Corneal deposits

The NSAIDs may cause visual disturbances. The nurse reports any complaints of blurred or diminished vision or changes in color vision to the primary health care provider. Corneal deposits and retinal disturbances may also occur. The primary health care provider may discontinue therapy if ocular changes are noted. Blurred vision may be significant and warrants thorough examination. 

Ophthalmologic effects Effects include blurred or diminished vision, scotomata, changes in color vision, corneal deposits, and retinal disturbances, including maculas. 

Corneal deposits during the long-term treatment of RA are not uncommon but the most prominent concern is the danger of producing irreversible retinal damage. At the usual antirheumatic doses these risks seem to be less for hydroxychloroquine than for chloroquine. 

NSAIDs. Hematopoietic side effects (e.g., leukopenia, hemolytic anemia, aplastic anemia, purpura, thrombocytopenia, and agranulocytosis) also may occur. Ocular effects (blurred vision, corneal deposits) have been observed in patients receiving indomethacin, and regular ophthalmological examinations are necessary when the drug is used for long periods. Hepatitis, jaundice, pancreatitis, and hypersensitivity reactions also have been noted. 

Rash, nausea, abdominal pain, diarrhea, dyspepsia, belching, headache, altered taste, uveitis, corneal deposits Rare (less than 2%)... 

Webber SK, Domniz Y, Sutton GL, Rogers CM, Lawless MA. Corneal deposition after high-dose chlorpro-mazine hydrochloride therapy. Cornea 2001 20(2) 217-9. 

Leung AT, Cheng AC, Chan WM, Lam DS. Chlorpromazine-induced retractile corneal deposits and cataract. Arch Ophthalmol 1999 117(12) 1662-3. 

Keratopathy is the most common ocular sign found in 69% to 100% of patients.The onset of keratopathy may be as early as 6 days after initiation of therapy, although it more commonly appears after 1 to 4 months of treatment. The corneal deposits are bilateral but are often asymmetric, and they are observed easily with the slit lamp. The development of keratopathy can be divided into four grades (Table 35-3). The development of each grade of keratopathy is shown in Figure 35-1, and a clinical photograph of amiodarone keratopathy is shown in Figure 35-2. 

Corneal deposits are generally reversible and do not affect vision. 

Patients should be counseled about corneal deposits however, no change in medication is normally required. Detection is the key to limiting any damage due to irreversible retinopathy. 

As the corneal deposits did not abate after withdrawal of the ciclosporin eye-drops, the systemic ciclosporin as well as its topical use may have contributed to the deposits. One should be aware that precipitation of ciclosporin on a compromised cornea can lead to severe visual impairment. 

Kachi S, Hirano K, Takesue Y, Miura M. Unusual corneal deposit after the topical use of cyclosporine as eyedrops. Am J Ophthalmol 2000 130(5) 667-9. 

Topical clarithromycin can cause self-resolving corneal deposits (16). 

Moller HU, Thygesen K, Kruit PJ. Corneal deposits associated with flecainide. BMJ 1991 302(6775) 506-7. 

Transient, non-infectious, crystalline, intrastromal corneal deposits have been reported after subconjunctival administration of 5-fluorouracil (75). The deposits were treated with glucocorticoids and completely resolved in 4 days. 

Yellow discoloration of the conjunctivae and sclerae can occur in patients taking mepacrine. The corneal deposits and mild diffuse cornea edema, which can cause blurring of vision, are reversible. 

Of more concern are two distinct tjrpes of adverse effects in the eye, which can be prodnced by various neuroleptic dmgs lenticular and corneal deposits. 

Severin M, Bulla M. Homhautablagerung bei Kindern mit Dialysebehandlung unter einer Therapie mit Vitamin D3 und 1,25 Dihydroxy-Cholecalciferol. [Corneal deposits in children... 

Palmar-plantar erythrodysesthesia (hand-foot syndrome) diarrhea stomatitis dermatitis bone marrow depression hyperbilirubinemia ocular irritation and corneal deposits... 

Amiodarone, for example (Figure 6.14), was introduced as a coronary dilator for angina. Concern about corneal deposits, discoloration of skin exposed to sunlight and thyroid disorders led to the withdrawal of the drug in 1967. However, in 1974 it was discovered that amiodarone was highly effective in the treatment of a rare type of arrhythmia known as the Wolff-Parkinson-White syndrome. Accordingly, amiodarone was reintroduced specifically for that purpose." ... 

Side effects of these drugs include CNS effects (e.g., headache, nervousness, insomnia, and others), rashes, dermatitis, pigmentary changes of the skin and hair, gastrointestinal disturbance (e.g., nausea), and reversible ocular toxicities such as cycloplegia and corneal deposits. Potentially serions retinal toxicity is uncommon when the currently recommended doses are used and is least common with hydroxychloroquine. However, because of the possibility of permanent damage associated with the retinopathy, an ophthalmologic evaluation should be done at baseline and every 3 months when chloroquine is used and every 6 to 12 months when hydroxychloroquine is used. If retinal abnormalities are noted, antimalarial therapy should be discontinued or the dose reduced. ... 

Adverse effects pulmonary fibrosis, corneal deposits, blue pigmentation ( smurf skin), pho-toxicity, thyroid dysfunction, T LDL-C, torsades, hepatic necrosis. 

Answer C. Ocular toxicity is characteristic of chloroquine and hydroxychloroquine. Corneal deposits are reversible, but retinal pigmentation can ultimately lead to blindness. Patients will complain about GI distress, visual dysfunction, ringing in the ears (note that tinnitus aiso occurs in salicylism), and itchy skin. Hydroxychloroquine also promotes oxidative stress that can lead to hemolysis in G6PD deficiency. DMARDs include gold salts (e.g., auranofin), methotrexate, and etanercept, but thioridazine is a phenothiazine used as an antipsychotic it lacks anti-inflammatory effect, but does cause retinal pigmentation. 

Abbreviations H, hypersensitivity BD, blood dyscrasia D-RCD, drug-related corneal deposits. 

Phototoxicity Corneal deposits Hepatic necrosis Thyroid dysfunction... 

Corneal deposits (reversible), hypo- or hyper- thyroidism (T4-like structure), photosensitivity, pulmonary fibrosis, bradycardia (rarely severe). 

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