Corneal Toxicity after Self-Application of Calotropis procera (Ushaar) Latex: Case Report and Analysis of the Active Components.

Calotropis procera (ushaar) produces a copious amount of latex, which has both inflammatory and anti-inflammatory pharmacological properties. Local application produces an intense inflammatory response and causes significant ocular morbidity. We report corneal toxicity following self-application of latex from C. procera in a 74-year-old man. He reported painless decreased vision in the affected eye with diffuse corneal edema, and specular microscopy revealed a reduced endothelial cell count. After he was treated with topical corticosteroids, his visual acuity improved from hand motion to 20/80. The composition of the active compounds in the latex was analyzed. When topically administered, the latex may cause severe ocular injuries and a loss of endothelial cells over a period of time. Public education, early recognition of such injuries, and timely intervention may prevent permanent ocular damage.

Comparative analysis of intravitreal triamcinolone acetonide-moxifloxacin versus standard perioperative eyedrops in cataract surgery.

PURPOSE: To compare the effectiveness of intravitreal injection of triamcinolone acetonide-moxifloxacin (Tri-Moxi) to a standard eyedrop regimen in controlling postoperative inflammation, corneal edema, and the rate of high intraocular pressure (IOP) among cataract patients. SETTING: Loma Linda University Eye Institute, California, USA. DESIGN: Retrospective longitudinal comparative study. METHODS: The electronic medical records of patients who underwent cataract surgery using triamcinolone acetonide-moxifloxacin injection along with a postoperative nonsteroidal antiinflammatory drug drop were reviewed (Group 1). Group 1 was compared with patients who received a standard eyedrop (Group 2) in terms of intraocular inflammation and corneal edema severity, and the rate of high IOP, postoperatively. RESULTS: A total of 1195 consecutive eyes (Group 1 [681 eyes], Group 2 [514 eyes]) of 919 patients were included in the study. The anterior chamber cell reaction severity decreased by 34.0% and 35.7% at 1 week and 1 month, respectively, after surgery following triamcinolone acetonide-moxifloxacin injection compared with standard eyedrop therapy (P = .001 and P = .02, respectively). Group 1 was associated with increased severity of corneal edema (odds ratio, 1.48; P = .001) on postoperative day 1, with no statistically significant difference at 1 week and 1 month postoperatively (P = .25 and P = .48, respectively). There was no statistically significant difference in the rate of high IOP between the two groups at different timepoints postoperatively. CONCLUSIONS: Triamcinolone acetonide-moxifloxacin injection is an effective method to control intraocular inflammation after cataract surgery. It is a promising substitute for standard eyedrop therapy, especially for patients who have poor compliance with eyedrop usage.

Topical ayurvedic ointment-induced chemical injury presenting as bilateral acute keratitis.

A 40-years-old female patient was referred to the cornea clinic as a probable case of bilateral keratitis. The patient had a history of headache followed by acute onset of redness, pain and discharge from both eyes for 15 days. The patient was diagnosed as bilateral keratitis by the first contact physician and was started on topical antibiotics, cycloplegics and lubricating eye-drops. At presentation, both eyes had visual acuity of perception of light, conjunctival congestion, limbal blanching, diffuse corneal oedema and epithelial defect. A detailed history revealed application of Vicks VapoRub [topical ayurvedic analgesic which contains (per 100 g of product) menthol (2.82 g), camphor (5.25 g) and eucalyptol (1.49 mL) and excipients include thymol (0.1 g), turpentine oil (5.57 mL), nutmeg oil (0.54 mL), cedar wood oil and petrolatum)] on the forehead and eyelids for headache several times over 2-3 days before the onset. The patient further confirmed the accidental application of the ointment in the eyes. A provisional diagnosis of acute chemical injury with Vicks VapoRub was made and treatment with topical antibiotic, cycloplegic, steroid, lubricant and vitamin C was started. On follow-up, both eyes showed gradual resolution of corneal oedema and epithelial defect. Visual acuity improved in the left eye to 6/60 with no change in right eye due to corneal haze.

Coenzyme Q10 in the Treatment of Corneal Edema in Kearns-Sayre: Is There an Application in Fuchs Endothelial Corneal Dystrophy?

PURPOSE: Corneal involvement in mitochondrial disease is seldom described. Kearns-Sayre syndrome (KSS) is a mitochondrial disorder characterized by retinitis pigmentosa, external ophthalmoplegia, and heart block. We report 2 patients with KSS with corneal lesions involving the endothelium, which improved with Coenzyme Q10 (CoQ10). Based on recent research regarding the role of dysfunctional oxidative metabolism in Fuchs Endothelial Corneal Dystrophy (FECD), we propose that mitochondrial diseases and FECD share a final pathway. METHODS: A chart review was performed and a review of the literature was completed with a PubMed search using the terms "Kearns-Sayre Syndrome", "mitochondria", "endothelium", "Fuchs endothelial corneal dystrophy", and "cornea". RESULTS: There are 19 reports of corneal involvement in clinical phenotypes of mitochondrial disease. Nine of these 19 cases had findings consistent with KSS. Our patients with KSS had microcystic changes throughout the cornea and excrescences on the endothelial surface seen with ultrasound biomicroscopy, similar to the clinical findings in FECD. CoQ10 improved corneal disease in both children. CoQ10 deficiency has been reported in a variety of mitochondrial diseases, and efficacy of supplementation has been demonstrated. It may be beneficial in these patients because of its antioxidant properties and role in oxidative phosphorylation. CONCLUSIONS: The common deletion found in patients with KSS has recently been implicated in FECD, which has recently been shown to be a disease related to dysfunctional oxidative metabolism. Future research should explore the use of antioxidants, such as CoQ10 in patients with FECD.

Protective effects of dispersive viscoelastics on corneal endothelial damage in a toxic anterior segment syndrome animal model.

PURPOSE: We evaluated whether viscoelastics have protective effects on the corneal endothelial cell damage in a toxic anterior segment syndrome (TASS) animal model depending on the types of viscoelastics. METHODS: A TASS animal model was established with an injection of 0.1 mL o-phthaldehyde solution (0.14%) into the anterior chamber of New Zealand white rabbits. One of two different viscoelastics, 1% sodium hyaluronate (cohesive group) or a 1:3 mixture of 4% chondroitin sulfate and 3% sodium hyaluronate (dispersive group), was injected into the anterior chamber. After five minutes, it was removed using a manual I/A instrument, and then 0.1 mL of o-phthaldehyde solution (0.14%) was injected into the anterior chamber. Damage to corneal endothelial cells was compared between the two groups. RESULTS: The corneal thickness increased quickly in both groups after the disinfectant injection. However, the dispersive group showed relatively mild corneal edema compared to the cohesive group. The mean corneal haze score in the dispersive group also was lower than that of the cohesive group. These partial protective effects of the dispersive viscoelastic were demonstrated by the different findings of a live/dead cell assay, TUNEL staining, and scanning electron microscopy between the two groups. CONCLUSIONS: The TASS animal model seems to be a useful means to evaluate corneal endothelial cell damage caused by toxic substances to find ways to protect or reduce endothelial cell damage. Dispersive viscoelastics were shown to have partial protective effects against corneal endothelial cell damage caused by a toxic disinfectant.

Corneal endothelial cytotoxicity of the Calotropis procera (ushaar) plant.

PURPOSE: To report 6 eyes of 5 patients with transient corneal edema after exposure to the milky latex of Calotropis procera (ushaar). METHODS: Interventional case series. RESULTS: Intracorneal penetration of ushaar latex can lead to permanent endothelial cell loss with morphologic alteration. Corneal edema resolved completely in approximately 2 weeks in all cases, despite reduced endothelial cell count and abnormal morphology. CONCLUSIONS: Corneal endothelial toxicity of ushaar latex is caused by its ability to penetrate the corneal stroma and induce permanent loss of endothelial cells. Corneal edema resolves if sufficient endothelial cell viability is still present after resolution of ushaar keratitis.

Euphorbia lactea sap keratouveitis: case report and review of the literature.

PURPOSE: To describe a case of Euphorbia lactea sap keratouveitis and to review all reported cases of ocular toxicity caused by Euphorbia species. METHODS: Case report and review of literature. RESULTS: A 79-year-old woman presented 34 hours after she felt some sap of an E. lactea plant spray into her right eye. Visual acuity was counting fingers at 1 m. Examination revealed ciliary injection, 90% corneal epithelial defect, marked stromal edema with Descemet folds, and anterior-chamber flare with a 1-mm hypopyon. There was no vitreitis, and funduscopy was unremarkable. No foreign body was seen on B scan ultrasound or computed tomography scan of the orbits. Corneal scraping excluded bacterial and herpetic keratitis. Intensive topical antibiotic therapy was started with cephalothin 5% and gentamicin 0.9%, and the pupil was dilated with atropine. Topical steroids were started once the epithelial defect had healed. Examination 11 weeks after the injury revealed minimal subepithelial corneal haze and marked improvement in visual acuity. CONCLUSIONS: To the best of our knowledge, this is only the third reported case of E. lactea sap keratouveitis. The clinical course of E. lactea sap keratouveitis is compared with that reported for other Euphorbia species.

Calotropis procera (ushaar) keratitis.

PURPOSE: To report a case of permanent endothelial cell injury after intracorneal penetration of milky latex from Calotropis procera (ushaar). DESIGN: Interventional case report. METHODS: A 40-year-old patient developed painless corneal edema despite minimal epithelial injury after exposure to ushaar latex. RESULTS: Confocal and specular microscopy confirmed permanent endothelial cell loss with morphologic alteration after intracorneal penetration of ushaar latex. Corneal edema resolved completely after 2 weeks, although reduced endothelial cell count and abnormal morphology persisted. CONCLUSION: Ushaar latex is capable of penetrating the corneal stroma and inducing permanent loss of endothelial cells. Corneal edema resolves if sufficient endothelial cell viability is still present after resolution of ushaar keratitis.

[The role of Brinzolamide 1% ophtalmic suspension in corneal edema]. / Utilizarea suspensiei de Brinzolamida 1% în edemul corneean--studiu experimental pe animale de laborator.

PURPOSE: The study is aimed at assessing the efficacy and safety of topical carbonic anhydrase inhibitor (IAC--i.e. ophthalmic suspension of brinzolamide 1%--Azopt) in the treatment of corneal edema. METHOD: For this purpose, we carried out an experimental, epidemiological-operational, randomised, placebo-controlled and double blind study, on three groups of laboratory animals (rabbits): group 1 (5 rabbits) included endothelial corneal injuries inflicted by ultrasound exposure by means of a phacoemulsification sound in both eyes group 2 (5 rabbits) included endothelial corneal injuries inflicted by direct trauma in both eyes group 3 (3 rabbits)--no endothelial corneal lesions (control group) In each group we instilled, all the animals, with ophthalmic suspension of brinzolamide 1% (Azopt), 1 drop t.i.d., in one eye for 14 days (starting the following day after infliction of endothelial injuries, when the corneal edema was evidenced by biomicroscopic examination) and placebo (saline solution 0.9% with the same osmolar and pH values as the Azopt) in the other eye. The assessment was performed throughout the following stages: To: preceding the infliction of corneal endothelial injuries, resorting to: biomicroscopic examination ultrasound pahimetry direct specular microscopy T1: the following day after infliction of corneal endothelial injuries, resorting to: biomicroscopic examination (the assessment of corneal edema) ultrasound pahimetry (measurement of corneal thickness and, hence edema) direct specular microscopy (cell density and endothelial ultrastructure evaluation: cellular polimegetism, pleiomorphism) T2: in the wake of 14 days therapy (after eye removal), adding to the previous examinations: indirect specular microscopy (with the same aim as the direct examination, yet examination carried out from the endothelial side) pathologic examination (using hematoxilin-eosin dye and Van-Gieson dye).

Hyperbaric oxygen therapy in the treatment of secondary keratoendotheliosis.

We evaluated the effectiveness of hyperbaric oxygen therapy in the treatment of keratoendotheliosis secondary to surgical treatment. A total of 33 patients were randomized to two arms of this study. The first arm consisted of 12 patients treated with pharmacologic therapy and hyperbaric oxygen daily for ten days. The second arm consisted of 21 patients treated with pharmacologic therapy alone (control group). Our evaluation of the results was based on testing visual acuity, grading of corneal alterations, and pachymetry findings. Hyperbaric oxygen treatment was effective in reducing corneal edema, particularly when administered early. Corneal neovascularization did not occur in any patient treated with hyperbaric oxygen.