Eyelids
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Epidermal growth factor receptor inhibitors: used in the treatment of solid tumours and can cause: (a) trichomegaly, (b) blepharitis, (c) dry eye syndrome.
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Imatinib: used in the treatment of chronic myeloid leukaemia and gastrointestinal tumours. Mild periorbital oedema occurs in two thirds approximately 6 weeks after commencing treatment.
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Ipilimumab: used for metastatic melanoma. Symptoms and signs similar to thyroid eye disease may rarely occur.
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Bortezomib: used for multiple myeloma and predisposes to recurrent chalazia.
Cornea
Vortex keratopathy (cornea verticillata)
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Signs: (a) fine greyish or golden-brown opacities in the inferior corneal epithelium, (b) progressing to a whorl-like pattern that originates from a point below the pupil and swirls outwards, sparing the limbus ( Fig. 21.1A ). Vision is usually not impaired, but some patients may experience halos around lights.
Fig. 21.1
Drug-induced keratopathy: (A) amiodarone-induced vortex keratopathy stained with fluorescein, (B) chlorpromazine.
(From Salmon JF, Kanski’s Clinical Ophthalmology: A Systematic Approach , 9th edition. Oxford, UK: Elsevier; 2020.)
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Causes: amiodarone (the higher the dose and the longer the duration of use, the more substantial the changes), quinolone antimalarials (chloroquine, hydroxychloroquine). Usually reversible on cessation of medication. Also, a sign of Fabry disease.
Chlorpromazine
Long-term therapy may cause subtle and visually innocuous yellowish-brown granular deposits in the endothelium, Descemet membrane and deep stroma ( Fig. 21.1B ).
Argyrosis
Keratopathy in argyrosis (silver deposition) is characterized by greyish-brown granular deposits in Descemet membrane; conjunctival involvement may also occur.
Chrysiasis
Chrysiasis describes the deposition of gold in tissues after prolonged administration (chrysotherapy), usually in the treatment of rheumatoid arthritis. Keratopathy is characterized by asymptomatic dust-like or glittering purple granules scattered throughout the epithelium and stroma.
Amantadine
Soon after commencement of therapy some patients develop reversible diffuse, white, punctate corneal opacities sometimes associated with epithelial oedema.
Ciliary body
Acute angle closure with myopia, may occur secondary to ciliochoroidal effusion. Causes include: (a) topiramate, (b) acetazolamide and other sulfonamides, (c) bupropion. The prognosis is good provided the complication is recognized and the medication is stopped. Laser iridotomy is not needed as the mechanism of angle closure is not pupillary block.
Lens
Steroids
Both systemic and topical steroids are cataractogenic. The relationship between dose and duration of systemic administration and cataract (posterior subcapsular) is unclear ( Fig. 21.2A ).
Other drugs
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Chlorpromazine: fine stellate yellowish-brown granules on the anterior lens capsule within the pupillary area ( Fig. 21.2B ) develop in 50% of patients who have received a cumulative dose of 1000 g. The deposits persist despite discontinuation of therapy, but do not cause visual symptoms.
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Busulphan: occasionally causes lens opacities.
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Gold : innocuous anterior capsular deposits in approximately 50% of patients treated for more than 3 years.
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Allopurinol: increases the risk of cataract formation in elderly patients with large cumulative doses.
Uveitis
Rifabutin
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Used in the treatment of pulmonary tuberculosis
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Acute anterior uveitis, typically unilateral and frequently associated with hypopyon; associated vitritis may be mistaken for endophthalmitis. Treatment involves withdrawal of the drug or reduction of dose.
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Drugs that inhibit metabolism of rifabutin (e.g. clarithromycin, fluconazole) increase the risk of uveitis.
Cidofovir
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Acute anterior uveitis with few cells, but a marked fibrinous exudate may develop following several intravenous infusions. Vitritis is common and hypopyon may occur with long-term administration.
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Treatment with topical steroids and mydriatics is usually successful, avoiding the need to discontinue therapy.
Retina
Chloroquine and hydroxychloroquine
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Pathogenesis of toxicity: these are melanotropic drugs that become concentrated in melanin-containing structures of the eye, such as the RPE and choroid. Chloroquine can result in retinal toxicity (the risk increases significantly when the cumulative dose exceeds 300 g.). Individual susceptibility is variable. Hydroxychloroquine is much safer than chloroquine, particularly if the dose is kept to less than 5 mg/kg real weight/day. The risk of retinal toxicity is 7.5% if used for more than 5 years. Significant damage can occur without signs on fundus examination and OCT scanning of the macula has therefore emerged as a key part of the screening strategy.
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Premaculopathy: (a) VA is normal, (b) scotoma to a red target located between 4° and 9° from fixation, (c) a subtle colour vision defect may be present on specialized testing.
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Early maculopathy: (a) VA 6/9–6/12, (b) a subtle ‘bull’s-eye’ macular lesion that may progress even if the drug is stopped.
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Moderate maculopathy: (a) VA 6/18–6/24, (b) obvious ‘bull’s-eye’ maculopathy ( Fig. 21.3A ), (c) with progressive loss of perifoveal outer retina, the preserved central foveal tissue results in the ‘flying saucer’ sign on OCT scanning ( Fig. 21.3B )
