Acute glaucoma in the unoperated eye after macular hole surgery

Main

Sir,

We read with interest the article by Bansal et al¹, and would like to report another case of angle closure glaucoma following pars plana vitreous surgery. This, however, occurred in the unoperated eye of a 68-year-old man following macular hole surgery.

Case report

The patient was initially referred 8 years earlier with a persisting inferotemporal retinal detachment in his right eye, following an unsuccessful buckling with cryotherapy a month earlier. A vitrectomy with gas and oversewing of the buckle was performed. The retina was attached but within 2 months developed an epiretinal membrane that was peeled. His vision improved from 6/60 to 6/12. At 3 years following this procedure, he was discovered to have raised intraocular pressure (IOP) in his right eye, with a narrow but open angle. His left IOP was normal and his angle was slightly narrow. He was commenced on a topical beta -blocker to his right eye. After 4 years, he developed a symptomatic cataract in the right eye and underwent phacoemulsification with an intraocular lens implantation. Over the next few months, he developed right metamorphopsia and his vision fell from 6/9 to 6/36 and was found to have developed a macular hole.

Therefore, a right internal laminar membrane peel was performed. An internal search revealed a retinal break at 12 o'clock that was lasered. An air/16% C3F8 exchange was performed. The postoperative instruction was to lie face down.

On the first postoperative day, the patient was found to have an IOP of 45 mmHg in his right eye with an attached retina. Systemic acetazolamide and topical beta blockers and alpha agonists were given and the IOP fell to 38 mmHg. The patient, however, complained of feeling unwell and of an ache over his forehead, which he blamed on pressure on his forehead from posturing. Further topical therapy was given and the right IOP fell to 32 mmHg, but the patient still complained of feeling unwell. The IOP in his left eye was checked and found to be 52 mmHg with an associated shallow anterior chamber. A diagnosis of acute angle closure glaucoma was made. Further systemic and topical treatment was given and the respective IOPs fell to 31 and 21 mmHg in the right and left eyes with associated relief of the symptoms. A left YAG peripheral iridotomy was subsequently performed.

Comment

The most likely cause of the acute glaucoma in the unoperated eye was the prolonged posturing in the face down position. Indeed, one provocative test for glaucoma is to place patients in the prone position.² The mechanism for this is the shifting of the lens-iris diaphragm anteriorly. This shallows the anterior chamber and narrows the angle. In our patient, the problem was compounded by the dilatation of the eye. Although it is unlikely that the episode of angle closure was solely precipitated by dilatation as both eyes had been dilated previously at vitreo-retinal clinic without incident. Also, gonioscopy had found a slightly narrow angle and the axial length was not particularly short. Biometry prior to the cataract surgery found axial lengths of 24 and 23.7 mm in the right and left eyes, respectively. Furthermore, it is unlikely that there was a phacomorphic component as there was no significant cataract in the left eye.

Raised IOPs can, therefore, be found in both the operated and unoperated eyes following pars plana vitreous surgery. Indeed for the unoperated eye this is not surprising, as vitreoretinal surgery often requires prone posturing and dilatation, both of which may precipitate angle closure glaucoma in those at risk.