抗利尿激素引起的暴发性紫癜的罕见表现。

Vanessa Awad, Preeth Nair, Sasmit Roy, Anish Yalamanchili, Sreedhar Adapa, Nirupama Vemuri
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摘要

暴发性紫癜(PF)是一种罕见的快速发展的皮肤缺血表现,特别是在危重病人。它被认为是为数不多的皮肤病紧急情况之一,死亡率很高,患者经常死于这种疾病。它可以表现为三种形式:新生儿,特发性和更常见的感染性,它可以继发于大多数细菌和罕见的病毒病因。据报道,它还与弥散性血管内凝血(DIC)、肝素诱导的血小板减少症(HIT)和急性肝衰竭(AHF)高度相关。遗传或获得性蛋白C缺乏和凝血级联(主要是蛋白C-血栓调节蛋白)的失调与发病机制有关。我们报告一位55岁男性因糖尿病酮症酸中毒(DKA)和感染性休克而住进重症监护病房。在启动DKA和广谱抗生素治疗方案的同时,他最初开始使用去甲肾上腺素治疗感染性休克。由于持续性难治性脓毒性休克,他随后开始使用苯肾上腺素和加压素来维持足够的血流灌注。次日,患者双膝、下肢和阴囊均有明显的黑色非漂白性变色,肢端除外。这种皮肤表现在整个住院过程中持续存在,尽管在停用抗利尿激素同时继续使用其他降压药后有所改善。抗利尿激素与少数皮肤坏死有关;然而,PF很少被记录,从来没有在1天内像我们这样。在排除DIC、HIT、血栓性血小板减少性紫癜和AHF的诊断后,本病例显示了一种可能由抗利尿激素引起的PF的独特发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

An Uncommon Presentation of Vasopressin-Induced Purpura Fulminans.

An Uncommon Presentation of Vasopressin-Induced Purpura Fulminans.

An Uncommon Presentation of Vasopressin-Induced Purpura Fulminans.

An Uncommon Presentation of Vasopressin-Induced Purpura Fulminans.

Purpura fulminans (PF) is a rarely encountered rapidly evolving dermatological manifestation of ischemia, particularly in critically ill patients. Considered one of the very few dermatological emergencies, it has high mortality rate where patients often succumb to the illness. It can manifest in three forms: neonatal, idiopathic, and the more commonly infectious variety, which can be secondary to mostly bacterial and rarely viral etiology. It is also reported to be highly associated with disseminated intravascular coagulation (DIC), heparin-induced thrombocytopenia (HIT), and acute hepatic failure (AHF). Hereditary or acquired deficiency of protein C and dysregulation of the coagulation cascade, mainly protein C-thrombomodulin, has been implicated in the pathogenesis. We present a 55-year-old male admitted to the intensive care unit for diabetic ketoacidosis (DKA) and septic shock. Along with initiating management protocol for DKA and broad-spectrum antibiotics, he was initially started on norepinephrine for septic shock. Because of persistent refractory septic shock, he was subsequently initiated on phenylephrine and vasopressin to maintain adequate perfusion. The following day, he was found to have sharply demarcated blackish non-blanching discoloration on bilateral knees, lower limbs, and scrotum, sparing the acral regions. This cutaneous manifestation persisted throughout his hospital course, although it improved after discontinuation of vasopressin while continuing with other pressors. Vasopressin has been implicated in a few instances of skin necrosis; however, PF has rarely been documented and never within 1 day like ours. This case demonstrates a unique development of PF likely from vasopressin after ruling out the diagnoses of DIC, HIT, thrombotic thrombocytopenic purpura, and AHF.

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