13, 16, 17 There have been a few cases of serious complications, such as vitreofoveal traction and retinal detachment, that occurred acutely after a single dose of 1% or 2% pilocarpine. The onset of posterior-segment complications from topical miotic use ranges in the literature from 10 hours to 2 months. Posterior-segment Complications Reported With Ocular Miotics 13 Mechanical pulling in areas of peripheral retinal compromise (thinning or weakness) could lead to the formation of retinal breaks. It is estimated that the ora serrata and underlying choroid move forward approximately 0.05mm for each diopter of accommodation. 15 When the muscle contracts and shortens, the choroidal insertion moves anteriorly. 4, 13 The longitudinal portion of the ciliary body has a fixed origin at the scleral spur and a potentially mobile insertion within the anterior choroid beneath the ora serrata of the retina. Contraction of the ciliary body muscle itself, particularly the longitudinal portion, may pull on the peripheral retina, resulting in forward translational movement of the ora serrata.4 Anterior displacement of the vitreous, combined with increased axial lengthening, could aggravate pre-existing areas of vitreoretinal traction (vitreoretinal tufts, lattice, stage 1 macular holes, etc.) or create traction at focal regions of firm vitreoretinal attachment. 4, 11 - 13 These sites are both strong vitreous attachment sites and in turn cause anterior shifting of the vitreous body. Ciliary body contraction causes forward displacement of the posterior lens surface and the vitreous base.Proposed mechanism of retinal break formation with drug-induced miosis and ciliary spasm. 10 There are 2 proposed mechanisms to explain why retinal side effects could occur with parasympathomimetic miotic use ( Figure 1).įigure 1. Posterior-segment complications that occur with miotics are linked to parasympathomimetic medications, and the risk for these complications is directly proportional to the ability of the medication to induce ciliary body spasm. Ciliary body contraction results in accommodation, mechanical opening of the trabecular meshwork, and expansion of Schlemm canal. 6 Parasympathomimetic drug-induced smooth muscle contraction of the iris sphincter causes miosis (reduced pupil size), as well as increased depth of focus. Pilocarpine mimics naturally occurring acetylcholine and binds to muscarinic receptors located within the pupillary sphincter and the ciliary body. 2, 6, 7 Agents utilized for their miotic effects that inhibit the dilator and avoid ciliary spasm include phentolamine and brimonidine. 6 The most effective ocular miotic agents are parasympathomimetic drugs that stimulate the parasympathetic pathway, such as pilocarpine, carbachol, and aceclidine. Pupillary miosis can be achieved by stimulating the iris sphincter muscle or inhibiting the dilator. 4, 5 Understanding the Mechanism Behind Posterior-segment Complications 2, 3 Other clinical uses of miotics include diagnostic testing of a dilated pupil, reversal of pupillary dilation, decreasing postoperative refractive surgery nighttime glare, and treating angle closure glaucoma. 1 More recently, there has been a renewed interest in miotics as a treatment option for presbyopia, and a variation of 1.25% pilocarpine (Vuity, Allergan/AbbVie) has re-emerged on the market and is commercially available (prescription only) for the treatment of presbyopia. The most used topical miotic is pilocarpine, which historically served as one of the key intraocular pressure-lowering medications, even for open angle glaucoma, prior to the advent of beta blockers, followed by adrenergic agonists. MIOTICS HAVE BEEN UTILIZED IN EYE CARE FOR MORE THAN 100 years.
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