Tierexperimentelle Untersuchungen zur Embolia cutis medicamentosa

Abstract

Embolia cutis medicamentosa (ECM) is a rare complication after intramuscular injection of certain drugs, resulting in local necrosis of skin and muscle at the injection site. The pathogenesis is still not clear. Drugs and their effective substances, from which an ECM recently was described (depot penicilline, antirheumatic drug combinations), were injected intraarterially, periarterially, and intramuscularly into the hind legs of rats. The legs were examined macroscopically and histologically. Complete skin and muscle necrosis of the hind leg was only found after intraarterial injection of the incriminated drugs. The most important single effective substance was phenylbutazone. From the experiments it is concluded that the intraarterial injection mode is the most likely pathomechanism of lokal skin and muscle necrosis in the ECM arising from the incriminated drugs.

Necrotising cutaneous lesions as a side effect of glatiramer acetate

“…Nicolau's syndrome, a rare complication after intramuscular injection of certain drugs also named embolia cutis medicamentosa, has been recently reported after GA injection [3]. The suspected pathogenesis is the accidental intra-arterial injection of the drug, which leads to either acute vascular spasm or intravascular thrombosis, causing muscular and cutaneous necrosis [1]. The most prominent symptom is the acute intense pain following the drug injection, after a few minutes cyanotic patches and livedoid pattern develop.…”

Embolia cutis medicamentosa after polidocanol injection of neovessels in Achilles tendinosis

“…Some authors have suggested that intra-arterial injection is the cause [11] but this does not seem to be the consensus view. For the past decade polidocanol injections have been used in the management of the pain associated with chronic Achilles tendinosis [12,13] .…”

Central Forehead Ischemic Skin Injury following Glabellar Botulinum: A Paradigm Microshift?

“…Correspondingly, several studies have since shown that Nicolau syndrome is likely to arise with pharmaceutical suspensions (capable of generating embolic/thromboembolic showers when accidentally injected intraarterially) or with solutions of an arterionoxic agent, such as thiopentone, capable of inducing intense arteriospasm and/or intravascular coagulation. 4,5…”

“…Correspondingly, several studies have since shown that Nicolau syndrome is likely to arise with pharmaceutical suspensions (capable of generating embolic/thromboembolic showers when accidentally injected intraarterially) or with solutions of an arterionoxic agent, such as thiopentone, capable of inducing intense arteriospasm and/or intravascular coagulation. 4,5 Type A botulinum toxin preparations, which have been available for intramuscular/dermal injection in the United States for more than 30 years, consist of lyophilized, albumin-stabilized powders that produce clear homogeneous solutions upon saline reconstitution. Numerous toxicity studies in primates have failed to reveal any potential for intravascular thromboembolic reactions, and its routine intramuscular use in humans regularly places it within well-vascularized tissues with an incredible record of safety.…”