Echothiophate iodide ophthalmic Disease Interactions

The use of miotic agents may occasionally cause retinal detachment due to drug-induced ciliary or accommodative spasm, which causes the lens and vitreous to move forward and create a retinal tear. Therapy with miotic agents should be administered with extreme caution, if at all, in patients with risk factors for retinal detachment, such as old age, retinal degenerative changes or other retinal disorders, aphakia, prior cataract extraction, or a history of severe myopia or retinal detachment.

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The use of miotic agents is contraindicated in patients with active anterior uveitis and/or glaucoma associated with iridocyclitis. Pupillary constriction produced by these agents may aggravate the inflammation and predispose these patients to the development of posterior synechiae.

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Miotic agents may cause a paradoxical transient increase in intraocular pressure, which can precipitate an acute attack in patients with angle-closure (narrow-angle) glaucoma or anatomically narrow angles. The risk is much higher with long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), since these agents can cause pupillary block and increase angle closure. Therapy with long-acting cholinesterase inhibitors should be administered cautiously, or avoided, in patients with chronic angle-closure glaucoma or in patients with anatomically narrow angles. The use of echothiophate iodide is specifically contraindicated in most cases of angle-closure glaucoma. Because chronic use of long-acting cholinesterase inhibitors may cause dilation of blood vessels and increased permeability, these agents should be avoided for at least 2 weeks prior to ophthalmic surgery so as to minimize the risk of hyphema. Miotic agents in general should not be used in patients with glaucoma secondary to unrelieved pupillary block.

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The use of miotic agents has been associated with the development of lens opacities characterized by the appearance of anterior subcapsular vacuoles. The incidence of cataracts appears to be highest in patients treated with long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate) and may also be related to age (higher in patients > 60 years of age), drug concentration, frequency of use, and duration of therapy (>= 6 months). Lens opacities usually regress if miotic therapy is withdrawn early in their development but often become progressive once they are established. Therapy with miotic agents should be administered cautiously in patients with or predisposed to cataracts. Slit-lamp examinations should be performed regularly, and miotic therapy discontinued if necessary.

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Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

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Topically applied cholinesterase inhibitors are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including central nervous system disturbances such as confusion and seizures. Children with Down's syndrome may be particularly susceptible to the CNS effects of these drugs. Echothiophate, specifically, has also been reported to cause hyperactivity in these children. Therapy with ophthalmic cholinesterase inhibitors, particularly the long-acting ones (e.g., demecarium and echothiophate), should be administered cautiously in children with Down's syndrome.

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