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Angle closure glaucoma secondary to hemiretinal vein occlusion
  1. Department of Ophthalmology, Mount Sinai School of Medicine of New York University, New York, USA
  1. Janet B Serle, MD, Box 1183, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA janet.serle{at}

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Editor,—Central retinal vein occlusion (CRVO) has been reported to cause shallowing of the anterior chamber with acute angle closure glaucoma.1 2 This is due to anterior displacement of the lens-iris diaphragm caused by either the transudation of fluid from retinal vessels into the vitreous cavity or swelling of the ciliary body due to spasm, oedema, or detachment which may cause relaxation of lens zonules with subsequent crowding and closure of the angle.2 3 We describe a patient who developed angle closure glaucoma without neovascularisation of the angle secondary to hemiretinal vein occlusion which responded to miotics and iridotomy suggesting a “pupillary block” mechanism. This is the first report of angle closure glaucoma following a hemiretinal vein occlusion.


A 63 year old African American man with controlled systemic hypertension noted reduced vision in his right eye for 1 month. Best corrected visual acuity was 20/200 right eye with +1.75 −0.75 × 85, and 20/25 left eye with +2.25 −1.00 × 95. Slit lamp examination was unremarkable, pupils were equally reactive without an afferent pupillary defect. Intraocular pressure (IOP) was 26 mm Hg right eye and 25 mm Hg left eye. Gonioscopy revealed grade 3 angles in both eyes. The superior half of the retina right eye had dilated tortuous veins and multiple superficial haemorrhages. The right optic nerve was oedematous and hyperaemic. Retinal examination was unremarkable left eye with a cup to disc ratio of 0.4 horizontally by 0.5 vertically. The patient was diagnosed with a hemiretinal vein occlusion right eye, elevated IOP in both eyes, and treated with betaxolol 0.25% twice daily in both eyes.

Two weeks later visual acuity was counting fingers right eye and unchanged left eye. IOP was 42 mm Hg right eye and 20 mm Hg left eye, on betaxolol. The patient was referred to our office.

On examination the anterior chambers were shallow right eye and deep left eye. IOP was 45 mm Hg right eye and 21 mm Hg left eye. The angle was closed without neovascularisation right eye and grade 3 left eye. B scan ultrasonography revealed an unremarkable posterior segment without choroidal detachments right eye. Brimonidine 0.2% and Cosopt were administered to the right eye. Thirty minutes later the IOP was 36 mm Hg right eye. Three hours later IOP right eye was 28 mm Hg. Mydriacyl 1%, neosynephrine 2.5%, and Cyclogyl 2% were administered and the IOP increased to 37 mm Hg. The patient was discharged on acetazolamide 250 mg by mouth four times daily, brimonidine 0.2% three times daily right eye, Cosopt twice daily right eye, and pilocarpine 2% four times daily right eye.

The following day, the anterior chamber had deepened and the IOP was 24 mm Hg right eye. Gonioscopy revealed a closed angle (Fig 1). Pilocarpine 2% was instilled and a laser iridotomy performed right eye. The following day the IOP was 16 mm Hg right eye. Gonioscopy revealed a grade 2 angle. Acetazolamide was discontinued, pilocarpine 4% four times daily right eye, brimonidine 0.2% three times daily right eye, and Cosopt twice daily right eye were continued.

Figure 1

Gonioscopy, no angle structures seen in the right eye.

Two months later, the anterior chambers were deep and the angles were grade 3 in both eyes. IOP was 14 mm Hg right eye on pilocarpine 4% four times daily and Timoptic XE four times daily 0.5% IOP on subsequent visits remained below 20 mm Hg, and the angle remained open (Fig 2). Visual acuity did not improve.

Figure 2

Gonioscopy, angle open to scleral spur with lightly pigmented trabecular meshwork, left eye.


Transient angle closure glaucoma, an infrequent sequela of CRVO, has not been reported following hemiretinal vein occlusion (HRVO). Angle closure may occur days to months following a CRVO. Neovascular glaucoma may develop weeks or months following a retinal vascular occlusion. Elevated IOP during an acute attack of primary pupillary block angle closure glaucoma can lead to a retinal vascular occlusion. Risk factors for CRVO and HRVO include systemic hypertension and diabetes mellitus. A history of glaucoma has been associated with CRVO, HRVO, and branch retinal vein occlusion (BRVO).1

The patient in this report developed angle closure glaucoma within a few weeks of the HRVO. He had a history of systemic hypertension. Elevated IOP was noted in both eyes on initial examination. Cycloplegic agents increased the IOP, suggesting the angle closure was not due to a ciliary block mechanism. Pilocarpine and a laser iridotomy reduced the IOP and opened the angle in this patient, suggesting a secondary pupillary block mechanism. At the time of diagnosis of angle closure glaucoma the contralateral eye had a deep anterior chamber and a wide open angle, making a diagnosis of primary pupillary block angle closure glaucoma unlikely.

Previous reports of angle closure glaucoma secondary to central retinal vein occlusion suggest treatment with cycloplegic/mydriatic agents is beneficial in some patients.2 Miotic agents have been reported to be of benefit in cases of angle closure glaucoma following a CRVO.3

Determining the mechanism of angle closure in an individual patient following a retinal vascular occlusion will guide the ophthalmologist to the appropriate treatment options, mydriatic or miotic therapy. Ultrasound biomicroscopy may be of benefit in differentiating between a ciliary block mechanism4 and a pupillary block mechanism.5


Supported in part by grant EY01867 from the National Eye Institute, National Institutes of Health, Bethesda, MD, an unrestricted grant from Research to Prevent Blindness Inc, New York, and the Louis and Rachel Rudin Foundation, Inc, New York, NY, USA.


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