Pingueculae and pterygia.

Pingueculae and pterygia are benign peribulbar lesions composed of degenerated basophilic subepithelial tissue. Pingueculae do not affect vision, and minor irritation can usually be managed with artificial tears. Pterygia may affect the visual axis and require surgical and adjunctive treatment. The various therapeutic strategies are reviewed. A conservative approach is advocated, as surgical removal of primary pterygia may result in recurrent ptergyia that are more difficult to manage than the primary lesions.

Stromal keratitis with anterior membrane dystrophy.

Anterior stromal nummular infiltrates developed in a 55-year-old woman with recurrent corneal erosion syndrome and associated anterior basement-membrane dystrophy. Gram and Giemsa stains showed no organisms, and cultures revealed no growth at 72 hours. Stromal keratitis can complicate recurrent corneal erosions associated with anterior basement-membrane dystrophy.

Mixed arteriovenous occlusive disease of the fundus.

Sudden loss of vision occurred in two young healthy patients who had the clinical findings of partial retinal artery and partial retinal vein occlusion. This might represent a severe variant of papillophlebitis.

Ocular involvement in the respiratory vasculitides.

The respiratory vasculitides are idiopathic inflammatory syndromes, characteristically involving the pulmonary vasculature as well as that of several other organ systems. The inflammatory response in these diseases is uniformly granulomatous. There are three distinct, recognized respiratory vasculitides: Wegener's granulomatosis, Churg-Strauss syndrome (allergic granulomatosis and angiitis), and lymphomatoid granulomatosis. Each of these entities may have ophthalmic manifestations, and ocular involvement may, in fact, be the presenting sign. The systemic and ocular manifestations, as well as the differential diagnosis and management of each of these entities are discussed.

The use of topical Healon tears in the management of refractory dry-eye syndrome.

We evaluated 28 patients with dry-eye syndrome in the setting of either primary or secondary Sjogren's syndrome, with topical Healon tears. In 26 of the 28 patients, we noted both subjective and objective improvement characterized by decreased itching, burning and foreign body sensation, decreased mucus stranding and Rose-Bengal staining of the cornea and conjunctiva, and increased corneal luster and tear break-up time.

Persistent corneal edema in the congenital rubella syndrome.

Corneal edema occurring in the congenital rubella syndrome can result from coexistent glaucoma or develop in the absence of an elevated intraocular pressure. We examined a 36-week-old female infant with documented congenital rubella syndrome who had bilateral corneal stromal edema without attendant congenital glaucoma. Histopathologic examination of the cornea revealed absent Descemet's membrane, deep interstitial keratitis, stromal corneal swelling, and deranged, focally absent endothelial cells. A viral infiltration of endothelium is postulated as the mechanism of the corneal edema and keratitis.

Primary infantile glaucoma (congenital glaucoma).

Primary infantile glaucoma, commonly termed congenital glaucoma or trabeculodysgenesis, is an unusual, inherited connatal anomaly of the trabecular meshwork and anterior chamber angle which leads to obstruction of aqueous outflow, increased intraocular pressure, and optic nerve damage. Its pathogenesis is still disputed; most observers have not been able to document ultrastructurally a continuous endothelial membrane, as initially advanced by Barkan. Medical therapy for primary infantile glaucoma is accorded a supportive role; the primary, definitive treatment is surgical. Both goniotomy and trabeculotomy ab externo give similarly good results in the majority of patients. The prognosis in this disease is related to the time of its initial presentation, initial surgical intervention, degree of optic nerve damage, nature and quality of corneal enlargement and astigmatism, progressive refractive error, and anisometropic amblyopia. The inability to easily quantitate visual acuity and extent of visual loss in neonates makes these parameters less helpful in following patients than measurement of corneal diameter and intraocular pressure. However, even these data should not be relied upon exclusively to determine the quality or quantity of success in primary infantile glaucoma.

Quantitation of tear lysozyme levels in dry-eye disorders.

A simple, rapid, reproducible method of quantifying tear lysozyme levels with a dual-channel spectrophotometer was used to compare normal subjects and those with dry-eye syndrome. The method was sensitive (80%) and specific (85%) and had a predictive value of a positive result of 83%. One patient with clinical manifestations of dry-eye syndrome and paradoxically elevated levels of tear lysozyme was found to have underlying sarcoidosis.

Syphilitic retinal detachment and uveal effusion.

A 32-year-old man developed a recurrent nonrhegmatogenous retinal detachment, uveal effusion, and visual loss as a result of latent secondary syphilis. Treponemes were found in the subretinal fluid and the Treponema pallidum hemagglutination test demonstrated substantially higher titers in the subretinal fluid than in the serum (1: 2,569 vs 1: 16). Despite scleral dissection and a scleral implant and treatment with penicillin, the patient's visual loss persisted and the last examination showed a thickened choroid, a flat nonrhegmatogenous retinal detachment, and reaccumulation of subretinal fluid.

Asymmetric anterior segment changes induced by chlorpromazine.

A 54-year-old man ingested chlorpromazine, 800 mg/day, for ten years and showed conjunctival, corneal, and lenticular changes. Because of a congenital Marcus-Gunn jaw-wink phenomenon in the right eye with subsequent ptosis, he presented an opportunity to compare the anterior segment changes induced by this drug in an eye exposed to sunlight with an eye relatively protected. The changes in the anterior segment were much more marked in the exposed left eye--supporting the hypothesis that chlorpromazine-induced ocular toxicity is a result of drug interaction with sunlight on anterior segment proteins, causing them to denature, opacify, and accumulate in conjunctiva, cornea, and lens.