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Arch Ophthalmol. 2004;122:399-404.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Cyclodialysis cleft is the result of separation of the meridonal ciliary muscle fibers from the scleral spur,¹ thereby providing a new drainage pathway of aqueous humor into the suprachoroidal space. Cyclodialysis has been used as a surgical option for aphakic glaucoma² but more often occurs inadvertently during anterior segment surgery or because of blunt ocular trauma. The new drainage channel increases uveoscleral outflow and may result in chronic ocular hypotony. Choroidal effusion, cystoid macular edema, optic nerve edema, engorgement and stasis of retinal veins, retinal folds, shallow anterior chamber, and cataract are recognized complications of chronic ocular hypotony.

Medical management of inadvertent cyclodialysis cleft is a trial of topical 1% atropine sulfate for 6 to 8 weeks. Topical or systemic corticosteroid therapy is not indicated. If medical management is ineffective, noninvasive methods of cleft closure, such as argon laser photocoagulation to the cleft, should be attempted. Should conservative therapy fail, . . . [Full Text of this Article]

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Ali Aminlari, MD; Christine E. Callahan, MD
Hershey, Pa

Corresponding author and reprints: Ali Aminlari, MD, Penn State University, Milton S. Hershey Medical Center, Department of Ophthalmology, PO Box 850, Hershey, PA 17033 (e-mail: aaminlari@psu.edu).