Acute primary angle-closure glaucoma (PACG) is a common form of glaucoma in East Asia, including Taiwan.1,2 Laser peripheral iridotomy (LPI) can halt the pupil block mechanism and relieve an acute episode. However, intraocular pressure (IOP) will rise again after long-term follow-up in about 60% of the patients with acute PACG and a patent iridotomy.3 Previous studies have shown that cataract surgery can be used to treat PACG.4–10 In this report, the patient had acutely elevated IOP after mydriasis and a history of acute PACG treated by LPI. Modern cataract surgery was used with success to treat this case.
A 70-year-old woman had acute PACG with IOP up to 69 mm Hg in the left eye in August 1992. After medical therapy, IOP decreased to 18 mm Hg. Sequential argon:YAG LPI was administered and focused with an Abraham contact lens onto the superonasal part of the peripheral iris. The laser settings were as follows: argon blue-green at 1.0 W, 50 μm spot size, 0.1-second exposure, followed by neodymium:YAG laser at 5 mJ. A prophylactic LPI was performed in the right eye. The iridotomy was 500 μm in diameter. During the 9-year follow-up period, IOPs were below 20 mm Hg in both eyes without medication, and the optic nerve did not deteriorate.
In April 2001, the patient complained of blurred vision in both eyes. Her medical and family history were unremarkable. Best corrected visual acuities were 20/50 in the right eye and 20/400 in the left eye with corrections of –3.5 –1.25 × 90 in the right eye and –3.75 –1.25 × 90 in the left eye. Intraocular pressures were 19 mm Hg in both eyes. Slit-lamp biomicroscopy revealed quiet conjunctiva, clear corneas, and shallow and quiet anterior segments. Patent iridotomies were noted in both eyes, with a middilated pupil in the left and a normal pupil in the right. The lens showed moderate and severe nuclear sclerosis in the right and left eye, respectively. Gonioscopy displayed appositional angle closure in both eyes, and peripheral anterior synechias (PAS) in the upper quadrant of the left eye. The A-scan ultrasonography disclosed short axial lengths (22.61 mm in the right eye, 22.51 mm in the left eye), increased lens thickness (5.42 mm in the right eye, 5.46 mm in the left eye), and shallow anterior chamber depths (2.11 mm in the right eye, 1.93 mm in the left eye). After mydriasis, fundus findings were unremarkable. The cup-disc ratios were 0.3 in the right eye and 0.5 in the left eye.
Two hours later, the patient complained of sudden severe ocular pain and red eye in the left eye. Acute elevation of IOP up to 40 mm Hg appeared with a fully dilated pupil and a visible iridotomy. Anterior chamber showed a mild reaction with mild corneal edema. The gonioscopy findings were as described above. Immediate medical treatment was given including topical 2% pilocarpine, topical 0.5% timolol, topical dexamethasone, oral acetazolamide 250 mg, and intravenous mannitol 300 mL. One hour later, IOP returned to 14 mm Hg. Topical 0.5% timolol was used as maintenance therapy. In the right eye, IOP always remained normal without medication. One week later, sutureless cataract surgery was performed in the left eye, including temporal clear corneal incision, phacoemulsification, and 3-piece soft acrylic posterior chamber intraocular lens (IOL) (AcrySof® MA30BA, Alcon Laboratories, Inc.) implantation in the bag. One day after surgery, IOP was 14 mm Hg. Two weeks later, the patient's right eye had the same procedure. Three months after these operations, uncorrected visual acuities were 20/25 in the right eye and 20/30 in the left eye. Intraocular pressures were normal without medication, even after inducing mydriasis for postoperative fundus examination. Optic disc findings were the same as those before the surgery. Gonioscopy revealed visible pigmented trabecular meshwork in both eyes and the persistence of synechial change in the upper part of the left eye. Deeper anterior chamber depths were found (3.54 mm in the right eye, 3.23 mm in the left eye).
In East Asia, acute PACG is commonly seen in patients with glaucoma.1,2 The anatomy of the acute PACG eye consists of shallow anterior chamber, thickened lens, anterior shift of iridolenticular diaphragm, and short axial length. These structural abnormalities predispose to pupil block and angle crowding. The main mechanism of an acute episode is pupil block, which can be treated by LPI in most cases. However, a proportion (58.1%) of eyes with acute PACG still develop an increase in IOP on long-term follow-up even with a patent iridotomy.3 This apparent “failure” in treatment is attributed to other mechanisms such as angle crowding, trabecular damage, and development of PAS.10
In the past, cases of recurrent acute attack after LPI were reported.11 Small size of iridotomy was the cause. A smaller iris opening created by laser results in a greater resistance of aqueous outflow. Therefore, Fleck12 suggested iridotomy should be between 150 and 200 μm. The diameter of iridotomy in our patient was 500 μm (Figure 1). The iridotomy opening was large enough to avoid recurrent acute attack.
Several studies4–9 demonstrated long-term reduction of IOP by lens removal in PACG cases. In acute, subacute, chronic, or uncontrolled PACG, IOP was reduced by either extracapsular cataract surgery or phacoemulsification.4,7,8 The mean number of glaucoma medications decreased after cataract surgery in most patients with PACG.4,5 It is postulated that the cataract operation can control IOP by eliminating lens-induced angle narrowing and increasing outflow facility. This postulation was confirmed by Scheimpflug image processing.5,8 Deepening of the anterior chamber depth and widening of the anterior chamber angle can be achieved after removal of the lens. However, only appositional angle closure may be terminated by performing cataract extraction.8 Synechial angle closure cannot be effectively treated by cataract surgery.8
In our case, chronic PACG did not develop after the acute attack during the 9-year follow-up period. Gonioscopy revealed appositional angle-closure with minimal PAS. Our patient's recurrent acute episode occurred only after mydriasis. Therefore, trabecular damage and synechial change are unlikely to be the causes of IOP elevation. In addition to appositional angle closure caused by crystalline lens swelling, mydriasis precipitated angle crowding, which resulted in the acute IOP spike. After removal of the crystalline lens, deepening and widening of the anterior chamber in both eyes were demonstrated. Relief of angle crowding achieved normalized aqueous outflow resistance. Following soft acrylic IOL implantation in the patient's left eye, no IOP elevations after mydriasis were noted. Additionally, cataract surgery may accelerate the glaucomatous disc change by inducing immediate or late elevation of IOP postoperatively. However, normal IOPs and stable optic disc findings were seen in this patient immediately after the operation and during more than 1 year of follow-up. Better than traditional extracapsular cataract surgery, small-incision phacoemulsification with a soft acrylic IOL can yield superior visual results owing to reduction in astigmatism, IOL tilt or dislocation, and posterior capsular opacity. In this patient, modern cataract surgery delivered reasonable visual results and IOP with an unusual history of acute PACG.
In summary, the patient had acute elevation of IOP after mydriasis, a patent iridotomy, and a history of acute PACG. This phenomenon resulted from appositional angle closure and angle crowding. Therefore, careful monitoring of IOP was necessary to detect recurrent PACG after mydriasis, even in patients with a large, patent iridotomy. This case was successfully treated with modern phacoemulsification cataract surgery, which produced remarkable visual results and IOP control by widening and deepening of the anterior chamber angle.
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