Superior limbic keratoconjunctivitis in contact lens wearers.

Forty patients with daily wear, cosmetic contact lenses (CL) presented with symptoms of ocular irritation and a keratoconjunctivitis clinically resembling superior limbic keratoconjunctivitis (SLK). Typically the patients were either successful hard CL wearers who changed to soft lenses and used a chemical aseptisizing solution or preserved saline solution, or successful soft CL wearers using salt tablets who switched to a preservative-containing system. In all cases, exposure to thimerosal-preserved solutions was documented. Upon discontinuation of lens wear, all signs and symptoms slowly resolved without permanent sequelae. Positive skin and ocular sensitivity reactions to thimerosal were present in one-third (5/15) of patients tested. Light and transmission electron microscopic examination of conjunctival specimens disclosed intercellular epithelial edema, pseudoepitheliomatous hyperplasia, acute and chronic inflammation, and decreased numbers of goblet cells. Exposure to thimerosal is implicated in the etiology of contact lens-superior limbic keratoconjunctivitis (CL-SLK).

Intracorneal lens implantation.

In previous experiments, we found that a high-water-content hydroxyethyl methacrylate (Permalens) hydrogel implant was not only well tolerated within the rabbit corneal stroma but also would successfully alter the anterior radius of curvature, and thus the refractive state, of the rabbit eye. The same lens material implanted in the cornea of a patient with aphakic bullous keratopathy was tolerated for six months and decreased epithelial edema but did not alter the refractive state. This cornea, containing the intrastromal lens, was obtained at subsequent penetrating keratoplasty and studied by light and transmission electron microscopy. Morphologically, the epithelium and anterior stroma were not edematous, whereas the stroma posterior to the lens remained edematous. Minimal fibroblastic activity was evident at the lens-stroma interface. There were no signs of inflammation, ulceration, or neovascularization.

Epithelial abrasion precipitates stromal ulceration in the vitamin A--deficient rat cornea.

Although the role of vitamin A deficiency in the development of xerophthalmia is well established, there is still some question as to whether the deficiency alone is sufficient cause for the development of keratomalacia. This article describes the clinical, histologic, and microbiologic changes occurring in eyes of vitamin A-deficient rats when keratomalacia-like stromal ulceration is induced by epithelial injury alone. The corneal epithelia of 21 severely vitamin A-deficient rats and 11 pair-fed controls were totally removed either by scraping or by n-heptanol. At 96 hr after epithelial removal, 93% of the deficient animals showed extensive epithelial defects and stromal ulceration. Histologically, an intense acute inflammatory response and abundant bacterial forms were consistently evident. Staphylococcus aureus and Streptococcus fecalis were the most frequent pathogens cultured from these ulcerating eyes. In contrast, the control corneas showed essentially complete re-epithelialization, with no ulceration, minimal inflammatory reaction, and an absence of morphologically demonstrable bacteria. Bacterial cultures from the control eyes showed abundant Pasteurella, with pathogens also present. These observations suggest that abnormal epithelial recovery, acute inflammation, and bacterial infection may be important factors for the development of keratomalacia-like corneal ulceration in experimental vitamin A deficiency.