Embolia cutis medicamentosa of the foot after sclerotherapy

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.