Ophthalmic toxicity intraocular pressure

Glucocorticoids that have been used for local ophthalmic treatment include medrysone, fluorometholone, tetrahy-droxytriamcinolone, and clobetasone. Loteprednol etabo-nate 0.5% increases intraocular pressure less than dexamethasone. Studies on animal models of uveitis and two randomized double-masked trials showed that loteprednol etabonate 0.5% was less potent than dexamethasone, prednisolone acetate 1%, or fluorometholone, which may partly explain the improved toxicity profile of loteprednol etabonate (429). 

The authors added that retinal toxicity of the local anesthetic agent did not affect the visual outcome in this patient. Scleral perforation is a well-known complication of eye blocks for ophthalmic surgery. The incidence with retrobulbar techniques is 0.075% and with peribulbar blocks 0.0002%. When recognized, ocular perforation usually requires a vitreoretinal procedure and is associated with a poor visual outcome. Risk factors include an anxious or oversedated patient, long sharp needles, superior injection, incorrect angle of needle insertion, and myopic eyes. If the intraocular pressure is increased, paracentesis may acutely reduce it, preventing retinal and optic nerve ischemia and possible permanent visual loss. 

Mannitol is an osmotic diuretic that has been used in acute oliguric renal insufficiency, acute cerebral edema, and the short-term management of glaucoma, especially to reduce intraocular pressure before ophthalmic surgery. Other indications include promotion of the excretion of toxic substances by forced diuresis, bladder irrigation during transurethral resection of the prostate, and oral administration as an osmotic laxative for bowel preparation. Mannitol is used as a diluent and excipient in pharmaceutical formulations and as a bulk sweetener. 

Both patients had clear anatomical causes for blindness, and unilateral (rather than bilateral) blindness suggested a limited role for systemic arsenic toxicity. Nevertheless, a weak contribution of ocular arsenic toxicity should not be ruled out. Both arsenic trioxide and all-trans retinoic acid can increase intracranial pressure, resulting in pseudotumor cerebri and a secondary increase in intraocular pressure, which may augment retinal injury. Also, arsenic trioxide can cause vasoconstriction and worsen retinal artery occlusion. Finally, elemental arsenic was detected in the eyes at 30-50% of the plasma concentration, a ratio comparable to that in cerebrospinal fluid. This may have direct retinal toxicity, especially with the high peak concentrations associated with intravenous arsenic trioxide. Full ophthalmic evaluation is recommended in patients receiving longterm or intravenous arsenic trioxide. 

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