A cyclodialysis cleft represents a disinsertion of the ciliary body from the scleral spur, allowing flow of aqueous humor from the anterior segment into the suprachoroidal space. Cyclodialysis clefts generally occur in three clinical settings: 1) as a surgical complication, 2) after trauma and 3) as an infrequently performed glaucoma operation. In all cases, the initial IOP may not be low, as cells or debris may be obstructing the cleft. Cyclodialysis clefts should be considered in the differential diagnosis for new-onset hypotony after anterior segment surgery or trauma.
Diagnosis of cyclodialysis clefts traditionally is made by gonioscopy, although some clefts are not visible by gonioscopy if the cleft is covered by part of the iris or ciliary body or if the peripheral anterior chamber is shallow or flat. Overfilling of the anterior chamber with viscoelastic through a paracentesis can open occult clefts and render them both visible gonioscopically and accessible to laser. Gentile et al. reported six cases of cyclodialysis clefts missed by gonioscopy and diagnosed only by high-resolution anterior segment ultrasound.1
The hallmark of a cyclodialysis cleft is a low IOP, which nearly always is 7 mmHg or less at the time of diagnosis.2 In a review of 58 cases by Ormerod et al.,2 visual acuity was occasionally as good as 20/20, with about half of patients having a vision of 20/200 or worse. IOPs of 4 mmHg or less were more frequently associated with visual acuities of 20/200 or worse, likely from accumulation of choroidal effusion leading to chorioretinal folds, photoreceptor misorientation and acquired hyperopia.
Clefts of 4 clock hours or less. These typically are treated with sequential medical management, laser and surgery, as needed. Clefts may occasionally close spontaneously and may be observed for up to six weeks with topical cycloplegia to relax the meridional ciliary body muscle fibers and help reappose the ciliary body to the scleral spur. Topical steroids are generally avoided to promote adhesion, but are purposefully used by some to try to generate a steroid-induced elevation in the IOP.
After six weeks of treatment with cycloplegia, laser treatment should be applied to both the ciliary body and scleral spur to induce scarring to close the cyclodialysis cleft. It is wise to treat the deeper, nonpigmented aspects of the cleft first to avoid pigment dispersion blocking the laser beam. Multiple treatments may be required. Retrobulbar anesthesia is desirable to facilitate application of higher levels of energy.3
If laser treatment is unsuccessful, several surgical procedures are available to close cyclodialysis clefts, including direct cyclopexy4 and cyclodiathermy.5
Clefts larger than 4 clock hours. These are less likely to respond to medical and laser treatment, and surgical procedures may be considered earlier.
Closure of a cyclodialysis cleft by any means can lead to a transient pressure spike of up to 60 mmHg,4 which can be delayed days to weeks after the procedure. This spike may occur due to a temporary increase in aqueous outflow resistance from an underperfused and underutilized trabecular meshwork. Closure of a cleft within two months of the onset of hypotony leads to a significantly greater likelihood of a final visual acuity of 20/25 or better, though acuities of at least 20/60 have been observed regardless of the duration of hypotony as long as no additional visually detrimental lesions were present.2 Failure of recovery of visual acuity with prolonged hypotony probably occurs as a result of permanent chorioretinal changes associated with hypotony maculopathy.
We recently examined a young man (an 18-year-old Asian college student) who was accidentally shot—while wearing no eye protection—with a paintball from a friend’s gun.
Ocular examination on the day of injury demonstrated that the patient had a contact lens in his right eye, but none in his left. Visual acuity in the right eye was 20/25, improving with pinhole to 20/20. In the left eye, the patient’s vision was count fingers at 3 feet without correction. There was no relative afferent pupillary defect. Eye movements were full, and confrontation visual field testing was normal.
Applanation tonometry revealed pressures of 12 mmHg and 11 mmHg in the right and left eyes, respectively. Slit-lamp examination was unremarkable in the right eye and demonstrated upper- and lower-lid ecchymosis, conjunctival injection, a small corneal abrasion, a 0.5 millimeter layered hyphema, several small iris sphincter tears and mild phacodonesis in the left eye. Dilated funduscopic examination was unremarkable in the right eye and demonstrated diffuse commotio retinae with a few small preretinal hemorrhages in the left eye.
The patient was started on cycloplegics, topical steroids and erythromycin ointment and was asked to return in 24 hours. At follow-up, his visual acuity was unchanged, his corneal abrasion had healed and his layered hyphema had disappeared, though he still had 4+ cells in the anterior chamber. His IOP had dropped to 4 mmHg by applanation. Fundus examination demonstrated radial striae around the macula.
Differential diagnosis of the patient’s hypotony in the left eye included cyclodialysis cleft, decreased ciliary body aqueous humor production and retinal detachment. Gonioscopy and scleral depression were deferred until five days after the injury. At that point, extensive angle recession in the left eye could be seen gonioscopically, with an extremely broad ciliary body band visible temporally. There was no visible cyclodialysis cleft. Ophthalmoscopy with scleral depression demonstrated dehiscence of the vitreous base with a possible retinal dialysis temporally.
B-scan and high-resolution anterior segment ultrasound showed a temporal cyclodialysis cleft (as evidenced by the presence of fluid in the suprachoroidal space), with associated iridodialysis and loose cleft coverage by both the ciliary body and peripheral iris.
After the diagnosis was made, the patient was treated with cycloplegics only and his steroids were discontinued. The patient was followed for one week; during that time, neither his visual acuity nor his IOP improved. He was subsequently lost to follow-up.
1 Gentile, R. C. et al. Ophthalmic Surg Lasers 1996;27:97–105.
2 Ormerod, L. D. et al. in Open-Angle Glaucoma, ed. G. W. Weinstein (New York: Churchill Livingstone, 1986), 201–225.
3 Ormerod, L. D. et al. Ophthalmology 1991; 98:1384–1393.
4 Kuchle, M. and G. O. Naumann. Ophthalmology 1995;105:322–333.
5 Maumenee, A. E. and W. J. Stark. Am J Ophthalmol 1971;71:320–327.
Dr. Ramulu is a resident in ophthalmology and Dr. Jun is assistant chief of service; both are at Johns Hopkins’ Wilmer Eye Institute.