Toxicology of the eye, third edition

Thomas, Charles C.

doi:10.3109/15569528709052171

Cited by 66 publications

(78 citation statements)

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“…4,5 Table 2 summarises the findings of this study, which was conducted in a tertiary referral centre, where 134/1024 (13.09%) of consecutive cases were classified as drug reactions. 1 Corneal involvement occurred in 119/134 (88%) of these cases and 38 (28%) had frank corneal epithelial defects or indolent ulcers. The commonest conjunctival reactions were toxic papillary, toxic follicular, and delayed hypersensitivity.…”

Section: Epidemiologymentioning

confidence: 98%

“…Benzalkonium side Eye effects include corneal vascularisation at high concentrations (0.1%), papillary conjunctivitis, punctate keratopathy, decreased epithelial microvilli reducing corneal wetting, it inhibits cell motility and healing, binds to soft contact lenses enhancing toxicity, causes allergic blepharoconjunctivitis, and has been associated with drug-induced pemphigoid. 1 Subclinical drug-induced scarring may occur without clinical inflammation, or clinically apparent scarring, in glaucoma patients on long-term miotic and nonmiotic therapy, such as phospholine iodide, pilocarpine, guanethidine, and adrenaline, although all topical antiglaucoma medications have to some degree been implicated. 12 While some shortening of the conjunctival fornix occurs with age, this is increased by topical therapy.…”

Section: Pathogenesismentioning

confidence: 99%

“…Toxic responses are often because of the preservatives (such as benzalkonium) or the excipients (such as EDTA) rather than the drugs, and drug information sheets often fail to supply relevant information regarding these. The effects of individual components may be established from pharmaceutical references and from those on side effects, for example Grants toxicology, 1 Martindale, 17 and the British National Formulary. 18 Easily accessible data on the probability for the development of an adverse reaction, or an index of toxicity, is not readily available from these sources either, and prediction of problems currently depends largely on clinical awareness and expertise.…”

Section: Predicting Toxic Reactionsmentioning

confidence: 99%

“…Classification systems for corneal toxicity are by disease, route of exposure and time course, or by agent 1,2 (see Table 1). The cornea may be involved alone or with the conjunctiva.…”

Section: Introductionmentioning

confidence: 99%

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Corneal toxicity: the epithelium and stroma in iatrogenic and factitious disease

Dart

2003

Eye

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Corneal toxicity is caused by chemical trauma and by iatrogenic and factitious disease, which are often overlooked, and which are reviewed here. The clinical signs of iatrogenic disease are usually nonspecific and identical to those resulting from other causes of surface disease. Factitious disease is either the result of mechanical trauma or the abuse of toxic eye drops. One epidemiological study, in a tertiary setting, identified 13% of keratoconjunctivitis cases as iatrogenic. Healing was prolonged taking 7-93 (median 28.5) days. Pathogenic mechanisms vary widely with different drugs and include subclinical scarring, pseudopemphigoid, drug-induced ocular cicatricial pemphigoid, and toxic follicular reactions. There is little readily available data either on the probability of the development of adverse reactions or for the comparison of different drugs. The assessment of the toxicity of topical drugs is currently by the Draize test in rabbits. New in vitro tests on human corneal epithelial cell cultures include ATP assays for cell viability, scanning EM of epithelial microvilli, and vital staining to assess cell membrane permeability and intracellular esterase. Despite their simplicity, these test systems can correlate well with clinical toxicity and provide a toxicity index for drug comparisons. Treatment requires drug withdrawal or substitution by nonpreserved and less toxic preparations. Factitious injury is rare, difficult to diagnose, and should only be considered when all other diagnoses have been excluded. Prevention requires a high level of awareness of the potential for iatrogenic disease, particularly in the high-risk setting of chronic ocular surface disease.

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Section: Epidemiologymentioning

confidence: 98%

Section: Pathogenesismentioning

confidence: 99%

Section: Predicting Toxic Reactionsmentioning

confidence: 99%

“…Classification systems for corneal toxicity are by disease, route of exposure and time course, or by agent 1,2 (see Table 1). The cornea may be involved alone or with the conjunctiva.…”

Section: Introductionmentioning

confidence: 99%

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Corneal toxicity: the epithelium and stroma in iatrogenic and factitious disease

Dart

2003

Eye

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“…Several systemic medications are known to cause ocular side-effects (Grant 1986;Fraunfelder & Meyer 1989;Imperia et al 1989;Pavan-Langston & Dunkel 1991;Rennie 1993;Novack 1997;Soukasian & Raizman 2000). Rifabutin, a broad spectrum antibiotic and inhibitor of RNApolymerase, is known to cause an anterior uveitis (Brogden & Fitton 1994; Ͻ8' Jacobs et al 1994;Saran et al 1994;Becker et al 1996;Chaknis et al 1996;Arevalo et al 1997;Fraunfelder & Rosembaum 1997), as well as a discoloration of skin and body fluids.…”

Section: Introductionmentioning

confidence: 99%

Retinal dysfunction and anterior segment deposits in a patient treated with rifabutin

Ponjavic

Gränse

Stigmar

et al. 2002

Acta Ophthalmologica Scandinavica

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ABSTRACT.Purpose: To describe the clinical and electrophysiological findings in a young boy with decreased vision possibly due to retinal damage by rifabutin. Methods: An 8-year-old boy with osteomyelitis was referred due to visual disturbance. During a period of 4 years, the boy was examined six times with electroretinography. Ophthalmological examination included testing of visual acuity, slit-lamp inspection, fundus inspection, fundus photography and kinetic perimetry. Two electrophysiological methods were performed for objective evaluation of retinal function, namely full-field electroretinography and multifocal electroretinography. Results: We found a slightly reduced visual acuity, a slowly increasing amount of yellow-white deposits on the posterior surface of the cornea and on the anterior part of the lens, a normal fundus appearance, and normal visual fields. However, the electroretinogram was abnormal on several occasions during therapy with rifabutin, but returned to normal 3 months after withdrawal of the medication. The multifocal electroretinogram returned to normal after the fullfield electroretinogram had done so. The anterior chamber deposits still remain. Conclusion: Long-term treatment with rifabutin may have a reversible and previously undescribed side-effect on retinal function. The drug may also accumulate irreversibly on the posterior surface of the cornea and on the anterior surface of the lens. We suggest that objective evaluation of retinal function with electrophysiological methods should be performed in patients with visual disturbance during treatment with rifabutin.

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The Spectrum of Ocular Inflammation Caused by Euphorbia Plant Sap

Eke

Al-Husainy²,

Raynor³

2000

Arch Ophthalmol

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To report the spectrum of clinical findings in patients with ocular inflammation caused by plant sap from Euphorbia species.Design: Clinical case series.Setting: Ophthalmology emergency referrals in the United Kingdom.Patients: We examined 7 patients, all of whom gave a history of recent ocular exposure to the sap of Euphorbia species.Interventions: All patients were treated with antibiotic drops or ointment (chloramphenicol). Cycloplegic and steroid drops were also used for some patients. Patients were observed until all signs and symptoms had resolved.Main Outcome Measures: Symptoms, visual acuity, and clinical signs of inflammation. All patients provided a specimen of the plant for formal identification.Results: Initial symptoms were generally burning or stinging pain with blurred vision. In most cases, visual acuity was reduced between 1 and 2 Snellen lines. In 1 patient with agerelatedmaculopathy,acuitydroppedfrom20/80tohandmotions before recovering. Clinical findings varied from a mild epithelial keratoconjunctivitis to a severe keratitis with stromaledema,epithelialsloughing,andanterioruveitis.Allsigns and symptoms had resolved by 1 to 2 weeks.Conclusions: These cases illustrate the range of severity of Euphorbia sap keratouveitis. The condition seems to be self-limiting when managed supportively. People who work with Euphorbia plant species should wear eye protection. Clinicians managing keratopathy caused by Euphorbia species should be aware of the danger of sight-threatening infection and uveitis, particularly during the first few days.

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Toxicology of the eye, third edition

Cited by 66 publications

References 0 publications

Corneal toxicity: the epithelium and stroma in iatrogenic and factitious disease

Corneal toxicity: the epithelium and stroma in iatrogenic and factitious disease

Retinal dysfunction and anterior segment deposits in a patient treated with rifabutin

The Spectrum of Ocular Inflammation Caused by Euphorbia Plant Sap

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