as allergens in sclerosant medications. Benzoyl alcohol is a
bacteriostatic agent used in many injectable pharmaceutical
agents. It is found in some injectable sclerosants and in bacteriostatic water, which is o en used to dilute a sclerosant to
a lesser concentration. Benzoyl alcohol has been associated
with toxic e ects such as respiratory failure, hypotension,
vasodilation, hemolysis, convulsions, hypersensitivity reactions, anddeath.
Carbitol is a contaminant that can be found in impure
compounded sclerosants. Impurities have been found in
samples of compounded POL, and Goldman has reported
signi cant concentrations of the contaminant carbitol in
37–39
samples of compounded STS.
e following text is reprinted from e Vein Book , rst
edition by Mitchel P.Goldman.
three principal manifestations of anaphylaxis are airway
edema, bronchospasm, and vascular collapse. Urticaria
alone does not constitute anaphylaxis and should not be
treated as such because of the potential side e ects of treatment with epinephrine, especially in older patients.
e signs and symptoms of anaphylaxis initially may be
subtle and o en include anxiety, itching, sneezing, coughing, urticaria, and angioedema. Wheezing may be accompanied by hoarseness of the voice and vomiting. Shortly a er
these presenting signs, breathing becomes more di cult,
and the patient usually collapses from cardiovascular failure resulting from systemic vasodilation. One helpful clue
in distinguishing between anaphylaxis and vasovagal reactions is heart rate. Sinus tachycardia is almost always present in a patient with anaphylaxis, whereas bradycardia or
cardiac rhythm disturbances are commonplace in vasovagal
reactions.
e recommended treatment is epinephrine, 0.2 to 0.5
ml 1:1000 subcutaneously. is can be repeated three or
four times at 5- to 15-minute intervals to maintain a systolic blood pressure above 90 to 100mm Hg. is should
be followed with establishment of an intravenous (IV)
line of 0.9% sodium chloride solution. Diphenhydramine
hydrochloride, 50 mg, is given next along with cimetidine,
300 mg; both the IV solution and oxygen are given at 4 to
6 L/min. An endotracheal tube or tracheotomy is necessary
for laryngeal obstruction. For asthma or wheezing, IV theophylline, 4 to 6 mg/kg, is infused over 15 minutes. At this
point it is appropriate to transfer the patient to the hospital. Methylprednisolone sodium succinate, 60 mg, is given
intravenously and repeated every 6 hours for four doses.
Corticosteroids are not an emergency medication because
their e ect appears only a er 1 to 3 hours. ey are given to
prevent the recurrence of symptoms 3 to 8 hours a er the
initial event. e patient should be hospitalized overnight
for observation.
MANIFESTATIONS OF
HYPERSENSITIVITY REACTIONS
Systemic reactions caused by sclerotherapy treatment
occur very rarely. Anaphylaxis is a systemic hypersensitivity response caused by exposure or, more commonly, reexposure to a sensitizing substance. Anaphylaxis is usually an
IgE-mediated, mast cell–activated reaction that occurs most
o en within minutes of antigen exposure. Other classes of
immunoglobulin such as IgG also may produce anaphylaxis.
Since the risk of anaphylaxis increases with repeated exposures to the antigen, one should always be prepared for this
reaction in every patient.
e principal manifestations of anaphylaxis occur in
areas where mast cell concentrations are highest: skin,
lungs, and gastrointestinal (GI) tract. Histamine release is
responsible for the clinical manifestations of this reaction.
Although urticaria and abdominal pain are common, the
SODIUM MORRHUATE
Although touted by the manufacturer as “the natural sclerosing agent,” sodium morrhuate causes a variety of allergic
reactions, ranging from mild erythema with pruritus to
generalized urticaria to GI disturbances with abdominal
pain and diarrhea to anaphylaxis. It has been estimated
that “unfavorable reactions” from the treatment of varicose leg veins occur in 3% of patients.
high number of allergic reactions with this product may be
related to the inability to remove all the sh proteins present in sodium morrhuate. In fact, 20.8% of the fatty acid
composition of the solution is unknown.
Many cases of anaphylaxis have occurred within a few
minutes a er injection or more commonly when therapy is
reinstituted a er a few weeks. Most of these cases occurred
before 1950. Rarely, anaphylaxis has resulted in fatalities, many of which have not been reported in the medical
120 • PRIMARY SUPERFICIAL VENOUS INSUFFICIENCY
40
e reason for the
literature. Bronchospasm developed in one patient being
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treated with the twel h injection under anesthesia. is
responded readily to antihistamine and epinephrine. e
patient was subsequently treated with STS without an
41
adverse reaction.
Prolonged dysrhythmia requiring placement of a perma-
42
nent pacemaker has been reported in two cases.
is complication has been attributed to a direct cardiotoxic e ect of
sodium morrhuate.
ETHANOLAMINEOLEATE
Ethanolamine oleate (Ethamolin) is a synthetic mixture of
ethanolamine and oleic acid with an empirical formula of
H 41 NO 3 . e minimal lethal IV dose in rabbits is 130
C
20
mg/kg. e oleic acid component is responsible for the
in ammatory action. Oleic acid also may activate coagulation in vitro by release of tissue factor and Hageman factor. Ethanolamine oleate is thought to have a lesser risk of
causing allergic reactions compared with sodium morrhuate
or STS. However, pulmonary toxicity and allergic reactions
have been associated with this sclerosingagent.
e product manufacturer has reported anaphylactic
shock a er injection in three cases (product information
[1989] from Glaxo Pharmaceuticals, Research Triangle
Park, NC). Another case of a nearly fatal anaphylactic
reaction during the fourth treatment of varicose leg veins
43
with 1 ml of solution also has been reported.
In one
additional case a fatal reaction occurred in a man with a
known allergic disposition (product information [1989]
from Glaxo Pharmaceuticals, Research Triangle Park, NC).
Another episode of a fatal anaphylactic reaction occurred
in a woman having her third series of injections. is represented one reaction in 200 patients from that author’s
practice. Generalized urticaria occurred in approximately
one in 400 patients; this symptom responded rapidly to an
44
antihistamine.
SODIUM TETRADECYL SULFATE
A synthetic detergent developed in the 1940s, STS has
been used throughout the world as a sclerosing solution.
A comprehensive review of the medical literature (in
multiple specialties and languages) until 1987 disclosed a
total of forty-seven cases of nonfatal allergic reactions in
a review of 14,404 treated patients; this included six case
45
reports.
A separate review of treatment in 187 patients
with 2,249 injections disclosed no evidence of allergic or
46
systemic reactions.
An additional report of 5,341 injec-
tions given to an unknown number of patients found “no
47
unfavorable reaction.”
Fegan 48 has reviewed his experience
with STS in 16,000 patients. He reported een cases of
“serum sickness, with hot, stinging pain in the skin, and an
erythematous rash developing 30 to 90 minutes a er injection.” ese patients subsequently underwent additional
uneventful treatment with STS a er premedication with
antihistamines. In ten additional patients, “mild anaphylaxis” developed that required treatment with an injection
of epinephrine. If one were to combine only those reviews
of over 1,000 patients, the incidence of nonfatal allergic
reactions would be approximately0.3%.
e product manufacturer notes two fatalities associated with the use of STS, both from the sclerotherapy procedure itself and not speci cally related to STS. One fatality
occurred in a patient who was receiving an antiovulatory
agent. Another death (fatal pulmonary embolism) was
reported in a 36-year-old woman who was not taking oral
contraceptives. Wyeth-Ayerst also was required to include
in its product insert the deaths of two additional patients
who were suspected of dying of anaphylactic shock a er
sclerotherapy treatment with STS (Mark Coyne, R.Ph.,
personal communication, Wyeth-Ayerst Pharmaceuticals,
August 19, 1998). e company did not have details of the
two cases except that one patient had a medical history of
asthma. Four deaths attributed to anaphylactoid reactions
were reported to the Committee on Safety of Medicines
for the United Kingdom between 1963 and 1988, with
twenty-two nonfatal allergic reactions such as urticaria
49
noted over the same period.
A fatality has been reported a er a test dose of 0.5 ml of
50
STS 0.5% was given to a 64-year-old woman.
An autopsy
performed by the Hennipin County, Minnesota, coroner’s
o ce revealed no obvious cause of death. Subsequently,
mast cell tryptase studies were performed on blood collected approximately 1 hour a er the reaction while the
patient was receiving life support. Anormal tryptase level
is less than 5 ng/ml; in experimental anaphylactic reactions
induced in the laboratory, levels up to 80 ng/ml have been
observed. In this patient the levels were extremely high at
6,000 ng/ml, suggesting that an anaphylactoid reaction had
caused her death. Unfortunately, tryptase levels are experimental at this time, and it is unclear how such a high level
could be obtained. erefore it is also unclear whether fatal
anaphylaxis is a signi cant possibility withSTS.
Since all reported cases of allergic reactions are of the
IgE-mediated immediate hypersensitivity type, it is recommended that patients remain in or near the o ce for 30
minutes a er sclerotherapy when STS is used. However,
allergic reactions also may develop hours or days a er the
procedure. erefore patients should be warned about
the possibility of allergic reactions and how to obtain care
should a reaction occur. In a review of 2,300 patients treated
over 16years, four cases of allergic reactions were reported
51
(0.17% incidence).
Reactions in this study were described
as periorbital swelling in one patient and urticaria in three.
All reactions were easily treated with oral antihistamines.
It is of interest that French phlebologists have advocated
a 3-days-before and 3-days-a er treatment course with an
antihistamine. P.Flurie noted no episodes of allergic reac-
51
tions in 500 patients treated in this manner.
COMPLICATIONS OF LIQUID SCLEROTHERAPY • 121
In a 2-year prospective study of 2,665 patients treated
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52
with STS by Paul ibault,
there were four cases of anaphylactoid reactions (0.15%). ese occurred 10 to 30
minutes a er injection of 3% solution, with patients having
facial ushing, urticaria, dizziness, tachycardia, shortness
of breath, and nally GI symptoms of nausea, vomiting,
and abdominal pain. All four patients responded well to a
subcutaneous injection of 0.5 ml of 1:1000 epinephrine followed by promethazine HCL 25 to 50 mg intramuscularly.
Urticaria occurred in an additional two patients (0.07%).
Between August 1985 and January 1990, thirty-seven
reports of adverse reactions to STS, of which ve cases of
suspected anaphylaxis and two cases of asthma induced by
injection, were reported to the Drug Experience Monitoring
Program of the Food and Drug Administration (FDA). One
of the cases of anaphylaxis resulted in the death previously
discussed. A er a detailed review it is unclear to us whether
anaphylaxis indeed occurred in every reportedcase.
e reports of the Clinical Drug Safety Surveillance
Group of Wyeth-Ayerst Laboratories are compiled from voluntary reporting to the manufacturer or the FDA, or both.
e following are summaries of those reports:January to July
1991 disclosed one episode of erythema multiforme; one episode of acute respiratory distress syndrome (ARDS); one episode of fever, lymphadenopathy, and rash; and three episodes
of abdominal pain, nausea, vomiting, and diarrhea. e case
report of erythema multiforme was reported in a woman a er
her thirteenth sclerotherapy treatment. Pruritus developed the
morning a er the last injection, with a generalized eruption
beginning on the legs 4days later. is was followed by fever
the following day. Arapid tapering course of oral prednisone
was given, with complete resolution of the rash in 2weeks.
From September 1991 to November 1992 there were
ve reports of urticaria and one episode of ARDS. From
December 1992 to September 1993 there was only one
case of a maculopapular rash. In short, anaphylaxis has been
reported, with rare fatal reactions. From September 1993
through October 1994 there was one case of angioedema,
and generalized weakness was reported in one patient a er
receiving 10 ml of 3% STS. From November 1994 through
January 1996 there was one case of anaphylaxis. From January
1996 through December 1996, there was one case of allergic vasculitis. From November 1997 through October 1999
there were three cases of urticaria and four cases of nonspeci c hypersensitivity reactions. ese reactions voluntarily
reported to Wyeth-Ayerst occurred with approximately
500,000 2-ml ampoules of 1% and 3% being sold yearly
within the United States. us the incidence of adverse reactions is rare. (All information regarding adverse reactions
from Sotradecol was provided by Paul Minicozzi, Ph.D.,
Wyeth-Ayerst Laboratories, through yearly correspondence.)
A similar low experience with adverse reactions was
reported by STD Pharmaceuticals, the manufacturers of
STS (correspondence from Robert Gardiner, Hereford, UK,
March 15, 1995, and the Adverse Drug Reaction Information
Tracking Product Analysis from the Medicines Control
Agency of Great Britain). e adverse drug reaction reported
in the United Kingdom between 1963 and 1993 was one
nonspeci c allergic reaction, two cases of anaphylactic shock,
six cases of gastrointestinal disorder, two cases of bronchospasm, four patients with a nonspeci c cutaneous eruption,
and two patients with urticaria. is summary comprised
30years, during which time an estimated 7,200,000 ml of
STD 1% and 3% was sold within the United Kingdom.
e most common systemic reaction consists of transient
low-grade fever and chills lasting up to 24 hours a er treatment. is has also been noted in one of our patients. Of
note is that three patients with allergic systemic reactions to
monoethanolamine oleate had no evidence of allergy toSTS.
With any sclerosing solution, reactions can occur that
are not allergic in nature but represent the e ect of the sclerosing solution on the vascular system. One such reaction
is hemolysis, which occurs through lysis of red blood cells
that are present in the treated vein. Ahemolytic reaction
occurred in ve patients in a series of more than 900 patients
with injection of more than 8 ml of STS 3%. Like a similar
reaction that occurred with ethanolamine oleate, patients
were described as “feeling generally unwell and shivery, with
aching in the loins and passage of red-brown urine. All rapidly recovered with bed rest and were perfectly normal the
next day.” Injections of less than 8 ml per treatment session
did not result in this reaction.
Although the lethal dose in humans has never been
reported, the IV median lethal dose (LD
53
mg/kg.
In our practice, it is not uncommon for patients
) in mice is 90
50
to be treated with up to 30 ml of 0.5% STS. We have not
observed an adverse reaction from this dose ofSTS.
My experience in over 20years in an estimated 20,000
patients is that no patient has developed a serious allergic reaction from the use of STS. Because STS from various sources
may have a variable purity, it appears possible that allergic
reactions may occur from the impurities such as carbitol and
54
not STS itself.
is may explain the decreased reported
incidence of allergic reactions with the use of Fibrovein
(STD Pharmaceuticals) as compared with Sotradecol
(Wyeth-Ayerst) and/or Trombovar (Omega Laboratories,
Montreal, Canada). Recently, Sotradecol has been approved
for manufacture and sale by Bioniche Life Sciences (Inverin
Co. Galway, Ireland). Bioniche claims to have a di erent
method for producing STS that does not involve distillation and thus contains no carbitol. e bene ts of this “new”
Sotradecol are unknown at the time of this writing.
POLIDOCANOL
Allergic reactions to POL also are quite rare and have been
reported in only four patients in a review of the world’s literature up to 1987, with an estimated incidence of 0.01%.
45
However, since 1987 rare allergic reactions have been
reported, including a case of nonfatal anaphylactic shock
122 • PRIMARY SUPERFICIAL VENOUS INSUFFICIENCY
to 1 ml of POL 2% injected into a varicose vein during the
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fourth treatment session.
55
reported seven cases of minor general urticaria in
Guex
nearly 11,000 patients treated over 12years. ese patients
cleared completely in 1 to 2days with antihistamine and
topical corticosteroid therapy, with one patient requiring
systemic corticosteroids. Kreussler GmbH, the product
manufacturer in Germany, has documented thirty- ve cases
of suspected sensitivity from 1987 to 1993 (personal correspondence, January 1994). Of these reports, most were
either vasovagal events or unproved allergic reactions. Nine
patients were given repeat challenges with POL, with only
three demonstrating an allergic reaction (urticaria or erythematous dermatitis). One patient died of anaphylactic
shock 5 minutes a er injection with 1 ml despite maximal
intervention. In 1994, Kreussler reported two patients with
urticaria. In 1995, two additional patients were reported
with urticaria, two with bronchospasm, and one with
angioedema. In 1996, there were four reports of urticaria,
two of anaphylactoid reactions, one with angioedema, one
with pruritus, and one with contact allergy. erefore POL
is not free from allergy, and, as with all sclerosing solutions,
physicians must be prepared to evaluate and treat patients
who have an allergic reaction to the sclerosing solution.
A detailed account of three serious cases of anaphylaxis
56
was reported from the Netherlands.
ese patients were
anaphylactic within 15 minutes a er injection of POL. Two
of them received the drug for the rst time. One patient, a
70-year-old woman with a complicated medical history of
two heart operations, two cerebrovascular accidents, and
hyperthyroidism, was successfully resuscitated a er cardiac
arrest. She was receiving multiple medications, including
digoxin, carbimazole, captopril, furosemide, mebeverine, and
acenocoumarol. She was treated without complications four
previous times with POL. e second patient showed signs
of ARDS a er being treated with epinephrine and systemic
methylprednisolone for shock. e third patient developed
urticaria, dyspnea, paresthesia, headache, and chest pain
with electrocardiographic (ECG) ndings of cardiac ischemia. No further studies were performed on these patients.
e Australian Polidocanol Open Clinical Trial at
2years, with over 8,000 treated patients, reported nine local
urticarial reactions and three generalized reactions, with two
patients developing a rash, for a frequency of approximately
30
0.2%. ere were no cases of anaphylaxis.
A er an additional 8,804 patients were evaluated, an additional three
patients developed urticaria, again without any additional
57
signi cant adverse sequelae.
A 5-year experience in 500
patients treated with POL 3% reported ve cases of allergic
reaction (1% incidence); one patient had nonfatal anaphylactic shock, with the other patients experiencing urticaria.
58
Two of 689 sequential patients were reported who
developed an immediate-type hypersensitivity reaction
59
with systemic pruritus and urticaria.
is represented an
incidence of 0.3% in their patient population and 0.91%
for the “true” population. ese two reactions occurred
without prior exposure to POL as a sclerosing agent. Since
POL is used as an emulsifying agent in preprocessed foods,
patients may have been exposed previously through ingestion. Both patients responded easily to either a single dose
of oral diphenhydramine, 50 mg, or 0.3 ml of subcutaneous
epinephrine plus 50 mg intramuscular diphenhydramine.
One speci c case report describes a 30-year-old woman
who underwent four separate sclerotherapy sessions with
POL. On the fourth session, 3 ml of POL 1.5% and 12 ml
of POL 0.5% were administered. e patient complained of
chest heaviness and constriction, which also appeared a er
two of her other sessions but was not brought to the attention of the medical sta . During the fourth episode she lost
consciousness and was found without a pulse or blood pressure with dilated pupils. Spontaneous respiration occurred
a er 2 to 3 minutes, she began to vomit and complained
of headache and earache. She recovered and was discharged
a er 10 hours well but returned the next day with dysosmia,
which lasted 6 weeks. Although a brain CT scan was nor-
60
mal the presumed cause was cerebral.
e median lethal dose (LD
) in rabbits at two hours
50
is 0.2 g/kg, which is three to six times greater than the LD
for procaine hydrochloride. e LD
in mice is 110 mg/kg.
50
e systemic toxicity level is similar to that of lidocaine and
61
procaine.
C H R O M A T E D G L Y C E R I N
CG 72% (Scleremo) is a sclerosing solution with a very
low incidence of side e ects (Scleremo product information, 1987). Hypersensitivity is a very rare complication.
Contact sensitivity to chromium occurs in approximately
63
5% of the population.
IV potassium dichromate leads to
complete desensitization in chromium-sensitized guinea
pigs. is e ect occurs because chromium needs to bind to
skin proteins to become an e ective antigen. is may be
related to the necessity for epidermal Langerhans’ cells to
produce an allergic response, whereas T-lymphocyte accessory cooperation is not optimal with IV injection and its
resulting endothelial necrosis. us it is more common for
a sclerotherapist to develop an allergic contact dermatitis
to CG than it is for a patient to have an allergic reaction to
IV use of CG. Indeed, Ouvry (personal communication,
1995)has developed an allergic contact dermatitis from
CG injected without the use of protective gloves.
64
Ramalet
has reported seven patients who developed an
allergic reaction to CG. One patient had a vasculitis, and
six patients had an eczematous reaction. All allergic patients
demonstrated a sensitivity to topically applied chrome.
Hematuria accompanied by urethral colic has been
reported to occur transiently a er injection of large doses of
CG. Ocular manifestations, including blurred vision and a
partial visual eld loss, have been reported by a single author,
65
with resolution in less than 2 hours.
Glycerin-induced (or
50
62
COMPLICATIONS OF LIQUID SCLEROTHERAPY • 123
any sclerotherapy-induced) hemolysis may not be a benign
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event. Hemoglobin can exert direct cytotoxic, in ammatory,
and pro-oxidant e ects that adversely a ect endothelial func-
66
Hemoglobin from destroyed red blood cells dimerizes
tion.
and is rapidly bound by the serum protein haptoglobin. e
haptoglobin-hemoglobin complex causes endocytosis and
67
degradation, which can lead to a variety of adverse e ects.
An additional case was reported of transient hypertension and visual disturbance a er the injection of 12 ml of
50% chromated glycerin into spider and “feeder” leg veins in
68
a fourth treatment session.
ese symptoms occurred 2½
hours a er treatment and lasted more than 3 hours without
treatment. is may have represented a retinal spasm or an
ophthalmic migraine.
Although transient hemoglobinuria is common in ath-
letes and without known long-term adverse e ects, hemo-
69
globulinemia can cause renal failure.
More commonly,
hemoglobulinemia can cause a dose-related gastrointestinal
dystonia and pain, including esophageal spasm and dysphagia. Refer to an excellent recent review that details more
70
clinical manifestations of hemoglobinemia.
Since we have been using glycerin alone without chromium but mixed 2:1 with 1% lidocaine with or without
1:100,000 epinephrine, we have yet to see an allergic reaction.
We have also yet to see hemoglobinuria or adverse e ects
with the use of up to 12 ml of this glycerin mixture except
for a minute or two of epinephrine-induced “rush” that can
occur in rare patients who have a sensitivity to epinephrine.
POLYIODIDEIODINE
Polyiodide iodine (Varigloban; Sclerodine 6)is a stabilized
water solution of iodide ions, sodium iodine, and benzyl
71,72
alcohol. Sigg etal.
reported on their experience with over
400,000 injections with Variglobin reported an incidence
of 0.13 allergic cutaneous reactions per 1,000. No systemic
allergic reactions were observed. Obvious contraindications
to the use of Variglobin are hyperthyroidism and allergies to
iodine and benzyl alcohol.
SODIUM SALICYLATE
Saliject (Omega Laboratories, Montreal) has not been
reported in a literature review to cause allergic reactions.
Dr.Beverly Kemsley has reported one of 6,000 patients who
developed an anaphylactic reaction a er the use of Saliject.
irty patients developed localized erythema and urticaria
that responded to the oral antihistamine terfenadine 120
mg (personal communication,1996).
HYPERTONICSALINE
Alone, hypertonic saline (HS) solution shows no evidence
of allergenicity or toxicity. Complications that may arise
from its speci c use include hypertension that may be exacerbated in predisposed patients when an excessive sodium
load is given, sudden hypernatremia, central nervous system
disorders, extensive hemolysis, and cortical necrosis of the
kidneys (Mary Helenek, written correspondence, American
Regent Laboratories, Inc., May 1990). ese complications
among others have led one manufacturer (American Regent
Laboratories) to add to its label the warning “For IV or SC
use a er dilution” in bold redink.
As discussed previously, hematuria can occur with any
sclerosing agent. Sometimes blood appears in the urine a er
one or two acts of micturition and occasionally at other times
throughout the day. Usually there are no other ill e ects, and the
hematuria resolves spontaneously. Hematuria probably occurs
because of hemolysis of red blood cells during sclerotherapy.
In summary, sclerotherapy with a wide variety of sclerosing solutions is a safe and e ective procedure for the treatment of varicose and telangiectatic leg veins. Space does not
permit a more complete discussion of other possible adverse
e ects. Table14.1 summarizes the di erent adverse e ects
Table14.1 SUMMARY OF COMPLICATIONS OF SCLEROSINGAGENTS
AGENTS
SOLUTION PIGMENTATION ALLERGIC REACTION NECROSIS PAIN
Sodium morrhuate ++ ++ +++* +++
Sodium tetradecyl sulfate ++ + ++* +
Ethanolamine oleate + ++ ++* ++
Polidocanol + + +* 0
Hypertonic saline + 0 +++* +++
Sclerodex (+0% saline 5% dextrose) + 0 + ++
Chromated glycerin 0 + 0 ++
Glycerin 0 0 0 +
Polyiodinated iodine ++ + +++* +++
+, Minimal; ++, moderate; +++, signi cant.
*Concentration dependent.
124 • PRIMARY SUPERFICIAL VENOUS INSUFFICIENCY
from a variety of available sclerosing solutions. e inter-
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ested reader is referred elsewhere for a complete review of
13
adverse e ects from sclerotherapy treatment.
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126 • PRIMARY SUPERFICIAL VENOUS INSUFFICIENCY
15.
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LASER TREATMENT OF TELANGIECTASIAS
AND RETICULARVEINS
Neil Sadick and Lian Sorhaindo
INTRODUCTION
e incidence of prominent venulectasias and/or telangiectasias on the lower extremities occurs in up to 41% of
women and 15% of men within the United States.
rent literature subdivides vascular pathology into super cial
“spider” veins or telangiectasias, deep reticular veins, and
protuberant varicosities. Etiologies include heredity, hormonal dysregulation, prolonged periods of standing obesity, pregnancy, and aging. Although patients may present
with symptoms of fatigue, aching, swelling, throbbing, and
occasionally pain, patients seek treatment primarily for aesthetic concerns. With this rise in consumer demand since
early 2000s, there has been a subsequent increase in the utilization of lasers and intense pulsed light (IPL) sources for
the treatment of lower extremityveins.
IDENTIFYING THE PROBLEM
e vasculature of the lower extremity consists of a complex,
intertwined network of super cial and deep venous plexuses.
e super cial veins lie directly underneath the skin surface.
e deep veins, in contrast, traverse the muscle of the leg. e
individual ow patterns of these two networks intertwine
such that super cial spider veins may be the direct result of
increased hydrostatic pressure in the deep reticularveins.
e varying sizes, depths, ow patterns, and vessel thickness of leg veins make the treatment of leg veins challenging. Presently, there is no gold standard of treatment for all
leg veins, and lasers o en are used as adjunctive therapy in
patients undergoing phlebectomy, sclerotherapy, or vein
stripping. Laser and light source technology has become
particularly useful in the treatment of small spider veins
or telangiectasias, and also in the setting of vessels that are
scleroresistant that may arise from prior surgical treatment
as a result of telangiectatic matting or angiogenic ushing
2
(see Box 15.1).
It can also be used in the treatment of large
spider and reticular veins; however, sclerotherapy remains
the gold standard for the treatment of these vessels. is
1
e cur-
chapter deals speci cally with the laser treatment of telangiectasias and reticular veins; other modalities of treatment
including sclerotherapy, ambulatory phlebectomy, and
endovenous ablation are discussed elsewhere in thebook.
PATIENT SELECTION:WHEN
AND HOW TO CHOOSE LASER/
IPL VERSUS SCLEROTHERAPY
Laser therapy is most e cacious for treating telangiectasias/venulectasias or reticular veins less than 3mm in diam-
3,4
As mentioned earlier, lasers have become indicated
eter.
in patients with areas of neovascularization with telangiectatic matting or angiogenic ushing, with scleroresistant/
noncannulable vessels, and who are needle-phobic. Relative
contraindications to the use of laser surgery include tanned
skin, pregnancy, the use of iron supplements or anticoagulation, history of photosensitivity disorder, or hypertrophic
and keloidal scarring (see Table15.1).
FUNDAMENTALS OF LASER
TREATMENT OF LEGVEINS
THEORY OF SELECTIVE
THERMOLYSIS:MAJOR PRINCIPLES
AND DETERMINANTS
e advent of laser technology for treatment of leg veins
began with the concept of selective photothermolysis devel-
5
oped in the late 1980s.
e theory of selective photothermolysis states that selective damage to a tissue structure is
achieved by means of a wavelength of light preferentially
absorbed by a chromophore in light-absorbing molecules
and laser exposure time less than or equal to the object’s
thermal relaxation time (i.e., the time required for the
object to lose 50% of its thermal energy). e thermal relaxation times of leg veins vary depending on vessel diameter
6
(see Table15.2).
127
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