Lemaitre-Labilloy Claire, Bodaghi Bahram, Cassoux Nathalie, Lehoang Phuc
Department of Ophthalmology, Pitie-Salpetriere Hospital, 43-87 boulevard de l'Hôpital, 75013 Paris, France.
Graefes Arch Clin Exp Ophthalmol. 2006 Jun;244(6):758-60. doi: 10.1007/s00417-005-0090-8. Epub 2005 Oct 21.
We report the case of a 43-year-old man haemodialysed for 20 years for systemic amyloidosis who underwent an acute choroidal occlusion after a haemodialysis accident.
The patient had cardiac, pulmonary, neurovegetative and renal localizations of amyloidosis. He complained during a haemodialysis session of discomfort with abdominal pain, headache, bradycardia, vomiting, confusion and blurred vision. Acute haemolytic anemia was confirmed. In the following days, eyes were red and the vision was still altered.
Examination showed decreased visual acuity (VA) to 20/80 OU, low intraocular pressure (IOP), major vitritis and pigmentary alterations of the fundus with yellow retinal deposits. Fluorescein and indocyanine green angiographies showed amyloid retinal deposits, pigmentary alterations, normal retinal perfusion and massive choroidal hypoperfusion persisting in the late sequence. Steroid therapy was tried unsuccessfully. The situation slowly improved within 3 months with complete clearing of the vitreous opacities and stabilisation of the pigmentary alterations. VA progressively recovered to 20/30, 1 year after the onset of the disease, but IOP remained low and choroidal perfusion did not improve 2 years after the accident.
Choroidal complications of amyloidosis have never been described so far. The acute occlusion observed here was the consequence of an intravascular haemolytic event that completed the preexisting amyloid vascular infiltration.
我们报告了一例43岁男性患者,因系统性淀粉样变性接受血液透析20年,在一次血液透析事故后发生急性脉络膜阻塞。
该患者有心脏、肺部、神经植物性和肾脏部位的淀粉样变性。他在一次血液透析过程中出现不适,伴有腹痛、头痛、心动过缓、呕吐、意识模糊和视力模糊。确诊为急性溶血性贫血。在接下来的几天里,眼睛发红,视力仍有改变。
检查显示双眼视力(VA)降至20/80,眼压(IOP)降低,严重玻璃体炎,眼底有色素改变及黄色视网膜沉积物。荧光素和吲哚菁绿血管造影显示淀粉样视网膜沉积物、色素改变、视网膜灌注正常,晚期序列中脉络膜大量低灌注持续存在。尝试使用类固醇治疗但未成功。3个月内情况逐渐改善,玻璃体混浊完全清除,色素改变稳定。发病1年后,视力逐渐恢复到20/30,但事故发生2年后眼压仍低,脉络膜灌注未改善。
迄今为止,淀粉样变性的脉络膜并发症尚未见报道。此处观察到的急性阻塞是血管内溶血事件的结果,该事件加剧了先前存在的淀粉样血管浸润。