术中虹膜松弛综合征的病理生理学：一场未解决的争论。
Pathophysiology of intraoperative floppy iris syndrome: An unsettled debate.
作者信息
Shen Yingchun, Frauches Rachel, Zhao Jingyu, Lo Chien-Hui, Ning Ke, Chen Siyu, Liu Zhiquan, Zhang Fan, Sun Yang
机构信息
Department of Ophthalmology, Stanford University School of Medicine, Palo Alto, CA 94306, USA.
Departments of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
出版信息
Surv Ophthalmol. 2025 Jun 4. doi: 10.1016/j.survophthal.2025.06.002.
Intraoperative floppy iris syndrome (IFIS)--characterized by iris blowing, prolapse, and progressive miosis during phacoemulsification surgery--poses significant challenges for eye surgeons. Despite being described almost 2 decades ago, its pathophysiology remains unclear. Initially, IFIS was thought to be a result of sympathetic signal blockage in the iris dilator muscle, since α-blockers such as tamsulosin were found to be a strong predisposing factor; however, many IFIS cases occur even in patients who discontinued α-blockers prior to cataract surgery. Several potential mechanisms through which α-blockers induces chronic changes in the iris - iris dilator atrophy, drug-melanin interaction, and loss of vascular tone - have been proposed as possible mechanisms. We address the prevailing theories on α-receptor-dependent mechanisms for IFIS and the current prophylactic measures undertaken to prevent IFIS-associated intraocular complications.
术中虹膜松弛综合征（IFIS）——其特征为在白内障超声乳化手术过程中出现虹膜膨隆、脱垂及渐进性瞳孔缩小——给眼科医生带来了重大挑战。尽管早在近20年前就已被描述，但它的病理生理学仍不清楚。最初，IFIS被认为是虹膜开大肌交感神经信号阻断的结果，因为发现坦索罗辛等α受体阻滞剂是一个很强的诱发因素；然而，许多IFIS病例甚至发生在白内障手术前已停用α受体阻滞剂的患者身上。已经提出了几种α受体阻滞剂诱导虹膜慢性变化的潜在机制——虹膜开大肌萎缩、药物 - 黑色素相互作用以及血管张力丧失——作为可能的机制。我们阐述了关于IFIS的α受体依赖性机制的主流理论以及目前为预防与IFIS相关的眼内并发症所采取的预防措施。
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