Bilateral acetazolamide-induced choroidal effusion following cataract surgery

Sir,

Idiosyncratic reactions to drugs including sulfonamide^{1, 2, 6} and corticosteroids^{3, 4} have been reported to cause choroidal detachment and secondary angle closure glaucoma. We report a case of bilateral angle closure glaucoma and extensive choridal effusion following administration of oral acetazolamide unresponsive to intravenous (i.v.) dexamethasone immediate postcataract surgery.

Case report

A 66-year-old man with chronic open angle glaucoma underwent left routine cataract surgery and intraocular lens implant under local anaesthesia. He received oral acetazolamide 250 mg overnight and immediately following the surgery. Three hours after surgery, he complained of severe pain in the operated eye. On examination the left eye (LE) showed corneal oedema shallow anterior chamber (AC), pupillary capture from 4 to 7 O' clock hours (Figure 1b) and an intraocular pressure (IOP) of 52 mm Hg. The right eye (RE) showed circumcorneal congestion, corneal oedema shallow AC with an immature cataract (Figure 1a), and IOP of 40 mm Hg. Gonioscopy showed 360° appositional angle closure with a convex iris configuration. He was treated with i.v. mannitol 2 mg/kg and oral acetazolamide 250 mg t.i.d., G.Timolol 0.5% bd, G Ofloxacin 0.3%, and G dexamethasone 1% q.i.d. The next day, the corneal oedema and shallow AC persisted with an IOP of 32 mm Hg in each eye. Ultrasound B-scan showed bilateral choroidal effusion (Figure 2a and b). Acetazolamide was thought to be the cause and was discontinued. i.v. dexamethasone 8 mg daily was started in an attempt to reduce inflammation related to the choroidal effusion but no positive effect therefore was discontinued. On day 5, the choroidal effusion showed resolution (Figure 2c and d) with clear cornea, normal AC depth and IOP of 18 mm Hg in each eye (Figure 1c and d). He achieved final best-corrected visual acuities of 6/6.

Figure 1

(a) RE first postoperative day showing corneal oedema and shallow AC. (b) LE first postoperative day showing corneal oedema and pupillary capture. (c) RE fifth postoperative day showing clear cornea and normal AC depth. (d) LE fifth postoperative day showing clear cornea, resolved pupillary capture, and deep AC.

Figure 2

(a) First postoperative day showing peripheral choroidal effusions in the superiotemporal and nasal quadrants. (b) LE 270° effusions extending anteriorly to the equator. (c and d) Fifth postoperative day showing resolved choroidal effusion in both eyes.

Comment

Acetazolamide-induced transient myopia and angle closure glaucoma has been reported in nonglaucomatous patient.^{1, 2, 6} Forward shift of crystalline lens caused by ciliary body oedema has been postulated as the mechanism.^{1, 2, 5} Ciliary body oedema has been based on an imbalance in eicosanoid (prostaglandin–thromboxane) metabolism (Figure 3).⁵

Figure 3

Flow chart for the mechanism of drug-induced secondary angle closure glaucoma.

In this patient, the cloudy cornea precluded laser iridotomy and cycloplegia was avoided as angle closure was a differential diagnosis. Dexamethasone was used empirically as an inflammatory aetiology was suspected.

The failure of laser iridotomy and cycloplegia was reported as the mechanical effect following forward rotation of ciliary body and displacement of iris–lens diaphragm secondary to choroidal effusion.⁶ Only when the latter resolved could the angle be opened. Corticosteroids have been shown to cause choroidal effusion^{3, 4} and are ineffective in managing this complication. Other methods of controlling IOP might have been considered to avoid this unusual complication.