Figure 5-26 Fibrous ingrowth appears as a thick, grayish, vascular retrocorneal membrane that results in high PAS and destruction of the trabecular meshwork. (Courtesy of Steven T. Simmons, MD.)
Trauma
Angle-closure glaucoma without pupillary block may develop following ocular trauma from the formation of PAS associated with angle recession or from contusion, hyphema, and inflammation. See Chapter 4 for discussion of trauma.
Retinal Surgery and Retinal Vascular Disease
Scleral buckling operations, especially encircling bands, can produce shallowing of the anterior chamber angle and frank ACG, often accompanied by choroidal effusion and anterior rotation of the ciliary body, causing a flattening of the peripheral iris with a relatively deep central anterior chamber. Usually, the anterior chamber deepens with the opening of the anterior chamber angle over days to weeks with medical therapy consisting of cycloplegics, anti-inflammatory agents, β-adrenergic antagonists, carbonic anhydrase inhibitors, and hyperosmotic agents. If medical management is unsuccessful, argon laser iridoplasty, drainage of suprachoroidal fluid, or adjustment of the scleral buckle may be required. Iridectomy is usually of little benefit in this condition. The scleral buckle can impede venous drainage by compressing a vortex vein, elevating episcleral venous pressure and IOP. Such cases may respond only to moving the scleral buckle or releasing tension on the band.
Following a pars plana vitrectomy, ACG may result from the injection of air, long-acting gases
such as sulfur hexafluoride and perfluorocarbons (perfluoropropane and perfluoroethane), or silicone oil. These substances are less dense than water and rise to the top of the eye, and an iridectomy may be beneficial. The iridectomy should be located inferiorly to prevent obstruction of the iridectomy site by the oil or gas. Eyes that have undergone complicated vitreoretinal surgery and have developed elevated IOP require individualized treatment plans. Treatment options include the following: removal of the silicone oil; release of the encircling element; removal of expansile gases; or primary glaucoma surgery, such as trabeculectomy, implantation of glaucoma drainage devices, or cilioablation.
Following panretinal photocoagulation, IOP may become elevated by an angle-closure mechanism. The ciliary body is thickened and rotated anteriorly, and often an anterior annular choroidal detachment occurs. Generally, this secondary glaucoma is self-limited, and therapy is directed at temporary medical management with cycloplegic agents, topical corticosteroids, and aqueous suppressants.
Central retinal vein occlusion (CRVO) sometimes causes early shallowing of the chamber angle, presumably because of swelling of the choroid and ciliary body. In rare cases, the angle becomes sufficiently compromised to cause ACG. The chamber deepens and the glaucoma resolves over 1 to several weeks. Medical therapy for the elevated IOP, combined with administration of topical corticosteroids and cycloplegia, is usually preferred. However, if the contralateral eye of a patient with CRVO has a potentially occludable anterior chamber angle, the ophthalmologist must consider an underlying pupillary block mechanism and the possible need for bilateral iridectomy.
Nanophthalmos
A nanophthalmic eye is normal in shape but unusually small, with a shortened axial length (<20 mm), a small corneal diameter, and a relatively large lens for the volume of the eye. Thickened sclera may impede drainage from the vortex veins. These eyes are markedly hyperopic and highly susceptible to ACG, which occurs at an earlier age than in primary angle closure. Intraocular surgery is frequently complicated by choroidal effusion and nonrhegmatogenous retinal detachment. Choroidal effusion may occur spontaneously, and it can induce ACG. Laser iridotomy, argon laser peripheral iridoplasty, and medical therapy are the safest ways to manage glaucoma in these patients. Surgery should be avoided if possible because of the high rate of surgical complications. When intraocular surgery is employed, prophylactic posterior sclerotomies may reduce the severity of intraoperative choroidal effusion. Additional treatment options include lensectomy for angles that remain compromised despite a patent iridotomy. In such cases, a limited core vitrectomy is sometimes needed to provide adequate ACD to accomplish safe lens removal.
Persistent Fetal Vasculature
The contracting retrolental tissue seen in persistent fetal vasculature (PFV; formerly known as persistent hyperplastic primary vitreous) and in retinopathy of prematurity can cause progressive shallowing of the anterior chamber angle with subsequent ACG. These conditions are discussed in more detail in BCSC Section 6, Pediatric Ophthalmology and Strabismus, and Section 12, Retina and Vitreous. In PFV, the onset of this complication usually occurs at 3–6 months of age during the cicatricial phase of the disease. However, the ACG may occur later in childhood.
PFV is usually unilateral and often associated with microphthalmos and elongated ciliary processes. The contracture of the hyperplastic primary vitreous and swelling of a cataractous lens may result in subsequent ACG.
Flat Anterior Chamber
A flat anterior chamber from any cause can result in the formation of PAS. Debate continues concerning how long a postoperative flat chamber should be treated conservatively before surgical intervention is undertaken. Hypotony in an eye with a postoperative flat chamber following cataract surgery or filtering surgery indicates a wound leak until proven otherwise. A Seidel test should be performed to locate the leak. Simple pressure patching or bandage contact lens application will often cause the leak to seal and the chamber to re-form. If the chamber does not re-form, the leak should be repaired surgically to prevent permanent synechial closure of the angle or other complications of hypotony.
Some ophthalmologists repair the wound leak and re-form a flat chamber following cataract surgery within 24 hours. Others prefer observation in conjunction with corticosteroid therapy for several days to prevent synechiae formation. Although iridocorneal contact is well tolerated, if the hyaloid face or an IOL is in contact with the cornea, the chamber should be re-formed without delay to minimize corneal endothelial damage. Early intervention should also be considered in the presence of corneal edema, excessive inflammation, or posterior synechiae formation.
Drug-Induced Secondary Angle-Closure Glaucoma
Topiramate, a sulfamate-substituted monosaccharide, is an oral medication prescribed in the treatment of epilepsy, depression, headaches, and pseudotumor cerebri. In some patients using this medication, a syndrome characterized by acute myopic shift and acute bilateral ACG can occur. Patients presenting with this syndrome experience bilateral, sudden loss of vision with acute myopia, bilateral ocular pain, and headache, usually within 1 month of initiating topiramate. In addition to myopia, ocular findings of this syndrome include a uniformly shallow anterior chamber with anterior iris and lens displacement, microcystic corneal edema, elevated IOP (40–70 mm Hg), a closed anterior chamber angle, and a ciliochoroidal effusion/detachment (Fig 5-27). The underlying mechanism of this syndrome is the ciliochoroidal effusion, which causes the relaxation of zonular fibers and the profound anterior displacement of the lens–iris complex, causing the secondary ACG and high myopia.
Figure 5-27 A, B-scan ultrasonogram of patient with very shallow anterior chamber (asterisk) and topiramate-induced angleclosure glaucoma. The choroidal effusion is clearly evident (arrows). B, Ultrasonographic view of extremely shallow anterior
chamber and closed angle (asterisk). The posterior choroidal effusion is clearly visible (arrow). (Courtesy of Jonathan Eisengart,
MD.)
The bilateral nature of this form of angle closure should alert the clinician to the possibility of an idiosyncratic response to topiramate. Treatment of this syndrome involves early recognition of the causal systemic medication and immediate discontinuation of the topiramate. In addition to discontinuation of the medication, medical treatment for the elevated IOP is initiated, generally in the form of aqueous suppressants. Systemic agents such as acetazolamide may also be administered orally or intravenously. Aggressive cycloplegia may help deepen the anterior chamber and relieve the attack. The secondary ACG usually resolves within 24–48 hours with medical treatment, and the myopia resolves within 1–2 weeks of discontinuing the topiramate. Because pupillary block is not an underlying mechanism of this syndrome, a peripheral iridectomy is not indicated. Other sulfonamides, such as acetazolamide, have been reported to cause a similar clinical syndrome.
Epstein DL, Allingham RR, Schuman JS, eds. Chandler and Grant’s Glaucoma. 4th ed. Baltimore: Williams & Wilkins; 1997. Ritch R, Shields MB, Krupin T, eds. The Glaucomas. 2nd ed. St Louis: Mosby; 1996.
Shields MB. Textbook of Glaucoma. 4th ed. Philadelphia: Williams & Wilkins; 2000.
Stamper RL, Lieberman MF, Drake MV, eds. Becker-Shaffer’s Diagnosis and Therapy of the Glaucomas. 7th ed. St Louis: Mosby; 1999.