#JAMACaseReport: Corneal Edema in a Gardener
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A woman in her 60s with a history of bilateral proliferative diabetic retinopathy complicated by a recent vitreous hemorrhage in her left eye presented with an acute onset of redness, irritation, and blurredvision in her lefteye.Her symptoms started 1 day after she rubbed her left eye with her hands after handling the milky latex (a fluid found in 10% of flowering plants) of a plant in her garden. She had no recent history of recent eye surgery, eye trauma, cold sores, or new illnesses.

On presentation, her visual acuity was 20/40OD and 20/200OS.Her pupils were equal, round, and reactive in both eyes. Her intraocular pressures were 16 mm Hg OD and 19 mm Hg OS. On anterior segment examination, she was found to have pinpoint epithelial defects, thickened stroma, and dense Descemet folds, along with a nuclear sclerotic cataract. Central pachymetry in the left eye measured 706 m, which was elevated from the mean expected pachymetry values of 540 to 560 m. A posterior pole examination was limited by corneal edema, but there was evidence of vitreous hemorrhage. The fellow eye had no corneal edema and was pseudophakic, with prior pan-retinal photocoagulation scars in the peripheral retina, the patient’s corneal edema was secondary to direct exposure to a plant of the genus Asclepias (milkweed family), which is commonly found in the tropics, subtropics, grasslands, and gardens. Plants in the Asclepiadaceae family are known to contain cardiac glycosides in their latex, leaves, stems, and roots. Cardiac glycosides can inhibit the Na+ -K+ -ATPase enzyme found in the corneal endothelium and are able to penetrate the cornea with minimal injury to the corneal epithelium. Two previous cases have described isolated endothelial decompensation and stromal edema after exposure to the milky latex of Asclepias curassavica and Asclepias fruticose. The onset of symptoms on exposure to the corneal toxin from these plants can begin within 12 hours. However, the effect of cardiac glycosides on the corneal endothelium can be self-limited, with corneal endothelial cell dysfunction lasting only 24 to 48 hours.

In this case, topical prednisolone acetate, 1%, was administered every 2 hours and a sodium chloride hypertonicity ophthalmic solution, 5%, was administered 4 times a day. Improvement in the corneal edema was seen within 2 days of treatment, and it had completely resolved by day 5, with improvement in visual acuity to 20/30 in the affected eye and a decrease in corneal pachymetry to 612 m. Her vitreous hemorrhage had also resolved at this time. Topical steroid therapy was tapered over the course of the following week, and the topical sodium chloride solution was discontinued. The patient had no recurrence of corneal edema in 7 months of follow-up.

Source: https://jamanetwork.com/journals/jamaophthalmology/article-abstract/2768636
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