To the Editor: We report a case of bilateral acute angle closure glaucoma associated with venlafaxine.

A 45-year-old woman with a history of bipolar affective disorder and borderline personality traits was admitted with increasing depression and suicidal ideation. She was taking sodium valproate (1500 mg/day) and slow-release lithium (450 mg/day). She had also taken dothiepin (50 mg nightly) for seven days, but this therapy was ceased on admission. Her only previous ophthalmological history was hypermetropia, and she had been taking low-potency neuroleptic medications and selective serotonin reuptake inhibitors in the past with no significant adverse effects.

She was treated with chlorpromazine (up to 150 mg daily), and venlafaxine therapy (extended release, 75 mg/day) was commenced.

After three days of taking venlafaxine, she developed left retro-orbital pain associated with nausea and vomiting, with subsequent swelling and drooping of the left upper lid and a dilated and fixed pupil. The eye was congested and visual acuity was reduced to counting fingers. She was diagnosed with acute angle closure glaucoma, treated with timolol, and transferred to a tertiary referral hospital. During this period, she sustained an injury to her right eye following an assault by a third party. A computed tomography scan revealed a right blow-out fracture with inferior rectus muscle entrapment.

On admission, intraocular pressures were 16 mmHg in the right and 50 mmHg in the left eye, and gonioscopy revealed closed angles (grade 1–2). Ninety minutes after being given intravenous mannitol, topical apraclonidine hydrochloride, latanoprost and pilocarpine eye drops, the intraocular pressure dropped to 35 mmHg in the left eye. Initial laser iridotomy was unsuccessful because of a hazy cornea. Laser iridotomy was repeated several times after topical steroid therapy until it was successful. The right orbital floor fracture was repaired with a Medpor implant (Porex Surgical Products Group, Atlanta, Georgia).

Eight days after starting venlafaxine therapy, she developed similar symptoms in her right eye, despite prophylactic treatment with pilocarpine eye drops four times a day. Venlafaxine was discontinued, and three days later a successful right laser iridotomy was performed. Her visual acuity was 6/5 in her right and 6/18 in her left eye. After eight weeks she was receiving no ophthalmic treatment and her intraocular pressures were well controlled.

In a MEDLINE search, we found no published reports of venlafaxine associated with acute angle closure glaucoma. The manufacturers report it as a rare adverse event (fewer than 1/1000; data on file; Wyeth-Ayerst Laboratories). There has been one previous report of increased intraocular pressures in two patients with known narrow-angle glaucoma who began taking venlafaxine.2 Glaucoma has also been reported with paroxetine.3-4 Our patient had no associated family history of glaucoma, but her eyes were predisposed to angle closure glaucoma owing to hypermetropia.

Patients with acute angle closure glaucoma usually have a structural defect that produces a narrow drainage angle, and thus moderate dilation of the pupil may precipitate an attack. Drugs like tricyclic antidepressants cause mydriasis and may cause the narrow angles to close as a result of anticholinergic effects. Venlafaxine, however, is a serotonin and noradrenaline reuptake inhibitor without anticholinergic activity. This fact and the time course suggest that a combination drug interaction may have occurred in this patient, perhaps by the hepatic inhibition of chlorpromazine metabolism by venlafaxine, increasing anticholinergic activity, or by a direct effect of venlafaxine on the eye unrelated to mydriasis.