卵巢过度刺激综合征(OHSS)的神经血管并发症:从病理生理学到最近的治疗选择。

Rocco S Calabro, Giuseppe Gervasi, Antonino Leo, Rosaria De Luca, Tina Balletta, Carmela Casella, Onofrio Triolo, Placido Bramanti
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引用次数: 8

摘要

卵巢过度刺激综合征(OHSS)是一种严重的医源性促排卵并发症,对患者的健康有非常严重的影响,因为它通常与高发病率和死亡率相关。事实上,重度OHSS患者表现为液体失衡体征(如体重迅速增加、腹水紧张、呼吸困难和进行性少尿),这与毛细血管通透性增加后液体从血管内腔转移到第三腔室有关。通过这种方式,心血管系统的表现包括血管内容积减少、血压降低、中心静脉灌注减少、代偿性心率和心输出量增加,并伴有动脉血管舒张。尽管静脉血栓栓塞现象可能是OHSS晚期的并发症,但动脉缺血累及脑循环是一种罕见的问题,但最近有报道。OHSS血栓栓塞的发病机制尚不完全清楚,尽管血液浓缩和血液高粘度似乎在静脉和动脉系统的血栓形成改变中起作用。有趣的是,心脏异常与遗传或获得性高凝状态的结合似乎增加了这些受试者发生脑梗死的风险,正如我们小组最近所显示的那样。本综述旨在探讨OHSS相关的神经血管并发症的病理机制和处理,包括新的治疗方案。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neurovascular complications of ovarian hyperstimulation syndrome (OHSS): from pathophysiology to recent treatment options.

Ovarian hyperstimulation syndrome (OHSS) is a severe iatrogenic complication of ovulation induction, which has a very serious impact on the patient's health, as it is often associated with a high morbidity and mortality risk. Indeed, patients classified as having severe OHSS presented with liquid imbalance signs (such as rapid weight gain, tense ascites, respiratory difficulty and progressive oliguria), which are related to the fluid shift from the intravascular space to third space compartments subsequent to an increased capillary permeability. In this way, cardiovascular system findings include decreased intravascular volume, decreased blood pressure, decreased central venous perfusion, and compensatory increased heart rate and cardiac output with arterial vasodilation might be found concomitantly. Notwithstanding that venous thromboembolic phenomena are a possible complication in advanced phases of OHSS, arterial ischemia involving the cerebral circulation is a rare but recently reported problem. The pathogenesis of thromboembolism in OHSS is not fully understood, even though hemoconcentration and blood hyperviscosity seem to play a role in developing thrombotic changes into both venous and arterial system. Interestingly, the presence of cardiac abnormalities in combination with inherited or acquired hypercoagulable state seems to increase the risk of cerebral infarct in these subjects, as recently shown by our group. This review is aimed at investigating the pathomechanism and the management of neurovascular complications related to OHSS, including new treatment options.

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