Department of Surgery, University of Virginia Health System, Charlottesville, VA, USA.
Crit Care Med. 2011 Apr;39(4):833-8. doi: 10.1097/CCM.0b013e318206d0eb.
Heparin-induced thrombocytopenia is a common adverse effect of treatment with heparin resulting in paradoxical thromboses. An immunoglobulin G class "heparin-induced thrombocytopenia antibody" attaches to a heparin-platelet factor 4 protein complex. The antibody then binds to the FcγIIa receptor on the surface of a platelet, resulting in activation, consumption, and thrombocytopenia in the clinical syndrome of heparin-induced thrombocytopenia. In contradistinction to other drug-induced thrombocytopenias that lead to a risk of hemorrhage, the state of thrombocytopenia in heparin-induced thrombocytopenia leads to an acquired hypercoagulability syndrome. Bilateral adrenal hemorrhage associated with heparin-induced thrombocytopenia has become an increasingly documented association. The adrenal gland has a vascular construction that lends itself to venous thrombus in the setting of heparin-induced thrombocytopenia and subsequent arterial hemorrhage. A literature search revealed 17 reported cases of bilateral adrenal hemorrhage in the setting of heparin-induced thrombocytopenia uniformly presenting with complete hemodynamic collapse.
An Ovid MEDLINE search of the English-language medical literature was conducted, identifying articles describing cases of bilateral adrenal hemorrhage in the setting of heparin-induced thrombocytopenia.
All cases with this association were included in the review.
A total of 14 articles were identified, describing 17 individual case reports of bilateral adrenal hemorrhage associated with heparin-induced thrombocytopenia. All cases confirmed known characteristics of heparin-induced thrombocytopenia and uniformly revealed hypotension due to adrenal insufficiency. There were five deaths, resulting in an overall mortality rate of 27.8%, and 100% mortality in the three cases where adrenal insufficiency went unrecognized.
The secondary complication of adrenal vein thrombosis leading to bilateral adrenal hemorrhage remains insufficiently recognized and undertreated. The nonspecific presentation of adrenal hemorrhage and insufficiency as a complication of heparin-induced thrombocytopenia, coupled with the catastrophic clinical course of untreated adrenal collapse, requires a high index of suspicion to achieve rapid diagnosis and provide life-saving therapy.
肝素诱导的血小板减少症是肝素治疗的常见不良反应，可导致矛盾性血栓形成。一种免疫球蛋白 G 类“肝素诱导的血小板减少症抗体”与肝素-血小板因子 4 蛋白复合物结合。然后，该抗体结合到血小板表面的 FcγIIa 受体上，导致肝素诱导的血小板减少症的临床综合征中的血小板激活、消耗和血小板减少症。与导致出血风险的其他药物诱导的血小板减少症不同，肝素诱导的血小板减少症中的血小板减少症导致获得性高凝状态综合征。与肝素诱导的血小板减少症相关的双侧肾上腺出血已成为越来越多的文献记载的关联。肾上腺具有血管结构，在肝素诱导的血小板减少症和随后的动脉出血的情况下容易发生静脉血栓形成。文献检索显示，在肝素诱导的血小板减少症背景下有 17 例双侧肾上腺出血的报道病例，均表现为完全血流动力学崩溃。
通过 Ovid MEDLINE 对英文医学文献进行了搜索，确定了描述肝素诱导的血小板减少症背景下双侧肾上腺出血病例的文章。
本综述纳入了所有具有这种关联的病例。
共确定了 14 篇文章，描述了与肝素诱导的血小板减少症相关的 17 例双侧肾上腺出血的个别病例报告。所有病例均证实了肝素诱导的血小板减少症的已知特征，并且均因肾上腺功能不全而出现低血压。有 5 例死亡，总死亡率为 27.8%，在 3 例未识别出肾上腺功能不全的病例中死亡率为 100%。
继发于肾上腺静脉血栓形成的双侧肾上腺出血的并发症仍然认识不足且治疗不足。肝素诱导的血小板减少症的并发症如肾上腺出血和功能不全的表现不具有特异性，加上未经治疗的肾上腺衰竭的灾难性临床病程，需要高度怀疑以实现快速诊断并提供救生治疗。
