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Infantile angle closure glaucoma (ACG) is a rare consequence of retinopathy of prematurity (ROP) and usually occurs a few years after laser treatment for ROP.1–3 A Medline search for ACG following laser photocoagulation extracted only one case. In the case, ACG occurred in 2 weeks after laser photocoagulation and although occurrence of iris bombe in both eyes was described, the mechanism for the ACG was not fully clarified.4
We present a case of bilateral ACG that occurred within a several weeks after the laser photocoagulation for ROP. We shall discuss the importance of ultrasound biomicroscopy (UBM) in the diagnosis.
A baby girl, born at 25 weeks gestation weighing 796 g, was diagnosed with stage 2 plus, zone 2 ROP bilaterally at 33 weeks. Diode laser photocoagulation, 986 applications right eye and 629 left eye, with 200–240 mW, 0.4 second duration, was performed by a paediatric ophthalmologist. On the following day, severe hyphaema was observed bilaterally but there was no evidence of choroidal detachment by B-mode ultrasound sonography. Topical atropine and corticosteroid were started and she was followed up conservatively. During the follow up period, total posterior synechia was formed in the both eyes and the anterior chamber became shallow.
At 39 weeks, the corneal diameter had increased, and the anterior chamber was extremely shallow bilaterally. The intraocular pressure (IOP) in the right eye was elevated to 28 mm Hg, and she was referred to our hospital.
Our examination showed that the corneal diameter was increased to 11 mm bilaterally. Slit lamp examination showed corneal oedema and shallow anterior chamber depth bilaterally, especially in the right eye. The corneal oedema made the funduscopy difficult bilaterally. The IOP under the general anaesthesia was 33 mm Hg right eye and 17 mm Hg left eye. Persistent pupillary membranes and iridohyaloid vessels were observed but rubeosis iridis was not observed (fig 1).
UBM images of anterior segments demonstrated iris bombe bilaterally, and the entire right iris surface was adherent to the corneal endothelium. As a result, the anterior capsule of the lens was also attached to the corneal endothelium (fig 2). Choroidal detachment and a retrolental mass were not observed by B-mode ultrasound sonography (fig 2).
Peripheral iridectomy was performed bilaterally (fig 1). Postoperatively, her peripheral anterior chamber deepened bilaterally although the lens in the right eye was still adherent to the corneal endothelium. Indirect ophthalmoscopy revealed normal cup to disc ratio. The IOP fell to normal levels bilaterally.
Shallow anterior chambers in ROP patients are known to be caused by various factors—for example, choroidal detachment after excessive photocoagulation, development of retrolental mass, or relative increment in lens thickness,5 but usually the cause of shallow anterior chamber cannot be determined. In our case, the development of hyphaema after photocoagulation induced posterior synechia, and the iris bombe followed. The displacement of the anterior chamber structures was induced by the forward movement of the iris-lens diaphragm in the right eye, and the ocular fragility in premature baby may explain this deformity.
Vitreous haemorrhage is known to occur in 7.9% of ROP cases after photocoagulation.6 In our case, there is a possibility that the hyphaema was derived from vitreous haemorrhage. Another possibility is an accidental photocoagulation of persistent pupillary membranes and/or iridocorneal vessels caused the hyphaema. We are not aware of such morphological changes after photocoagulation for ROP.
ACG that occurs immediately after retinal photocoagulation in ROP patients is rare, but is still an important complication. In ROP patients, the lens and its ligament are weak, and therefore not only ACG but also lens displacement occurred. It is important that we be aware of the possible development of ACG following retinal photocoagulation for ROP.