Central Retinal Vein Occlusion and Nonarteritic Ischemic Optic Neuropathy in 2 Patients with Mild Iron Deficiency Anemia

Abstract

We report on 2 patients with ophthalmologic complications associated with mild iron deficiency anemia. Case 1, a 37-year-old female patient, presented after 4 days of blurred vision in her left eye. Ophthalmoscopic and angiographic findings were consistent with the diagnosis of central retinal vein occlusion (CRVO). Further hematologic investigation into possible causes disclosed mild iron deficiency anemia (Hb 9.4 g/dl, hematocrit 30.5%). After the patient’s visual acuity had worsened progressively to 20/50, an initial thrombolytic treatment and continuous intravenous heparinization was started on day 8, followed by oral substitution therapy with ferrous sulfate. On day 14, her visual acuity recovered to 20/20 OS and remained stable during follow-up. Case 2, a 50-year-old female patient, presented with a 1-week-history of blurred vision and metamorphopsia. Her visual acuity was 20/200. Further examination revealed a nonarteritic ischemic optic neuropathy and an iron deficiency anemia as the underlying disease (Hb 7.3 g/dl, hematocrit 25%). Despite intravenous heparinization and systemic treatment with steroids, there was no improvement in visual acuity. Clinicians involved in the management of chronic iron deficiency anemia should be aware of possible ophthalmic manifestations in this disease.

Evaluation of Choroidal Thickness in Children With Iron Deficiency Anemia

“…17,18 In previous studies, retinal vein occlusion, ischemic retinopathy, and ischemic optic neuropathy have been reported in patients with IDA. 6,19 In addition, Turkyilmaz et al 20 reported that the average retinal nerve fiber layer and the retinal nerve fiber layers of the superior and inferior quadrants were significantly thinner in the IDA group than in the control group. Furthermore, Carraro et al 7 suggested that severe anemia plays a significant role in the pathogenesis of retinal abnormalities.…”

“…This disturbance causes retinopathy, including retinal vein and retinal artery occlusion. 6,21 The mechanism of the disturbance of the retinochoroidal circulation in patients with IDA remains unclear; however, iron deficiency may contribute to a hypercoagulable state by affecting blood flow patterns within the vessels because of reduced deformability and increased viscosity of microcytic red blood cells. 22 The other postulated mechanism behind hypercoagulability was reduced antioxidant defense due to IDA and reduced activity of glutathione peroxidase, which corresponds to increased platelet aggregation, reactive thrombocytosis, and elevated factor VIII levels.…”

“…5 Central retinal vein occlusion, retinal hemorrhage, ischemic retinopathy, and papilledema have been reported in patients with IDA. 6,7 The exact pathophysiology of fundus lesions is still unknown, but it has been suggested, is related to hypoxia. In retinal tissue, iron is particularly important for the visual phototransduction cascade.…”

Iron Deficiency Anemia with Marked Thrombocytosis Complicated by Central Retinal Vein Occlusion

“…The disturbance causes various ophthalmic disorders, including retinal vein occlusion and retinal artery occlusion (6)(7)(8)(9). It has been speculated that the disturbance of retinochoroidal circulation is caused by formation of thrombosis due to hypoxia-induced injury of angioendothelial cells, deregulation of the coagulation/fibrinolytic system and thrombocytosis in iron deficiency anemia (5,7).…”

Massive subhyaloidal hemorrhage associated with severe PAI-1 deficiency

“…Interestingly, there have been a few reports on an association with hematologic disorders [1,11], including anemia. Patients with this condition have a substantially elevated risk of intraretinal hemorrhages or retinal vein occlusion [4]. However, in light of the fact that our patient's hemoglobin level was only mildly decreased (11.9 g/dl), and platelet count or hematocrit levels were normal, it seems less likely that these factors may have conributed to the development of her subhyaloidal hemorrhage.…”