Brachtel R, Meinertz T
Arch Dermatol Res (1975). 1977 May 27;258(3):281-8. doi: 10.1007/BF00561131.
The pathogenesis of local skin necroses after intramuscular injection of various drugs such as phenylbutazone (Embolia cutis medicamentosa, Nicolau's syndrome) is not clear. In an attempt to simulate this clinical feature experiments were performed on the rabbit ear lobe. A 20% phenylbutazone solution was injected paraarterial, intraarterial and paraarterial after perforation of the vessel. The drug produced a violent inflammation with all kinds of application. The local inflammation induced by paraarterial injection resulted in a fine scarring. Both other kinds of application produced necroses or even perforations. The histological examinations in these cases revealed massive destructions of the inner arterial wall. In control-experiments necroses or perforations were nerve observed. From these data the following conclusions on the etiology of Nicolau's syndrome can be drawn: Phenylbutazone injected into the vascular or perivascular tissue causes an obligatory inflammation. After lesion of an artery complete destruction of the vessel followed by necrosis of the skin may occur. It seems obvious that this secondary effect can not completely be avoided.
肌肉注射诸如保泰松等各种药物后发生局部皮肤坏死（药物性皮肤栓塞，尼科劳综合征）的发病机制尚不清楚。为了模拟这一临床特征，在兔耳叶上进行了实验。将20%的保泰松溶液经动脉旁、动脉内注射以及在血管穿孔后经动脉旁注射。无论采用哪种注射方式，该药物都会引发剧烈炎症。经动脉旁注射引起的局部炎症导致形成细小瘢痕。其他两种注射方式均导致坏死甚至穿孔。这些病例的组织学检查显示动脉内壁有大量破坏。在对照实验中未观察到坏死或穿孔现象。从这些数据可以得出关于尼科劳综合征病因的以下结论：注入血管或血管周围组织的保泰松会引发必然的炎症。动脉受损后，可能会发生血管的完全破坏，继而导致皮肤坏死。显然，这种继发效应无法完全避免。
