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At least 19 recordsLinked to original sources
PubMed1979

Corneal edema with several hard corneal contact lenses.

Five patients were each fitted with polymethylacrylate (PMMA), BP Flex, and Polycon corneal contact lenses of the same dimensions. Corneal edema was monitored with a slit-lamp biomicroscope and pachometer. Lenses were worn in a double-masked and random sequence for periods of 6 hr. Patients developed less corneal edema with Polycon lenses than with PMMA lenses. There was no significant difference in corneal edema with PMMA and BP Flex lenses. Those patients who developed little corneal edema with optimum-fitting PMMA lenses also developed little edema with the BP Flex and Polycon lenses. Steeper-fitting PMMA and BP Flex lenses produced more corneal edema than optimum-fitting lenses made of the same materials, while steeper-fitting Polycon lenses produced only slightly more edema than the optimum-fitting Polycon lenses.

Adult↗
PubMed1979

Vision through an abnormal cornea: a pilot study of the relationship between visual loss from corneal distortion, corneal edema, keratoconus, and some allied corneal pathology.

Visual function was assessed by classic acuity measures as well as contrast thresholds over a wide spatial frequency range for subjects with experimentally induced corneal distortion and induced corneal edema. These results were compared with similar results for patients with uniocular keratoconus, bilateral keratoconus, and allied corneal pathology. Distortion and edema were found to produce characteristically different types of contrast attenuation at threshold (amplitude) and have quite different suprathreshold abnormalities (phase) for objects within the resolution limit and therefore could form the basis of a useful functional classification of the visual degradation from corneal pathology.

Cornea↗
PubMed1979

Corneal edema in essential iris atrophy.

In a clinical study of the essential iris atrophies, corneal edema occurred in 49 of 90 patients, and a characteristic hammered-silver appearance of the posterior cornea was visible in 54 cases. Intraocular pressure in the eyes with corneal edema ranged from normal to extreme elevation with glaucomatous damage, and lowering the pressure relieved the corneal edema in many cases with penetrating keratoplasty being effective when other measures failed. Electron microscopy of two keratoplasty specimens revealed extremely few, distinctly abnormal cells lining a collagenous layer posterior to Descemet's membrane.

Adolescent↗
PubMed1977

[Recurrent corneal edema without ocular hypertension, pigment degeneration combined with deafness, progressive dystrophy of the outer eye-muscles in a patient with proportional dwarfism and diabetes mellitus (author's transl)].

A 27-year-old woman has been suffering from recurrent corneal edema without ocular hypertension since her early childhood. When the cornea is clear, visual acuity-with correction for high myopia-is 5/10 to 5/15 and Nieden I; when the cornea is swollen, it decrease to 5/50 and 1/10, respectively, and Nieden VII. Furthermore, there is an atypical pigment degeneration of the retina combined with deafness, a progressive ptosis since her 10th year of life, and a progressive dystrophy of the outer eye muscles, having developed in the past few years. In addition, the mentally normal developed patient presents a proportional dwarfism (no dysostosis) and a diabetes mellitus. This combination of symptoms is compared with the well known Bardet-Biedl syndrome and the De Grouchy syndrome and is found to constitute a new syndrome.

Adult↗
PubMed1979

Effects of monomeric methylmethacrylate on ocular tissues.

Toxic effects of high doses of monomeric methylmethacrylate were demonstrated in rabbit eyes. These effects were not related to surgical manipulation. Monomeric methylmethacrylate caused limbal hyperemia, corneal edema, corneal neovascularization, iris engorgement, anterior chamber inflammation, iris atrophy, and cataract. The doses of monomeric methylmethacrylate needed to produce these lesions were much higher than the amount of monomer available for leaching out of implanted intraocular lenses.

Animals↗
PubMed2026

Descemet Stripping Only in Fuchs Endothelial Corneal Dystrophy: Results of a Randomized Clinical Trial of Topical Ripasudil and Directions for Future Innovation.

PURPOSE: To review history of Descemet stripping only (DSO) in Fuchs endothelial corneal dystrophy, describe the results of a clinical trial of topical ripasudil after DSO (K-321-201 study), and discuss future directions. METHODS: A 1-year, phase 2, randomized, placebo-controlled multicenter clinical trial of two doses of K-321 (ripasudil) administered for 12 weeks after DSO surgery in Fuchs endothelial corneal dystrophy was performed. The primary endpoint, central corneal endothelial cell density (ECD) at 12 weeks after surgery, was determined by an independent reading center that was masked to study group assignment. Duration of corneal edema, need for medical or surgical rescue therapy, corneal thickness, and central ECD throughout the entire study period were also examined. Adverse events and exploratory endpoints were collected. RESULTS: Sixty-five subjects were enrolled (21 in the QID group, 22 in the BID, and in the placebo group). Over 95% of subjects completed the trial. The QID group had a higher central ECD 12 weeks after DSO than the placebo group (531 &#xb1; 312 cells/mm2 vs 228 &#xb1; 298 cells/mm2, P = .0065). Corneal edema cleared in 17/21 (81.0%) of the QID group at 12 weeks, compared with 2/22 (9.1%) of the placebo group (P < .0001). Rescue was required in 2/21 (9.5%) subjects in the QID group and 6/22 (27.3%) subjects in the placebo group (P = .0092). Adverse events were mild and did not lead to discontinuation of treatment. CONCLUSIONS: Topical K-321 given QID improves DSO outcomes, as demonstrated by a higher ECD, more rapid resolution of corneal edema, and reduced failure rate. The medication was well-tolerated.

Humans↗
PubMed1979

Pseudophakic bullous keratopathy. A clinical-pathologic analysis.

Of 226 patients who had an intraocular lens implanted over a three year period, 6.2% developed bullous keratopathy compared with 2.2% of 90 patients who had a standard cataract extraction performed by the same surgeon. An additional 4.0% of the lens implant patients developed peripheral or intermittent corneal edema. The factors related to the higher incidence of this complication in lens implant patients included corneal touch during implantation, prolonged postoperative iritis and, in cases of mild or peripheral corneal edema without bullous keratopathy, recurrent lens dislocation. The most consistent pathologic findings in 10 corneas that required keratoplasty were epithelial edema and loss of corneal endothelium. Means to prevent this complication are discussed.

Aged↗
PubMed1979

Corneal decompensation in Chandler's syndrome. A scanning and transmission electron microscopic study.

A corneal button obtained from a 58-year-old woman with Chandler's syndrome was studied by light and electron microscopy. Clinically, the patient had mild unilateral glaucoma, slight changes in the iris, endothelial dystrophy, and corneal edema that was increasingly sensitive to intraocular pressure. Corneal pathology included loss of large numbers of endothelial cells with consequent exposure of Descemet's membrane. Endothelial cells demonstrated irregular shape, partial loss of tight junctions, and increased numbers of cytoplasmic filaments. Some endothelial cells appeared metaplastic or perhaps were replaced by cells from some source other than the cornea. Proliferation of cells was not apparent. A thin layer of acellular tissue, containing long-spacing collagen and 15-nm-wide fibrils, was interposed between normal Descemet's membrane and the endothelium. These observations suggest a basis for the corneal edema that distinguishes Chandler's syndrome from other forms of essential iris atrophy.

Cornea↗
PubMedDate not supplied

Production of anterior segment ischemia.

Anterior segment ischemia changes can occur without detachment of any muscles. The most common cause of such ischemic changes of the anterior segment is the removal of too many rectus muscles in one operation. Twenty dog eyes and eight monkey eyes were subjected to the disinsertion and detachment of various combinations of extraocular muscles. They were sacrificed at intervals from 30 to 90 days. During the observation period, they were observed for gross and slit lamp changes. The enucleated eyes were studied microscopically for signs of ischemic and necrotic changes. Two patients who were studied, observed, and treated for anterior segment ischemia following muscle surgery are described. The changes which occur after muscle surgery are extensive and include corneal edema, cataract, chemosis, corneal changes, decreases in intraocular pressure, decreases in outflow or glaucoma and frank necrosis. The variables which lead to this reaction is described in detail. Also, some unanswered queries, such as the duration of the reaction and the time interval of the reaction after multiple muscle surgeries, are discussed.

Adult↗
PubMed1977

Production of anterior segment ischemia.

Anterior segment ischemic changes can occur without detachment of any muscles. The most common cause of such ischemic changes of the anterior segment is the removal of too many rectus muscles in one operation. Twenty dog eyes and eight monkey eyes were subjected to the disinsertion and detachment of various combinations of extraocular muscles. The dogs were sacrificed at intervals from 30 to 90 days. During the observation period, they were observed for gross and slit-lamp changes. The enucleated eyes were studied microscopically for signs of ischemic and necrotic changes. Two patients who were studied, observed, and treated for anterior segment ischemia following muscle surgery are described. The changes which occur after extraocular muscle surgery are extensive and include corneal edema, cataract, chemosis, corneal changes, decreases in intraocular pressure, decreases in outflow or glaucoma, and frank necrosis. The variables which lead to this reaction are described in detail. Also, some unanswered queries, such as the duration of the reaction and the time interval of the reaction after multiple muscle operations are discussed.

Adult↗
PubMedDate not supplied

Progressive essential iris atrophy, Chandler's syndrome, and the iris nevus (Cogan-Reese) syndrome: a spectrum of disease.

Progressive essential iris atrophy, Chandler's syndrome, and the iris nevus (Cogan-Reese) syndrome are considered to be variations of a single disease process, which is characterized by abnormalities of the cornea, anterior chamber angle, and iris. In each variation, the typical patient is a white woman with unilateral disease, negative family history, and an onset of symptoms in early to middle adulthood. Since the membrane theory of Campbell suggests that the disease is a fundamental abnormality of the corneal endothelium, rather than the iris, the term "iridocorneal endothelial syndrome," as proposed by Yanoff, may be an appropriate inclusive term for the spectrum of disease, although further study of the pathogenesis is needed. For each variation of the disease, corneal edema and secondary glucoma are both treated primarily by medical or surgical reduction of the intraocular pressure, although penetrating keratoplasty is occasionally required for cases with advanced corneal edema.

Adult↗
PubMed1979

The management of patients with intraocular lenses. Guidelines for those who do not perform this operation.

The management of patients with intraocular lenses can be done quite well by any knowledgeable ophthalmologist. Every examination must include the measurement of intraocular pressure and a thorough slit-lamp examination, specifically noting: Corneal edema, local or diffuse; Increasing corneal guttata; Touch of lens or iris suture to the cornea; Aqueous ray or cells, KP, LP (lens precipitates); Lens displacement; Iris suture problems; Pupil margin erosion; Secondary cataract; Vitreous face: loss or thickening; Retrolenticular membrane formation; Vitreous cells. Ophthalmoscopy should include examination of the peripheral retina for detachment, but visual fields should be done whenever detachment is suspected. Contact lens--slit-lamp examination of the macula for cystoid edema should be supplemented by Flourescein angioscopy when needed. Lens removal should be done only after careful consideration. The damage induced by such surgery must be weighed against the problems of leaving the lens in place. Consultation is mandatory. When in doubt, refer.

Edema↗
PubMed1979

Oxygen-transmitting hard contact lenses.

Nine PMMA contact lens wearers with persistent corneal edema were refitted with CAB contact lenses. All of the patients showed less corneal swelling with CAB lenses than with PMMA lenses.

Acetates↗
PubMed1975

Rabbit corneal damage produced by Pseudomonas aeruginosa infection.

Gross, light microscopic, and electron microscopic examination of the rabbit corneal destruction produced by experimental Pseudomonas aeruginosa infections revealed a combination of acute inflammation and liquefaction necrosis of the cornea. Degeneration of the epithelial cells and the start of polymorphonuclear leukocyte infiltration of the cornea occurred initially. These changes were followed by loss of the epithelium, degeneration and loss of the keratocytes and endothelium, loss of the characteristic weblike pattern of the proteoglycan ground substance, dispersal of ultrastructurally normal collagen fibrils, extensive accumulation followed by degeneration of polymorphonuclear leukocytes, and accumulation of plasma proteins and fibrin in the necrotic cornea. Histochemical examination of the cornea suggested a loss of the proteoglycan ground substance but not of collagen. Rabbit corneas injected with Clostridium histolyticum collagenase showed gross and cellular changes similar to those observed during the pseudomonal infections; however, histochemical examination suggested a loss of collagen, and electron microscopy revealed ultrastructurally abnormal collagen fibrils. The results support the idea (i) that a bacterial or host-derived collagenase is not required for extensive corneal damage during a P. aeruginosa corneal infection, and (ii) that a P. aeruginosa corneal infection may severly damage the cornea by producing extensive corneal edema and by causing the loss of the corneal proteoglycan ground substance, thus resulting in dispersal of undamaged collagen fibrils, weakening of the cornea, and subsequent descemetocele formation and corneal perforation by the anterior chamber pressure.

Clostridium↗
PubMed1978

Keratoplasty for bullous keratopathy with intraocular lens.

The presence of a pseudophakos does not appear to introduce any greater hazard when keratoplasty is required because of corneal edema. This, together with the histories obtained from patients requiring such keratoplasty, strongly suggests that the insult to the corneal endothelium takes place at the time of placement of the intraocular lens in the great majority of cases. Of possible further significance is the fact that five of the sixteen patients who underwent keratoplasty had had secondary procedures to stabilize or to reposition the lens following the original lens implantation. The increased trauma inherent in the intraocular lens operation has been pointed out by many authorities. The fact that twelve of the sixteen patients requiring keratoplasty had been operated by experienced, nationally known intraocular lens surgeons further emphasizes this. The immediate problem appears to be the development and refinement of surgical techniques to avoid some of the complications which have been described. The prognosis for keratoplasty in cases of bullous keratopathy with an intraocular lens has been found to be at least as good as in cases without an intraocular lens.

Corneal Diseases↗