Ocular siderosis includes a series of degenerative changes caused by iron poisoning in the eye, such as keratopathy, heterochromia iridum, tetanicpupils, dilated pupils, secondary glaucoma, and complicated cataracts[3–5]. The complications in the posterior segment of the eye caused by ocular siderosis include cystic macular oedema, diffuse pigment changes, arteriole stenosis, retinal ischaemia, retinal detachment and severe proliferative vitreoretinopathy. The causes of retinal detachment due toocular siderosis are retinal glial cell proliferation and subretinal leakage. Until now, there have been no reports about retinal detachment caused by ocular siderosis.
This study is the first to observe the clinical characteristics of retinal detachment caused by ocular siderosis. The clinical characteristics of this group of patients can be summarized as follows: 1. the location of foreign body deposition is relatively hidden; 2. poor vision prognosis; and 3. retinal detachment is highly likely to recur in patients with retinal tears. There were 7 cases (7 eyes), accounting for 58.33%, in which foreign bodies were located in the plane part of the ciliary body or the peripheral part of the retina in this group. Because the location of foreign body deposition is relatively hidden and the size of iron foreign bodiesis usually small, the early clinical symptoms of patients with injuries are often not obvious, and the presence of foreign bodies is difficult to identify by routine examination, so the course of disease is prone to be delayed.Failure to seek early treatment is also an important practical cause ofocular siderosis with retinal detachment.
Although the exact mechanism by which iron causes widespread retinal degeneration and vascular lesions is unclear, many hypotheses exist. One hypothesis is that ions released by iron produce free radicals that cause severe oxidative damage to retinal cells[6, 8, 9]. The Haber-Weiss reaction, in which Fe3+ and O2− are converted to strong oxidizing hydroxyl radicals, is thought to occur in vivo, as these reactants may persist for a long time in the case of iron deposition. Fe3+ is the catalyst in the reaction, which means it is present as a reactant in the first step and is regenerated in the last step, so only a small amount of Fe3+ can push the reaction forward indefinitely. While O2− is produced by light and molecular oxygen, long-term exposure to the strong oxidative environment of superoxide dismutase and catalase cannot remove or neutralize the harmful chemicals in these cells. Another hypothesis, based on the cytotoxic mechanisms of silicosis and asbestosis, postulates that the accumulation of iron in cells leads to the release of lysosomal enzymes, which damage tissues. This hypothesis suggests that cytoplasmic aggregates of ferritin, known as ferriosomes, occur in ocular iron deposition, triggering a toxic cascade. Therefore, patients with ocular siderosis complicatedby retinal detachment tend to have poor vision, and the improvement of visual function is extremely limited even after surgical treatment. Moreover, even after the removal of intraocular foreign bodies, the visual function of some patients continues to decline. The possible reason is that the residual iron ions still promote intraocular toxicity even after the removal of intraocular foreign bodies. Small iron particles can still be released at the inner retinal surface following surgical removal, potentially inducing further toxicity[10, 11]and leading to further damage to retinal cells, resulting in the continuous decline of visual function. The overall postoperative visual acuity of all the patients in this group was poor, but the statistical results showed that the visual acuity of the patients after surgery was still significantly improved compared with that before surgery (P < 0.05), which may indicate that the surgical treatment of retinal detachment caused by ocular siderosis is still of clinical significance.
Amongcases of retinal detachment caused by ocular siderosis, there is a special case whereexudative retinal detachment is accompanied by retinal tears caused by foreign bodies. In this study, 4 patients (4 eyes) had retinal tears. All 4 patients underwent filling with silicone oil during the first operation, and silicone oil was removed within 3 to 6 months after vitrectomy. Unfortunately, 4 of the patients experienced retinal detachment recurrence within 1 to 3 weeks after the removal of silicone oil. All of the patients with recurrent retinal detachment were subsequently treated with a second retinal reattachment, and the eyes were filled with silicone oil for the second time. Among them, two patients underwent silicone oil removal again within 6 to 12 months after the second retinopathy surgery, and retinal detachment recurrence occurred again, while the other two patients who underwent filling with silicone oil for a second time did not undergo silicone oil removal during the follow-up period. These results may suggest that patients with ocular siderosis complicated by rhegmatogenous retinal detachment have a low rate of complete retinal reattachment and are highlylikely to develop silicone oil-dependent eyes. The reason may be that iron ions tend to bind to retinal pigment epithelial cells, resulting in degeneration and inactivation of these cells. Iron retinotoxicity leads to dysfunction of all the layers of the retina, with more severe damage occurring in the inner retina than in the outer retina in the late stages of the disease[8, 11];thus,effective and strong adhesion is difficult to form between the retinal neuroepithelium and pigment epithelium. This results in retinal tears not being completely closed even with retinal laser photocoagulation or retinal freezing. When the silicone oil in the eye is removed, the retinal tear can easily reopen, which leads to retinal detachmentrecurrence. When silicone oil is removed from the eye, the retinal tear tends to reopen, leading to retinal detachmentrecurrence. Further, the eyeballs of patients with ocular siderosis complicated by rhegmatogenous retinal detachment likely become silicone-oil-dependent eyes. Animal studies of ocular siderosis have also shown that the retina will completely degenerate, and degeneration of the pigment epithelium can cause the retina to fail to fuse with the choroid in the late stage of the disease. Therefore, ocular siderosis complicated by rhegmatogenous retinal detachment is a special type of disease thathas a different prognosis from thatof exudative retinal detachment caused by ocular siderosis. Certainly, if iatrogenic retinal tears occur during surgical procedures for exudative retinal detachment due to ocular siderosis, the prognosis is the same. Full awareness and communication with the patient should be completed before the surgeon performs surgical treatment so that the patient can fully understand the severity of the disease.
This study is limited by its retrospective design. Furthermore, the sample size of this study is small, which does not fully reflect the overall situation of the disease. This study is only a single group of case cohort observations.