Press Archive
- Charles Francis: Weakening eye surgery laws places WV patients in jeopardy
- Mark D. Mayle, MD - 2022 Secretariat Award Recipients
- Dr. Larry Schwab recognized with 2020 International Blindness Prevention Award
- Wow Moment with Joseph A. LoCasio | Bio-Tissue | #WowWednesdays
- WVU Today | Moore, Oppe named recipients of Heebink award for Distinguished Service
- Cornea Transplant Restores Young Boy’s Sight After Fishing Accident
- Keep your eyes healthy and safe in the workplace
- Glaucoma Awareness Month
- Ophthalmologists Say 90 Percent of Work-Related Eye Injuries Can be Avoided by Wearing Eye Protection
- Five Tips to Avoid Toy-Related Eye Injuries
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A 46-year-old woman presented with pain and an intraocular pressure of 63 mmHg in the left eye 2 years after plaque brachytherapy for uveal melanoma. Examination revealed pigmented material in the anterior chamber (Fig 1), a choroidal mass (Fig 2), and marked pigmentation in an open trabecular meshwork with gonioscopy. Histopathology of this blind, painful eye confirmed the diagnosis of spindle B type uveal melanoma (Fig 3), with foci of necrosis and pigment laden macrophages (melanophages). Melanophages (black arrow) were deposited on the ciliary body (CB), iris (I) and in the trabecular meshwork (white arrow, Fig 4; C indicates cornea).
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Corneal hydrops is an uncommon condition occurring in 2%−3% of patients with keratoconus. It is caused by a leak of aqueous into the cornea through a tear in Descemet's membrane causing severe corneal edema (Fig 1). Acute hydrops occurred in a 51-year-old man. The hydrops resolved over 4-months with conservative medical treatment, and a penetrating keratoplasty was performed. The histopathology (hematoxylin and eosin and periodic acid-Schiff) revealed thinning of the apical stroma (Fig 2, asterisk), breaks in Bowman's membrane (Fig 3, white arrow) and subepithelial bullae (Fig 4, open arrow).
Read more: Changes in the Corneal Architecture Following Corneal Hydrops
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We thank Dr Cullen for his interest in our editorial and thoughtful comments. With regard to the expressed notion that hyperemia and edema should indicate optic nerve head ischemia, one should recognize that in bona fide ischemic optic neuropathy such as in giant cell arteritis that Dr Cullen refers to in an earlier article from his Singapore series on ischemic optic neuropathy (ION),1 it is pallor rather than hyperemia that is the predominant sign. We believe that the noted hyperemia in so-called nonarteritic anterior ischemic optic neuropathy (NAION) is indicative of an altogether different process at hand.
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A 92-year-old woman had her right eye removed for a submacular choroidal melanoma. Four weeks before surgery her vision was counting fingers and intraocular pressure 17 mm Hg. The tumor measured 14.6×9.6 mm and was 4.4 mm thick. The nasal portion of the optic disc was visible and interpreted as normal (Fig A). In the laboratory, the eye was opened horizontally. Histologically, cavernous degeneration of the optic nerve was located nasally (N) opposite the melanoma (Figs B and C). Pial septi were widely dilated.
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Katz and associates are most appreciative of the new concept we propose in our editorial. That it is dynamic shear force injury due to epipapillary membrane vitreoglial separation from peripapillary and papillary axons that leads to pathology, heretofore described as nonarteritic anterior ischemic optic neuropathy (NAION). Their eloquent appraisal of our editorial and examples of other English misnomers is music to our ears.
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We read with relish the editorial of Parsa and Hoyt arguing for a change in prism through which we see what we had heretofore called nonarteritic anterior ischemic optic neuropathy (NAION).1 Their elegant and cogent summary of consequences and associations of vitreopapillary traction, when collated as they have done, convincingly argue their point. As the English horn is neither English nor a horn, so too, NAION is not ischemic, at least, not primarily so.