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.

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.

Inadvertent intracorneal injection of local anesthetic during lid surgery.

PURPOSE: To report a case of inadvertent intracorneal injection of anesthetic agents during lid anesthesia and corneal penetration without full-thickness perforation. METHOD: Case report. RESULTS: Corneal edema with acute loss of vision was noted. The patient was treated with topical, antibiotic, cycloplegic, hyperosmotic agent and lubricant. While the edema slowly subsided, a loss in endothelial cell count was noted. CONCLUSIONS: The effects of intracorneal injection of lignocaine, bupivacaine, and its preservatives have not previously been reported in the literature. A lower postinjection endothelial cell count and associated clinical features in our case indicate that endothelial toxicity occurred. This potential complication should be kept in mind with necessary precautions taken during injection of the eyelid, particularly in cases with preexisting lid laxity.

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.

Severe corneal toxicity after topical fluoroquinolone therapy: report of two cases.

PURPOSE: To describe 2 cases of sterile corneal ulcers that persisted after several weeks of therapy with topical moxifloxacin 0.5% but that resolved when antibiotic therapy was changed. METHODS: Small case series. RESULTS: Both cases presented here describe corneal ulcers that persisted and showed signs of worsening during weeks of frequent topical dosing with moxifloxacin. Descemet folds and an atypically large amount of stromal edema were present in both cases, and there appeared to be possible endothelial dysfunction as well. There was no sign of bacterial, viral, or fungal infection in either case. In both cases, healing began a few days after moxifloxacin was discontinued, and topical gatifloxacin and corticosteroids were initiated. CONCLUSION: These cases suggest that moxifloxacin may interfere with the healing of corneal ulcers.

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.

Corneal endothelial safety of intracameral preservative-free 1% xylocaine.

PURPOSE: To evaluate the effect of intracameral preservative-free 1% xylocaine on the corneal endothelium as an adjuvant to topical anaesthesia during phacoemulsification and Acrysof foldable IOL implantation. MATERIAL & METHODS: This is a prospective, controlled, randomised, double-masked study. 106 patients with soft to moderately dense (Grade 1-3) senile cataract and corneal endothelial cell density of >1500/mm2 were randomised to the xylocaine group (n=53) and control group(n=53). Central endothelial specular microscopy and ultrasound corneal pachymetry were performed preoperatively. On the first postoperative day the eyes were evaluated for corneal oedema and Descemet's folds. Ultrasound corneal pachymetry was performed at 1, 3 and 12 months. Specular microscopy was performed at 3 and 12 months. Cell loss was expressed as a percentage of preoperative cell density. Six patients could not complete one year follow-up. Chi-square and paired t test (2 tail) statistical tests were applied for analysis. RESULTS: Four (7.54%) patients in the xylocaine group and 5 (9.43%) in the control group had a few Descemet's folds associated with mild central stromal oedema. Corneal thickness increased from 549.3micro +/- 37.2micro to 555.5micro +/- 36.5micro in the xylocaine group and from 553.1micro +/- 36.2micro to 559.3micro +/- 40.5micro in the control group at the one-month postoperative visit. Thickness returned to the preoperative level in xylocaine group 549.6micro +/- 34.5micro and control group 554.7micro +/- 41.1micro at three months. (P=0.484) The percentage of cell loss was 4.47 +/- 2.53% in the xylocaine group and 4.49 +/- 3.09% in the control group at one year. (P=0.97) CONCLUSION: Intracameral preservative-free 1% xylocaine does not appear to affect corneal endothelium adversely during phacoemulsification.

The effect of photodynamic therapy with rose bengal on posterior capsule opacification in rabbit eyes.

We investigated the in vivo effect of photodynamic therapy (PDT) using rose bengal on the development of posterior capsule opacification (PCO). Endocapsular phacoemulsification was performed on white rabbits, which were divided into 4 groups: control group; group 1, treated with visible light only; group 2, treated with rose bengal only, and group 3, treated with PDT. In the case of the PDT group, rose bengal dissolved in sodium hyaluronate was injected into the empty capsular bag and treated with visible light. Three months after surgery, the rabbits were sacrificed and the eyeballs enucleated. The obstruction rate of visible light caused by PCO was measured with an optical powermeter. The mean obstruction rate was 30.6% in the control group, 28.3% in group 1, 19.3% in group 2, and 14.3% in group 3. Group 3 showed a statistically significant decrease in PCO compared with the control group and group 1 (p = 0.0014). Our results suggest that PDT using rose bengal effectively decreased PCO in rabbit eyes.

Suppression of croton oil-induced rabbit corneal edema by sideritis javalambrensis.

This investigation was designed to evaluate the anti-inflammatory activity of the aqueous and hexane extracts of Sideritis javalambrensis, to which pharmacological properties have been attributed in Spanish traditional medicine. The extracts were applied as eye drops in a croton oil-induced corneal edema model in rabbits. Corneal thickness was estimated before the induction of inflammation and 3, 6, 8, 12, 48, 72 and 96 h after induction. Significant inflammation inhibition percentages were shown during both the acute and chronic stages of inflammation by both extracts and by the reference drug dexamethasone, with most therapeutic effect shown during the chronic phase. However, the hexane extract exhibited potent anti-inflammatory activity from 6 to 24 h post-induction, achieving greater percentage inhibition values during this stage than those obtained for dexamethasone.

Ecbalium elaterium (squirting cucumber)--remedy or poison?

BACKGROUND: Ecbalium elaterium is a plant endemic to the Mediterranean basin. Its roots and cucumber-shaped fruit have been used in folk medicine since antiquity. The alleged uses of the fruit juice are as a potent cathartic, analgesic, and antiinflammatory agent. Cucurbitacin B, a triterpene derivative is the active antiinflammatory principal. PATIENTS: We present a series of 13 patients who were exposed to the juice of Ecbalium elaterium in its natural form. In 3 patients, exposure was intranasal for the treatment of sinusitis or liver cirrhosis. In 3 other cases, children ingested the fruit unwittingly. In 6 patients, exposure was ocular and, in one, dermal. Within minutes of exposure, the patients exhibited irritation of mucous membranes at various degrees of severity manifested as edema of pharynx, dyspnea, drooling, dysphagia, vomiting, conjunctivitis, corneal edema, and erosion, depending on the route of the exposure. Recovery began within several to 24 hours after administration of oxygen, steroids, antihistamines, and beta-2-agonists. Ocular exposures responded to topical steroid and antibiotic eyedrops within a few days. The toddler with the dermal exposure remained asymptomatic. CONCLUSION: Exposure to the juice of Ecbalium elaterium, mainly in its undiluted form, may cause irritation of mucous membranes, supposedly of inflammatory nature. Patients exposed orally or intranasally should be closely followed for upper airway obstruction. Patients exposed ocularly should have their eyes promptly irrigated to prevent corneal and conjunctival injury.

Comparison of preservative-free bupivacaine vs. lidocaine for intracameral anesthesia: a randomized clinical trial and in vitro analysis.

PURPOSE: To determine whether intracameral bupivacaine hydrochloride 0.5% is as effective as lidocaine hydrochloride 1.0% in controlling discomfort of patients during phacoemulsification and posterior chamber intraocular lens implantation. In rabbits, corneal endothelial cell function, ultrastructure, and viability were evaluated after in vitro perfusion of bupivacaine 0.5%. METHODS: In a double-masked, controlled trial, 48 eyes of 48 patients with uncomplicated age-related cataract were randomly assigned to receive bupivacaine 0.5% or lidocaine 1.0% intracamerally before phacoemulsification with a posterior chamber intraocular lens. Outcome measures such as pain, visual acuity, amount of sedation, length of surgery, pupil size, intraocular pressure, corneal clarity, and anterior chamber reaction were compared. In laboratory studies, paired rabbit corneas were evaluated by endothelial cell perfusion with either bupivacaine 0.5%, bupivacaine 0.5% and glutathione bicarbonate Ringer solution in a 1:1 ratio or bupivacaine 0.5% buffered to a pH of 7.0. The paired control corneas were perfused with glutathione bicarbonate Ringer solution and rates of corneal swelling were determined. Cell ultrastructure and viability were also evaluated. RESULTS: In the randomized trial, there was no significant difference in the pain patients had during surgery or in the early or late postoperative period. No statistically significant difference was seen between the two groups in terms of pupil size, intraocular pressure, corneal edema, anterior chamber reaction, or visual acuity immediately after the operation or on postoperative day 1. Paired rabbit corneas perfused with bupivacaine 0.5% and bupivacaine 0.5% buffered to a pH of 7.0 swelled significantly (P<.001, P = .009, respectively), and had corneal endothelial cell damage. Dilution of the bupivacaine 1:1 with glutathione bicarbonate Ringer solution prevented corneal edema and damage to the corneal endothelium. Endothelial cell viability was also decreased after perfusion of bupivacaine 0.5% (P<.001). CONCLUSIONS: Clinically, bupivacaine 0.5% is as effective as lidocaine 1.0% for anesthesia during phacoemulsification and posterior chamber intraocular lens implantation. However, in vitro perfusion of bupivacaine 0.5% damaged the corneal endothelium of rabbits except when the drug was diluted 1:1 with glutathione bicarbonate Ringer solution. Surgeons who use 0.2 to 0.5 ml of intracameral bupivacaine 0.5% should be aware of its potential to cause endothelial cell damage because of its lipid solubility. The bupivacaine 0.5% should be diluted at least 1:1 with balanced salt solution before intracameral injection, followed immediately by phacoemulsification. The surgeon should ensure that the bupivacaine 0.5% is nonpreserved and packaged in single-use vials or flip-top containers.

Ocular inflammation models by topical application: croton-oil induced uveitis.

PURPOSE: The aim of the present investigation was to develop a new ocular inflammation model in the rabbit by comparison of the inflammation response induced by the topical application of several irritating agents (carrageenan, Freund's adjuvant, alkali and croton oil). METHODS: The following parameters were determined after the application of each irritant to the eyes of female, white, New Zealand rabbits: Corneal edema and the Tyndall effect (slit-lamp biomicroscopy), corneal thickness (biometer-pachometer) and aqueous humor levels of the prostaglandin E2 (R.I.A), total protein (Weichselbaum technique), albumin, albumin/globulin (Doumas technique) and leukocytes (coulter counter). RESULTS: Croton oil 1-4% (40 microl) produced edema and a Tyndall which showed a proportional increase with croton oil concentration. Ultrasonic pachometer measurement of the variation in corneal thickness (3-168 h) showed a dose-dependent response (p<0.01) from the 8th to the 168th hour. Uveitis and considerable increases in the levels of the prostaglandin E2 (4.50+/-0.40 pg/0.1 ml vs. 260.03+/-2.03 pg/0.1 ml), total protein (0.25+/-0.05 g/l vs. 2.10+/-0.08 g/l), albumin, albumin/globulin and leukocytes were observed in the aqueous humor 24 h after topical application of croton oil 3% (40 microl). All the values obtained were statistically significant (p<0.01). CONCLUSIONS: The topical application of 3% croton oil (40 microl) was most appropriate for the evaluation of the inflammatory process in the anterior chamber and for the determination of the effects of intraocular penetration. The inflammatory mechanism in this model is thought to involve the activation of the arachidonic acid pathway accompanied by the breakdown of the blood-aqueous barrier permitting high molecular weight proteins to enter the aqueous humor. Typology: anterior uveitis with corneal edema.

Corneal endothelial toxicity of topical anesthesia.

PURPOSE: To determine the relative corneal endothelial toxicities of the following topical anesthetic agents: bupivacaine HCl 0.75%, unpreserved lidocaine HCl 4%, proparacaine HCl 0.5%, and tetracaine HCl 0.5%. METHODS: The experiment was conducted using pigmented rabbits. Approximately nine animals each were randomly assigned to eight groups. Right eyes received injections of 0.2 ml of one of the four anesthetic agents at one of two concentrations and left eyes received injections of 0.2 ml of balanced salt solution. Corneal thickness and clarity were measured before surgery and on postoperative days 1, 3, and 7. RESULTS: A statistically significant increase (P < 0.05) in corneal thickness and opacification over preoperative measurements was noted with injections of bupivacaine, lidocaine, and proparacaine, controlling for changes occurring in control eyes from surgery alone. Proparacaine was statistically more toxic than were the others. The toxicity of tetracaine was statistically indistinguishable from balanced salt solution, although mild toxicity was evident clinically. Injection of 1:10 dilutions of the same anesthetic agents failed to produce a statistically significant increase in corneal thickness or opacification on any postoperative examination. CONCLUSIONS: Anterior chamber injection of bupivacaine HCl 0.75%, unpreserved lidocaine HCl 4%, and proparacaine HCl 0.5% produces corneal thickening and opacification that is clinically and statistically significant. Tetracaine HCl 0.5% injection produces corneal thickening and opacification that is clinically apparent in some eyes but statistically insignificant. Ophthalmic surgeons should be aware of the potential for endothelial cell injury if anesthetic agents enter or are injected into the eye during cataract surgery in the concentrations supplied commercially.