Drug-Induced Cataract

Several drugs and exposures induce lens opacities, mostly by direct toxicity, oxidative damage or osmotic injury. Risk depends on dose, duration and individual susceptibility.

• Corticosteroids (all routes: oral, inhaled, nasal, topical eye, periocular and intravitreal, dermal): posterior subcapsular cataract. Risk increases with daily prednisolone doses over 10 mg for more than 1 year, but can occur sooner, and in children.
• Amiodarone: anterior subcapsular deposits (vortex keratopathy and anterior lens opacity).
• Phenothiazines (chlorpromazine over 500 mg daily for years): anterior stellate pigment deposits.
• Busulfan and other alkylating agents; allopurinol (long term, high doses); tamoxifen (crystalline retinopathy and subcapsular opacities); statins (association only); miotics (echothiophate iodide, pilocarpine: anterior vacuoles); chlorpromazine; gold; psoralen with ultraviolet A therapy; isotretinoin (rare).
• Ionising radiation (cranial irradiation, bone marrow transplant conditioning; threshold about 2 Gy acute, with posterior subcapsular cataract), infrared, and ultraviolet B light.
• Smoking and heavy alcohol are risk factors.

• Gradual loss of vision, glare, and trouble reading in bright light as posterior subcapsular opacities enlarge.
• Posterior subcapsular plaque (granular, vacuolated, with a central "breadcrumb" pattern) in steroid cataracts; anterior stellate subcapsular deposits in phenothiazine and amiodarone use.
• Often bilateral, reversing in some early drug induced forms if the drug is stopped, especially in children.
• Associated drug side effects: raised intraocular pressure with corticosteroids; retinal toxicity with tamoxifen and chloroquine.

• Medication history: agent, route, dose, duration, and cumulative exposure, including inhaled and topical steroids.
• Slit lamp examination under dilation, including retroillumination of the posterior capsule.
• Intraocular pressure and optic disc in steroid use; dilated fundus and optical coherence tomography.
• Radiation exposure history.
• Differentiate from diabetic, myopic, uveitic and age related posterior subcapsular cataract.

• Identify and reduce or stop the causative drug where possible: use the lowest effective steroid dose, alternate day dosing, steroid sparing agents (methotrexate 15 to 25 mg weekly, azathioprine 2 mg/kg daily, mycophenolate 1 g twice daily), inhaled steroid with spacer and mouth rinse, and replace topical steroid with loteprednol or an NSAID where suitable.
• Switch amiodarone or phenothiazine only if clinically safe; discuss with the prescribing physician.
• Regular ophthalmic surveillance (every 6 to 12 months) for patients on long term steroids, monitoring cataract, pressure and optic disc.
• Radiation: protective measures, and lens shielding for therapy where feasible.
• Cataract surgery when visual function falls: phacoemulsification with intraocular lens; anticipate zonular weakness in some, and postoperative inflammation and cystoid macular oedema with prophylaxis (prednisolone acetate 1 percent tapered, nepafenac 0.1 percent).
• Posterior capsule opacification is common (especially in young patients), treated by laser capsulotomy.
• Paediatric steroid cataracts: early surgery and amblyopia therapy.