CD induced by antiglaucoma eye drops is considered to occur because of 2 mechanisms: suppression of aqueous humor production (timolol, dorzolamide, and acetazolamide) and increased uveoscleral outflow (prostaglandin analogues such as latanoprost, bimatoprost, and travoprost) (Table). The mechanism of CD induced by the aqueous humor suppression group was suggested in detail by Vela. The ciliary body is first damaged and/or sensitized by the long-term suppression of aqueous humor or filtering surgery. After retreatment with the drug, the sensitized ciliary body responds with a dramatic reduction in aqueous production causing hypotony. On the other hand, the mechanism underlying CD induced by the increasing uveoscleral outflow group was the increase in the uveoscleral outflow of the aqueous humor via a reduction in the levels of collagen types I, III, and IV in the ciliary smooth muscles and adjacent sclera. This hypothesis was also supported by Martínez-Belló et al, who showed that 4 of 28 eyes with trabeculectomy showed persistent supraciliochoroidal effusion observed with ultrasound biomicroscopy for 6 months after trabeculectomy without CD. They suggested that observed supraciliochoroidal effusion may be produced by increased uveoscleral outflow resulting from iatrogenic cyclodialysis due to trabeculectomy technique with scleral spur excision, which removes the barrier between the anterior chamber and the suprachoroidal space. We might excise the scleral spur in this case and topical bimatoprost further increased uveoscleral outflow, leading to CD.
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