ARTICLE
Sclerotherapy of varicose veins can cause many side effects. Initial
side effects are: anaphylactic shock, ischemia after intrarterial injection,
air embolia, transitional impairment of sight and urticaria. Later side
effects are: pigmentation, matting, necrosis, varicophlebitis and artificial
periphlebitis after paravenous injection [1].
Embolia cutis medicamentosa, as we will describe in the following case
study, is another rare side effect occurring after the injection of sclerosing
agents for intracutaneous varicose veins, which to date has not been reported
in the literature.
Case report
A 71-year-old woman was treated with sclerotherapy for intracutaneous
varicose veins at the left medial ankle. Sclerotherapy was performed with
a 1% polidocanol solution.
During the injection, the patient noticed a dysesthesia at the heel
and the sole of the left foot. There was no pain reported.
A few hours later an aching pain occurred at the sole of the left foot.
The same evening, the patient noticed a livid color change at the plantar
and at the medial side of the foot.
Four days later she visited her physician again with these skin lesions.
Seven days after sclerotherapy she attended our out-patient clinic with
livedo-like livid skin lesions of the medial and lateral foot, reminiscent
of embolia cutis medicamentosa. These lesions were very painful (Figs.
1A and 1B).
The color-Doppler examination showed a normal
superficial and deep venous system. The bidirectional Doppler-sonographical
examination showed a normal arterial system of the legs without signs
of arterial occlusions.
Sensibility, motricity and coordination of the legs were normal.
We treated the patient with alprostadil intravenously (3 x 20 µg
daily) for 4 weeks. The therapy was continued with pentoxifyllin orally
(3 x 400 mg daily) for a further 3 months.
Initially methylprednisolon (16 mg daily) was given orally with a dosage
reduction over two weeks and an anticoagulant (3 x 8,000 IU heparin s.c.
daily) for four weeks. Locally, we applied unguentum leniens and cotton-wool
pads as a protection against cold.
During this treatment the skin slowly normalized and the lesions healed
completely without necrosis. At a control check one year later only a
slight hyperpigmentation remained (Figs.
2A and 2B)
Discussion
Embolia cutis medicamentosa was first described by Juliusberg, Freudenthal
and Nicolau between 1924 and 1928 [2-4]. The first reports were made after
bismuth injections for lues-therapy [2].
After an intramuscular injection, in most cases, a livedo-like, hemorrhagic
skin lesion occurs with a possible skin necrosis that seems to heal very
slowly.
Embolia cutis medicamentosa has been reported after the intramuscular
injection of sulfonamides, depot penicillin, streptomycin, tetracyclins,
expectorants, antirheumatic agents and bismuth. It has also been reported
after the subcutaneous injection of interferon-alpha [5, 6].
The pathogenesis has not been completely clarified.
Ischemia, livedo racemosa and a possible necrosis occur after wrongly
injected intra-arterial drugs, followed by an embolic bloodflow disorder.
A periarterial and/or an intramural injection can also cause an arterial
spasm and therefore the same clincal picture.
In embolia cutis medicamentosa a strong pain sensation usually occurs
immediately after the injection. This is probably caused by reactive spasms
of the vessels [5].
In sclerotherapy of intracutaneous veins, the
sclerosing agent is injected intracutaneously and intravenously. In this
case embolia cutis medicamentosa could also be explained by an overflow
of the sclerosing agent into small skin arteries if there are arterio-venous
shunts at this level [7].
To our knowledge, this is the first reported case of embolia cutis medicamentosa
after sclerotherapy of intracutaneous veins.
Within a few hours of injection, a hard, livid erythemateous lesion
develops at the site of the injection. Sometimes a hard livid infiltration
with a livedo racemosa-like aspect also occurs. These lesions cause local
and radiating pain. The healing is sometimes accompanied by hyperpigmentation,
as in our case.
In more severe cases, after 24-72 hrs a first central demarcation and
necrosis occurs.
Also bacterial superinfection and transitional paralysis are possible.
Over the next weeks and months, secondary wound-healing of deep ulcers
with remaining atrophic scars takes place [5].
At the beginning of the skin changes, therapy with vessel-dilating drugs
(alprostadil, pentoxifyllin, nicotic acid) can be used to reduce the development
of hemorrhagic necroses [5]. Systemically non steroidal antiphlogistics
and steroids can be used to reduce inflammatory reactions.
In the case of a secondary wound-infection, systemic antibiotics have
to be used.
Locally, steroids can be applied. Necrosis by embolia cutis medicamentosa
must be treated locally with the appropriate topical therapy. Very large
necrotic areas should be treated surgically [3, 5].
In our case the combined therapy with alpostadil, corticosteroides and
heparin in a prophylactic dosage led to a complete remission of the skin
changes without necrosis.
REFERENCES
1. Staubesand J, Schöpf E. Neuere Aspekte der Sklerosierungstherapie.
Springer-Verlag, Berlin Heidelberg New York 1990: 70-81.
2. Freudenthal W. Lokales embolisches Bimogenol-Exanthem. Arch Dermatol
Syph 1924; 147: 155-60.
3. Köhler LD, Worret WI, Hofmann H. Atypische zosteriforme segmentale
Embolia cutis medicamentosa. Hautarzt 1997; 48: 492-5.
4. Nicolau S. Dermite livédoïde et gangréneuse de
la consécutive aux injections intramusculaires dans la syphilis.
A propos d'un cas d'embolie artérielle bismutique. Ann Mal Vener
1925; 20: 321-9.
5. Braun Falco O, Plewig G, Wolff HH. Dermatologie und Venerologie.
Springer-Verlag, Berlin Heidelberg New York 1995: 366-7.
6. Rasokat H, Benedick C, Wemmer U, Steigleder GK. Aseptische Hautnekrose
nach subkutaner Injektion von Interferon-alpha. Dtsch Med Wschr
1989; 114: 458-60.
7. Biegeleisen K. Primary lower extremity teleangiectasias relationship
of size and color. Angiology 1987; 38: 760-8.
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