Grillo Lola M, Nguyen Huy V, Tsang Stephen H, Hood Donald C, Odel Jeffrey G
College of Physicians and Surgeons (LG, HVN), Columbia University, New York, New York; Department of Ophthalmology (SHT, DCH, JGO), Columbia University, New York, New York; Department of Pathology and Cell Biology (SHT), Institute of Human Nutrition, and Irving Comprehensive Cancer Center, Columbia University, New York, New York; and Department of Psychology (DCH), Columbia University, New York, New York.
J Neuroophthalmol. 2016 Dec;36(4):383-388. doi: 10.1097/WNO.0000000000000400.
Ocular cobalt toxicity is a rare phenomenon reported with increased frequency due to the rise of cobalt-chromium metal hip implants. We report the case of a 66-year-old previously healthy man who developed decreased vision due to cobalt-chromium toxicity from a metal-on-metal hip arthroplasty. Our objective was to determine whether the origin of his visual loss was due to toxicity of the optic nerve, of the retina, or of both.
Ocular examination, 10-2 SITA-Standard Humphrey Visual Field (VF), standard full-field electroretinogram (ERG) as indicated by the International Society for Clinical Electrophysiology of Vision (ISCEV), multifocal electroretinogram (mfERG), multifocal visual evoked potentials (mfVEP), and optical coherence tomography (OCT) were conducted.
Ocular examination revealed decreased visual acuity, poor color vision, normal funduscopy, and cecocentral scotomas on VF testing. Because his right eye was amblyopic since childhood, test results from only the left eye are shown. Electrophysiology studies revealed an ISCEV standard full-field ERG with photopic and scotopic responses within normal limits, mfERG with amplitudes and latencies within normal limits, and mfVEP with latencies within normal limits, but with decreased central amplitudes. Peripapillary and macular OCT showed retinal nerve fiber layer and retinal ganglion cell-inner plexiform layer thickness within normal limits.
Because decreased color vision and cecocentral scotoma on 10-2 VF are most consistent with toxic optic neuropathy, and decreased central amplitudes on mfVEP are suggestive of neural dysfunction, we hypothesize that our patient presented with an early stage of optic nerve toxicity that was not yet apparent as a structural abnormality on OCT.
由于钴铬金属髋关节植入物的增加,眼部钴中毒是一种报告频率上升的罕见现象。我们报告了一例66岁既往健康男性的病例,该患者因金属对金属髋关节置换术导致的钴铬中毒而出现视力下降。我们的目的是确定其视力丧失的根源是视神经毒性、视网膜毒性还是两者皆有。
进行了眼部检查、10-2 SITA标准汉弗莱视野(VF)检查、国际临床视觉电生理学会(ISCEV)规定的标准全视野视网膜电图(ERG)检查、多焦视网膜电图(mfERG)检查、多焦视觉诱发电位(mfVEP)检查以及光学相干断层扫描(OCT)检查。
眼部检查显示视力下降、色觉减退、眼底镜检查正常以及VF测试出现中心暗点。由于其右眼自幼弱视,仅展示了左眼的测试结果。电生理研究显示,ISCEV标准全视野ERG的明视和暗视反应在正常范围内,mfERG的振幅和潜伏期在正常范围内,mfVEP的潜伏期在正常范围内,但中心振幅降低。视乳头周围和黄斑OCT显示视网膜神经纤维层和视网膜神经节细胞-内丛状层厚度在正常范围内。
由于10-2 VF上的色觉减退和中心暗点最符合中毒性视神经病变,且mfVEP上的中心振幅降低提示神经功能障碍,我们推测该患者呈现出视神经毒性的早期阶段,在OCT上尚未表现为结构异常。