Bilateral Central Retinal Artery Occlusion

Kabakow, Bernard

doi:10.1001/archopht.1955.00930020676007

Cited by 35 publications

(3 citation statements)

References 24 publications

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“…1 For sickle cell trait (HgSA) patients (Table 1), there were five reports of unilateral CRAO in patients with multiple coexisting conditions including systemic lupus erythematosis (SLE), 15 rheumatic heart disease, 15 trauma with increased intraocular pressure, 15−17 syphilis, 13 diabetes mellitus, 13 hypertension 13 and carotid artery disease. 13 There were two reports of bilateral CRAO in HgSA patients associated with pulmonary tuberculosis and SLE in one patient, 18 and hemolytic uremic syndrome with severe dehydration in the other. 19 We could find only one case of spontaneous unilateral CRAO in a HgSA patient 20 and no reports of spontaneous bilateral CRAO.…”

Section: Discussionmentioning

confidence: 99%

Bilateral Central Retinal Artery Occlusion Associated with Moyamoya Syndrome in a Sickle Cell Disease Patient

Goodwin

Vaphiades

Johnson³

et al. 2008

Neuro-Ophthalmology

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Section: Discussionmentioning

confidence: 99%

Bilateral Central Retinal Artery Occlusion Associated with Moyamoya Syndrome in a Sickle Cell Disease Patient

Goodwin

Vaphiades

Johnson³

et al. 2008

Neuro-Ophthalmology

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“…Documented retinal pathology associated with Hb AS includes retinal haemorrhages and exudates (Nagpal et al 1977), angioid streaks (Lieb et al 1959), acute chorioretinal infarctions (Lieb et al 1959), chorioretinitis, vitreous hemorrhage (Kabakow et al 1955), retinal vasculature abnormalities – retinal vein tortuosity/dilation (Lieb et al 1959), microaneurysms (Lieb et al 1959), central retinal artery occlusion (Kabakow et al 1955; Michelson & Pfaffenbach 1972; Sorr & Goldberg 1975) and retinitis proliferans (Lieb et al 1959).…”

Section: Discussionmentioning

confidence: 99%

“…hypertension, TB, diabetes, sarcoidosis, syphilis, rheumatoid arthritis) (Nagpal et al 1977). However, four cases have been reported in association with severe blunt ocular trauma in the absence of systemic disease (Kabakow et al 1955; Michelson & Pfaffenbach 1972; Sorr & Goldberg 1975; Jackson et al 1995). All patients presented with markedly reduced visual acuity, raised intraocular pressures and traumatic anterior uveitis.…”

Section: Discussionmentioning

confidence: 99%

Latent proliferative sickle cell retinopathy in sickle cell trait

Mehta

Whittaker

Tsaloumas

2001

Acta Ophthalmologica Scandinavica

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ABSTRACT.Purpose: To describe a patient with sickle cell trait who developed latent proliferative sickle cell retinopathy after mild blunt trauma. P roliferative sickle cell retinopathy is characterized by vascular proliferation and is most commonly observed in patients with Hb SC, Hb S-thalassemia and Hb SS. We report a case of a patient with sickle cell trait (Hb AS) who developed latent, uniocular, proliferative sickle cell retinopathy after an episode of mild blunt ocular trauma. Case ReportA 20-year-old Ghanaian student presented complaining of flashing lights and floaters in his left eye associated with a periorbital aching pain. He was elbowed in the left eye playing football two days earlier, resulting in 'tunnel vision' which settled within one hour. He had no past medical history of note.He had sustained a similar injury to the left eye, playing football three years previously. An ophthalmic assessment then revealed moderate anterior chamber inflammation, intraocular pressure (IOP) 30 mmHg and normal dilated fundoscopy. He was discharged from follow-up after the IOP returned to normal.Current examination showed unaided visual acuity 6 / 5 RE 6 / 6 LE. Pupillary reactions, anterior segments and intraocular pressures were normal. There was no aniscoria. Dilated fundal examination showed no vitreous abnormalities and a normal right fundus. The left fundus showed five areas (150 ae) of peripheral sea-fan neovascularization (Stage 3) with an ischaemic ridge from 9-4 o'clock delineating avascular from vascular retina. He was normotensive and systemic examination was unremarkable.Full blood count, chest X-ray, urea & electrolytes and blood glucose were normal. Haemoglobin electrophoresis revealed the genotype Hb AS (HbA 60%, HbS 40%) with normal mean cell haemoglobin/mean cell volume.Fundus fluorescein angiography delineated the areas of neovascularization and also showed areas of capillary drop out in the peripheral fundus of the left eye (Fig. 1). There was no abnormality in the vasculature in the right eye.

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