Diagnosis: Topiramate-induced, bilateral, secondary angle closure glaucoma
Acute angle closure glaucoma is an ophthalmic emergency caused by sudden blockage of the outflow tract of the eye, or trabecular meshwork, causing an acute, significant, elevation in intraocular pressure. In addition to decreased vision, and pain, the elevated IOP can cause rapid, irreversible damage to the optic nerve, causing permanent vision loss. Therefore, prompt diagnosis and management of this condition is critical.
The most common mechanism for acute angle closure glaucoma is referred to as “pupillary block.” In a healthy eye, aqueous humor is produced by the ciliary body, travels over the lens, then through the pupil to enter the anterior chamber (see diagram below). Once in the anterior chamber, it exits the eye through the trabecular meshwork, and then is drained via Schlemm’s canal into the venous system. In acute angle closure glaucoma, the pupil becomes dilated, typically prompted by an environment with dim illumination, such as a movie theatre or room with lights off. The iris in its dilated state then mechanically obstructs the angle, or outflow tract of the eye. Simultaneously, fluid continues to be produced by the ciliary body. However, because it cannot exit the eye, a relative pressure differential is created between the posterior chamber, including the ciliary body where aqueous humor is being produced, and the anterior chamber, where the aqueous humor is trying to exit the eye. The increased pressure in the posterior chamber, causes shallowing of the anterior chamber, and because of this shallowing, the iris becomes pushed against the lens, thereby blocking any fluid from passing from the posterior to the anterior chamber. This mechanism is therefore referred to as a “pupillary block” mechanism. The iris essentially becomes “stuck” in this dilated position, because it is pressed against the lens (Above left image credit: Troy Teeples & Griffin Jardine, MD. Acute Angle Closure Glaucoma. MoranCORE, Moran Eye Center.).
The treatment for pupillary block angle closure glaucoma, is essentially the creation of a “new pupil” or passageway for fluid to pass from the posterior to the anterior chamber. This is achieved through performing a laser peripheral iridotomy. Using laser, a small hole is a created in the peripheral iris to restore flow of fluid from the posterior to anterior chamber. With flow restored, the relative pressure differential between the posterior and anterior chamber is resolved, allowing the anterior chamber and angle to deepen, and re-establishing space between the lens and the pupillary margin (see Case 8 for more information).
However, other “non-pupillary block” mechanisms can cause obstruction of the outflow tract, and can cause secondary angle closure glaucoma. Neovascular glaucoma, is one example of a secondary angle closure glaucoma, whereby abnormal blood vessels grow within the outflow tract, mechanically blocking it, and often pulling the angle closed through contraction of these abnormal blood vessels (see Case 6).
Another mechanism of secondary angle closure is caused by ciliary body swelling. Ciliary body edema, is often drug-induced, such as by sulfa drugs, commonly topiramate. It typically occurs within the first 2 weeks of starting the medication. The drug induced ciliary effusion effectively “pushes” the lens-iris complex forward, thereby blocking the trabecular meshwork. The anterior rotation of the lens-iris diaphragm also causes a myopic shift in the refractive error, and contributes to the sudden change in vision. Because the mechanism of this outflow obstruction is a “push” mechanism, rather than pupillary block, a laser iridotomy is not effective in breaking the attack.
In drug-induced angle closure glaucoma, the swelling of the ciliary body needs to be reduced, and this is achieved by discontinuation of the offending medication, and topical, or sometimes oral steroids. Additionally, supportive therapy with aqueous suppressant drops, (see case 5) is indicated to lower the IOP, until the angle opens back up, restoring outflow and normal intraocular pressure. Topical cycloplegic drops also help to rotate the ciliary body posteriorly to reduce the anterior “push” mechanism.
Fortunately, if identified early, drug induced, secondary angle closure glaucoma, often resolves within a few days with discontinuation of the medication and treatment as discussed above. Myopic shift typically resolves within 1-2 weeks.
Here’s how the eye might appear on UBM after resolution of the attack (arrow pointing to wide space between iris and cornea indicating an open angle, also note resolution of the supraciliary effusion).
References and Additional Resources:
1. Abtahi MA, Abtahi SH, Fazel F, Roomizadeh P, Etemadifar M, Jenab K, Akbari M. Topiramate and the vision: a systematic review. Clin Ophthalmol. 2012;6:117-131.
2. Symes RJ, Etminan M, Mikelberg FS. Risk of angle-closure glaucoma with bupropion and topiramate. JAMA Ophthalmol. 2015;133(10):1187-1189.
3. Fraunfelder FW, Fraunfelder FT, Keates EU. Topiramate-associated acute, bilateral, secondary angle-closure glaucoma. Ophthalmology. 2004;111(1):109-11.
Case 9 Index