While beneficial therapeutically, almost all medications have untoward effects on various body tissues and functions, including the eye in which organ toxic reactions are readily detectable. Every part of the eye and all ocular functions could be affected adversely. In this review, we describe the most commonly recognized
drug-induced ocular disorders, their specific clinical features, the medications that can cause the problem, the differential diagnosis and possible mechanisms of action, as well as guidelines for the management of the adverse reactions. The eyelids are most frequently involved in
drug toxicity that commonly manifests as
inflammation,
hypersensitivity reaction or
dermatitis.
Drug-induced keratoconjunctival disorders present mainly as conjunctival hyperaemia (red eye), with or without superficial corneal involvement. Frequently,
drug preservatives in topical ocular medications induce these adverse effects. Treatment of
blepharospasm with
Botox may lead to drooping of the eyelids and corneal exposure. Intraoperative floppy iris syndrome is a
drug-induced reaction in patients treated with
tamsulosin and who undergo
cataract surgery. Certain sulfa-based drugs can cause swelling of the ciliary body and lead to the development of
angle-closure glaucoma. In addition,
adrenergic agents, certain beta(2)-adrenergic agonists and
anticholinergic agents may induce pupillary dilation and precipitate
angle-closure glaucoma in susceptible patients.
Glucocorticoids administered systemically, topically or intravitreally are known to increase intraocular pressure, which can lead to the development of
open-angle glaucoma in susceptible patients. This painless form of
glaucoma has also been associated with the use of the
anticancer agents docetaxel and
paclitaxel. The toxic effects of systemic and topically applied drugs may manifest as cloudiness of the lens. Long-term use of
glucocorticoids produces a characteristic posterior subcapsular
cataract and, although the opacities may remain stationary or progress, they rarely regress upon
drug withdrawal. Systemic administration of
phenothiazines or
busulfan induce cataractous changes in the anterior or posterior cortex, respectively. Many systemic drugs reach the retina through the vascular supply.
Aminoquinolines induce a characteristic bull's eye
maculopathy.
Phenothiazines bind to
melanin granules and can cause a severe phototoxic retinopathy. Typical
tamoxifen retinopathy manifests as crystalline deposits in the inner retina. Some patients treated with
retinoids have decreased night vision and abnormal dark-adaptation. Patients on long-term treatment with
linezolid may develop an
optic neuropathy (swollen or pale optic disc), symmetric painless decrease of visual acuity and colour vision, and bilateral visual field defects. A probable link exists between
amiodarone and a bilateral
optic neuropathy that is very similar to nonarteritic ischaemic
optic neuropathy (
NAION). The most common adverse effects of cGMP-specific
phosphodiesterase type 5 inhibitors (
erectile dysfunction drugs) are changes in colour perception, blurry vision and increased
light sensitivity; recently these drugs have been also implicated in the development of
NAION. A bilateral, retrobulbar
optic neuropathy that manifests as loss of visual acuity or colour vision and visual field defect is associated with the use of
ethambutol. Many different kinds of medications can cause similar ocular adverse reactions. Conversely, a single medication may affect more than one ocular structure and cause multiple, clinically recognizable disorders. Clinicians should be mindful of
drug-induced ocular disorders, whether or not listed in product package inserts, and, if in doubt, consult with an ophthalmologist.