DEEXA (Dexamethasone sodium phosphate)
Dexamethasone decrease inflammation by suppression of neutrophil migration. I decreases the production of inflammatory mediators and reversal of increased capillary permeability. It also suppresses normal immune responses.
When given topically to the eye, dexamethasone is absorbed into the aqueous humor, cornea, iris, choroid, ciliary body and retina. Systemic absorption occurs butt may be significant only at higher dosages. Tissue distribution studies in animals show a high uptake of dexamethasone by the liver, kidney and adrenal glands; a volume of distribution has been quoted as 0.58 l/kg. Dexamethasone sodium phosphate is rapidly converted to dexamethasone within the circulation. Up to 77% of dexamethasone is bound to plasma proteins, mainly albumin. This percentage, unlike cortisol, remains practically unchanged with increasing steroid concentrations. The mean plasma half-life of dexamethasone is 3.6 +/- 0.9h. In man, over 60% of circulating steroids are excreted in the urine within 24 hours, largely as unconjugated steroid.
Dexamethasone sodium phosphate is used for management of steroid responsive inflammatory conditions of the palpebral and bulbar conjunctiva, cornea, and anterior segment of the globe such as allergic conjunctivitis, acne rosacea, superficial punctate keratitis, herpes zoster keratitis, iritis, cylitis, and selected infective conjunctivites when the inherent hazard of steroid use is accepted to obtain an advisable diminution of foreign bodies. It is also indicated for otic use to treat steroid-responsive inflammatory conditions of the external auditory meatus.
Contra indicated in epithelial herpes simplex (dendritic keratitis), vaccinia, varicella, and most other viral diseases of the cornea and conjunctiva; mycobacterial infection of the eye, fungal disease of ocular structures; perforation of a drum membrane; and in those persons who have shown hypersensitivity to any component of the formulation.
Prolonged use may result in ocular hypertension and/ or glaucoma, with damage to the optic nerve, defects in visual acuity and fields of vision and posterior subcapsular cataract formation. Monitor intraocular pressure if topical ophthalmic products are used for 10 days or longer.
Prolonged use may suppress the host response and thus increase the hazard of secondary ocular infections
Perforations may occur in diseases which cause thinning of the cornea or sclera
Pediatric: safety and effectiveness in pediatric patients have not been established.
Geriatric: refer to adult dosing. Use cautiously in the elderly in the smallest possible dose.
Hepatic impairment: no dosage adjustment required
Pregnancy: category C. There are no adequate or well-controlled studies in pregnant women. Studies in animals have shown that topically applied steroids can be absorbed systemically and can cause abnormalities of the foetal development in pregnant animals. Although the relevance of these findings to human beings has not been established, the use of dexamethasone sodium phosphate ophthalmic solution during pregnancy should be avoided.
Lactation: it is not known whether dexamethasone is excreted in human milk; caution should be exercised when dexamethasone sodium phosphate ophthalmic solution is administered to nursing women.
Dosage and administration
Eye: the usual dose is 1 drop, 4 to 6 times daily in the affected eye to be treated
In severe cases, treatment may be started with 1 drop every hour but dosage should be reduced to one drop every 4 hours when favorable responses is observed. Gradual tapering off is recommended in order to avoid a relapse
Ear: instill 3-4 drops into the aural canal 2-3 times a day, reduce dose gradually once a favorable response is obtained. Alternatively, may pack the aural canal with a gauze wick saturated with a solution; remove from the ear canal after 12-24 hours. Repeat as necessary
Burning, cataract formation, filtering blebs, glaucoma (with optic nerve damage), perforation of globe, secondary ocular infections, stinging, visual acuity defects, visual field defects.
The risk of increased intraocular pressure associated with prolonged corticosteroid therapy may be more likely to occur with concomitant use of anticholinergics, especially atropine and related compounds, in patients predisposed to acute angle closure.
The risk of corneal deposits or corneal opacity may be likely to occur in patients presenting with compromised cornea and receiving polypharmacy with other phosphate containing eye medications. The therapeutic efficacy of dexamethasone may be reduced by phenytoin, phernobarbitone, ephedrine and rifampicin. Glucocorticoids increase the need for salicylates as plasma salicylate clearance is increased.