Frog saliva-induced toxic keratopathy: a case report.

Corneal toxicity due to exposure to many chemicals and medications have been described in the literature. We present a case of toxic keratopathy by corneal exposure to salivary secretion of a frog. A 40-year-old male patient reported a sudden splash of frog saliva in his right eye while he was examining it at a close distance. Corneal punctate epitheliopathy and stromal oedema and Descemet folds were the initial clinical findings, which completely recovered on the 2nd control day of topical dexamethasone and ofloxacin treatment. We aimed to show the toxic effects of animal-derived secretions on the cornea as a rare cause of toxic keratopathy.

Corneal Toxicity Secondary to Latex From Asclepias curassavica in a Pediatric Patient.

PURPOSE: To report a case of corneal milkweed toxicity on the corneal endothelium with epithelial damage in a pediatric patient. METHODS: We report a case of a 13-year-old boy who presented to the emergency department with complaints of left eye pain and photophobia after direct corneal exposure to milkweed latex. He was found to have a large corneal epithelial defect and diffuse stromal edema suspected to be secondary to the cardiac glycosides present in the milkweed plant. Clinical examination and course are reported. RESULTS: The patient was seen in the outpatient clinic on multiple visits. His epithelial defect had resolved within 3 days, and all corneal damage had healed within 18 days from injury. He was treated with antibiotic and steroid eye drops. CONCLUSIONS: Corneal exposure to cardiac glycosides from milkweed plants is known to damage the endothelial sodium-potassium pumps and to cause corneal edema and decreased visual acuity. All previously documented case reports of corneal milkweed toxicity are secondary to indirect exposure to the plant's latex. Here, we report the first case of corneal endothelial toxicity because of direct latex inoculation from an Asclepias plant and the first such toxicity reported in a pediatric patient.

Calotropis procera -induced keratitis.

Calotropis procera produces copious amounts of latex, which has been shown to possess several pharmacological properities. Its local application produces intense inflammatory response. In the 10 cases of Calotropis procera -induced keratitis reported here, the clinical picture showed corneal edema with striate keratopathy without any evidence of intraocular inflammation. The inflammation was reversed by the local application of steroid drops.

Ocular toxicity by latex of Calotropis procera (Sodom apple).

We report the spectrum of ocular toxicity following accidental inoculation of latex of Calotropis procera (Sodom apple) in 29 eyes between January 2003 and December 2006. All patients presented with sudden painless dimness of vision with photophobia. Twenty-five (86%) patients had initial visual acuity of less than 20/60. All eyes had conjunctival congestion and mild to severe corneal edema with Descemet's folds. Three (10%) eyes had an epithelial defect, nine (31%) had iridocyclitis, and seven (24%) had associated secondary glaucoma. After treatment with topical corticosteroids, antiglaucoma agents, cycloplegics, hypertonic saline and tears supplements, 27 (93%) eyes recovered completely within 3-14 days. After three months, 17 (74%) out of 23 eyes showed a significant low endothelial cell count compared to the normal fellow eye ( P 0.001). The latex of Calotropis procera causes significant ocular morbidity which may be preventable by simple health education. The long-term effect on corneal endothelium has to be studied further.

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.

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.

Phacomorphic Angle-closure Following Silicone Oil Tamponade in a Pediatric Patient.

PURPOSE: The purpose of this study was to report a case of phacomorphic glaucoma following retinal detachment repair with silicone oil (SO) in a pediatric patient. STUDY DESIGN: Case report. METHODS: A chart review was conducted at St. Michael's Hospital and The Hospital for Sick Children (Toronto, Canada), where the patient received ophthalmic care from July 28, 2015 onwards. RESULTS: A 14-year-old boy with a history of traumatic retinal detachment and proliferative vitreoretinopathy in the left eye, requiring 2 pars plana vitrectomies, membrane peel, and SO tamponade, presented with 1-day history of decreased vision in the left eye, severe headache, nausea, and vomiting. Visual acuity was hand motions; intraocular pressure (IOP) was 54 mm Hg; the pupil was middilated and minimally reactive with a reverse relative afferent pupillary defect. Slit-lamp examination revealed an injected eye with diffuse microcystic corneal edema, a shallow anterior chamber (AC), and an intumescent cataract. Gonioscopy demonstrated closed angles in 3 quadrants. Compared with his last examination 6 weeks prior, where only a mild posterior subcapsular cataract was noted, the patient's presentation was suggestive of rapid lens intumescence causing acute angle-closure glaucoma. He was given topical and systemic treatment, including intravenous mannitol, and his IOP reduced to 22 mm Hg after 7 hours. Urgent lensectomy was performed the following day. Preoperative ultrasound biomicroscopy revealed a greatly increased lens thickness of 5.12 mm and an AC depth of 1.12 mm. The integrity of both anterior and posterior lens capsules was confirmed intraoperatively, and SO remained confined to the posterior segment. Postoperatively, the iris returned to a normal configuration with open angles, and IOP was 16 mm Hg with no antiglaucoma medications at the last follow-up. CONCLUSIONS: Acute angle-closure in children is a rare event. To our knowledge, this is the first reported case of phacomorphic glaucoma secondary to vitreoretinal surgery in the pediatric population. Although uncommon, ophthalmologists should be aware of this potential complication with the intraocular use of SO and administer urgent treatment accordingly.

Corneal edema and permanent blue discoloration of a silicone intraocular lens by methylene blue.

BACKGROUND AND OBJECTIVE: To report a silicone intraocular lens (IOL) stained blue by inadvertent intraoperative use of methylene blue instead of trypan blue and the results of experimental staining of various lens materials with different concentrations of the same dye. MATERIALS AND METHODS: A "blue dye" was used to enhance visualization during capsulorhexis in a patient undergoing phacoemulsification with implantation of a three-piece silicone lens. Postoperatively, the patient presented with corneal edema and a discolored IOL. Various IOL materials were experimentally stained using methylene blue. Sixteen lenses (4 silicone, 4 hydrophobic acrylic, 4 hydrophilic acrylic, and 4 polymethylmethacrylate) were immersed in 0.5 mL of methylene blue at concentrations of 1%, 0.1%, 0.01%, and 0.001%. These lenses were grossly and microscopically evaluated for discoloration 6 and 24 hours after immersion. RESULTS: The corneal edema resolved within 1 month after the initial surgical procedure. After explantation, gross and microscopic analyses of the explanted silicone lens revealed that its surface and internal substance had been permanently stained blue. In the experimental study, all of the lenses except the polymethylmethacrylate lenses were permanently stained by methylene blue. The hydrophilic acrylic lenses showed the most intense blue staining in all dye concentrations. CONCLUSIONS: This is the first clinicopathological report of IOL discoloration due to intraocular use of methylene blue. This and other tissue dyes may be commonly found among surgical supplies in the operating room and due diligence is necessary to avoid mistaking these dyes for those commonly used during ocular surgery.

Toxic anterior segment syndrome and possible association with ointment in the anterior chamber following cataract surgery.

PURPOSE: To report clinical and laboratory findings of 8 cases of toxic anterior segment syndrome (TASS) related to an oily substance in the anterior chamber of patients following cataract surgery with intraocular lens (IOL) implantation. SETTING: John Moran Eye Center, University of Utah, Salt Lake City, Utah, USA. METHODS: Eight patients had uneventful phacoemulsification by the same surgeon via clear corneal incisions with implantation of the same 3-piece silicone IOL design. Postoperative medications included antibiotic/steroid ointment and pilocarpine gel; each eye was firmly patched at the end of the procedure. On the first postoperative day, some patients presented with diffuse corneal edema, increased intraocular pressure, and an oily film-like material within the anterior chamber coating the corneal endothelium. The others presented with an oily bubble floating inside the anterior chamber, which was later seen coating the IOL. Additional surgical procedures required included penetrating keratoplasty, IOL explantation, and trabeculectomy. Two corneal buttons were analyzed histopathologically. Two explanted IOLs had gross and light microscopic analyses (as well as surface analyses of 1 of them), and 4 other explanted IOLs had gas chromatography-mass spectrometry. RESULTS: Pathological examination of the corneas showed variable thinning of the epithelium with edema. The stroma was diffusely thickened and the endothelial cell layer was absent. Evaluation of the explanted IOLs confirmed the presence of an oily substance coating large areas of their anterior and posterior optic surfaces. Gas chromatography-mass spectrometry of the lens extracts identified a mixed chain hydrocarbon compound that was also found in the gas chromatography-mass spectrometry analyses of the ointment used postoperatively. CONCLUSIONS: The results indicate that the ointment gained access to the eye, causing the postoperative complications described. These cases highlight the importance of appropriate wound construction and integrity, as well as the risks of tight eye patching following placement of ointment.

Amines as occupational hazards for visual disturbance.

Various amines, such as triethylamine and N,N-dimethylethylamine, have been reported to cause glaucopsia in workers employed in epoxy, foundry, and polyurethane foam industries. This symptom has been related to corneal edema and vesicular collection of fluid within the corneal subepithelial cells. Exposure to amine vapors for 30 min to several hours leads to blurring of vision, a blue-grey appearance of objects, and halos around lights, that are probably reversible. Concentration-effect relationships have been established. The visual disturbance is considered a nuisance, as it could cause onsite accidents, impair work efficiency, and create difficulties in driving back home. Occupational exposure limits have been established for some amines, but there is shortage of criteria. Volatility factors, such as vapor pressure, should be considered in industrial settings to prevent human ocular risks, while trying to reduce levels of hazardous amines in the atmosphere.

Toxic Keratopathy Following the Use of Alcohol-Containing Antiseptics in Nonocular Surgery.

IMPORTANCE: Corneal abrasion is the most common ocular complication associated with nonocular surgery, but toxic keratopathy is rare. OBSERVATION: Three patients developed severe toxic keratopathy after orofacial surgery on the left side with general anesthesia. All patients underwent surgery in the right lateral tilt position with ocular protection but reported irritation and redness in their right eyes after the operation. Alcohol-containing antiseptic solutions were used for presurgical preparation. Ophthalmic examination showed decreased visual acuity ranging from 20/100 to 20/400, corneal edema and opacity, anterior chamber reaction, or stromal neovascularization in the patients' right eyes. Confocal microscopy showed moderate to severe loss of corneal endothelial cells in all patients. Despite prompt treatment with topical corticosteroids, these 3 patients eventually required cataract surgery, endothelial keratoplasty, or penetrating keratoplasty, respectively. After the operation, the patients' visual acuity improved to 20/30 or 20/40. Data analysis was conducted from December 6, 2010, to June 15, 2015. CONCLUSIONS AND RELEVANCE: Alcohol-containing antiseptic solutions may cause severe toxic keratopathy; this possibility should be considered in orofacial surgery management. Using alcohol-free antiseptic solutions in the periocular region and taking measures to protect the dependent eye in the lateral tilt position may reduce the risk of severe corneal injury.

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.

Ocular toxicity of low-molecular-weight components of silicone and fluorosilicone oils.

Silicone oil (SiO) and fluorosilicone oil (FSiO) are injected into the vitreous cavity in difficult cases of retinal detachment surgery. SiO and FSiO contain linear and cyclic low-molecular-weight components (LMWC) that are thought to cause ocular toxicity. Using the purified oils (without LMWC) and some of the individual LMWC, the authors evaluated the relation of the LMWC to the short-term ocular toxicity of the oils. When octamethylcyclotetrasiloxane or other single small species of linear and cyclic LMWC of SiO were injected into the rabbit anterior chamber, severe inflammation and corneal edema were induced. The ocular responses to the single species of the LMWC of SiO decreased with an increase of the molecular weights. Cyclic LMWC of FSiO (a mixture of trimethyl-3,3,3-trifluoropropylcyclotrisiloxane and tetramethyl-3,3,3-trifluoropropylcyclotetrasiloxane) also induced inflammation and corneal edema. However, unpurified SiO and FSiO, as well as purified oils (via solvent fractionation), did not cause significant adverse ocular response, presumably because the amounts of LMWC (especially the smallest species) in the oils were relatively small. Using gas chromatography, the authors analyzed SiO and FSiO recovered from rabbit and human vitreous cavities up to 2 yr after injection. In most of the cases, the concentrations of LMWC in SiO decreased after injection. This is consistent with the possibility that LMWC diffused from the oils into the ocular tissues. The long-term effect of LMWC in intraocular SiO and FSiO has not been determined. However, diffusion of LMWC into ocular tissues may relate to the chronic ocular toxicity of the oils.

The effect of povidone iodine on the corneal endothelium.

PURPOSE: Povidone iodine has been proven to be a valuable antiseptic solution in preparing the eye for surgery and is an alternative to postoperative topical antibiotics. No study has addressed the intraocular toxicity of povidone iodine after injection into the anterior chamber. We investigated the potential toxicity of povidone iodine on the corneal endothelium after injections into the anterior chamber in a rabbit model. METHODS: In this study we used 24 eyes of 12 albino rabbits. The eyes were divided into the following three groups according to the drugs tested: group A, 5% povidone iodine; group B, 10% povidone iodine; group C, balanced salt solution. The injected eyes were evaluated by biomicroscopy, specular microscopy, corneal pachymetry, and transmission and scanning electron microscopy. RESULTS: Corneal edema was observed in all eyes of groups A and B. In groups A and C, the endothelial cell morphology was not significantly changed and the mean endothelial cell count of the eyes did not change significantly (p = 0.5054). There was no significant difference in corneal thickness between groups A and C (p = 0.3823), but there was a significant difference between groups B and C ( = 0.0002). Transmission and scanning electron microscopy results were normal in group C but not in groups A and B. CONCLUSION: Povidone iodine in both 5% and 10% concentrations demonstrates severe toxicity when one drop of either concentration is placed directly in the anterior chamber. When povidone iodine is used in preparing the eye for intraocular surgery and as an alternative to postoperative antibiotics, the inadvertent leakage of povidone iodine into the anterior chamber must definitely be prevented.

Silicone oil-induced corneal hydrops?

A 27-year-old man with a personality disorder, who did not have keratoconus previously, recently presented with a clinical picture resembling acute corneal hydrops OS three years after silicone oil injection for a complicated retinal detachment. Although self-induced trauma could not be excluded completely, this case might represent a newly described late corneal complication of intracameral silicone oil.

Role of toxic ingredients in silicone oils in the induction of increased corneal endothelial permeability.

Silicone oils may induce pathological changes in corneas or retinas by unknown mechanisms but the effects are probably related to certain specific components. Low molecular weight compounds have been implicated in the induction of toxic tissue reactions. Several of these components, that occur as contaminants or by-products in crude silicone oils, were tested for their ability to alter corneal endothelial permeability. In vitro inulin/dextran permeability was measured after one week of in vivo exposure to a non-toxic oil to which various low molecular weight components were added. At least 75% of the anterior chamber volume was replaced with oil +/- additives. A long-chain silanol-terminated polydimethylsiloxane (1000 cps) at 2 mg/ml, tetramethyl-ammonium siloxanolate (a catalyst) at 1 mg/ml and a mixture of a series of linear compounds (MM through MD10M) each at 10 mg/ml all caused a large corneal endothelial permeability increase. A mixture of two short-chain silanol-terminated compounds was less damaging, as was a mixture of a cyclic series. Evidently certain compounds can induce toxic effects on the corneal endothelium whereas other compounds are much less toxic. The linear series and the catalyst, that induce corneal endothelial changes, have been shown to occur in silicone oils.

Intraocular tolerance to silicone oils of different specific gravities. An experimental study.

Different methylphenylsilicone (MPS) and fluorosilicone (FS) oils having a higher specific gravity than water were investigated as vitreous replacements. Their intraocular tolerance in vitrectomized aphakic rabbit eyes was evaluated for periods of up to 4 months and compared to that of regular polydimethylsilicone oil (PDMS). Weakly fluorinated FS and weakly phenylated MPS showed a presumably toxic effect on the retina. As compared to highly fluorinated FS, highly phenylated MPS showed better intraocular tolerance; however, inflammatory reaction was slightly more extensive than in eyes filled with PDMS.

Acute corneal decompensation after silicone oil removal.

PURPOSE: To assess acute corneal decompensation after silicone oil removal in some aphakic eyes with clear corneas whose anterior chambers were completely filled with silicone oil for a considerable period of time. METHODS: Eight eyes of 8 patients who underwent vitrectomy and intraocular silicone oil injection were studied. All the eyes were aphakic and anterior chambers were completely filled with silicone oil. In all eyes, corneas were clear and no corneal finding indicating keratopathy was detected by slit-lamp microscopy before silicone oil removal. The mean silicone oil removal time was 4 months (range 2-7 months). A specular microscope was used for the evaluation of corneal endothelial changes and corneal pachometry was performed to observe corneal changes before and after the silicone oil removal in 5 eyes besides slit-lamp microscopy. The follow up period after silicone oil removal was 2-12 months (mean 6 months). RESULTS: In all eyes severe corneal stromal edema and clouding was detected in the first day following silicone oil removal. Increased corneal thickness was seen in all eyes. Decreased (at or below critical levels) corneal cell density was detected by specular microscopy before and after silicone oil removal. No significant improvement was observed during the follow up period. CONCLUSION: Eyes whose anterior chambers completely filled with silicone oil could be evaluated as clear corneas by slit lamp microscopy despite severe endothelial damage. We recommend that eyes with silicone oil in the anterior chambers should be monitored by a combination of slit-lamp microscopic examination and specular microscopy to determine the relative corneal endothelial tolerance to the silicone oil and endothelial damage. Early removal of the silicone oil can be considered when the retinal adhesion allows.