Anterior chamber depth and intraocular pressure following panretinal argon laser photocoagulation for diabetic retinopathy

To the Editor: Ocular photocoagulation uses heat produced through the absorption of light by ocular pigments. Absorption of light can take place either in the tissue to be photocoagulated or in a neighboring tissue, from which heat is then transferred to the tissue of interest by thermal conduction. Thermal damage is caused by chemical changes that result when the ocular tissues are heated to temperatures high enough to denature proteins or other large molecules.1–3 A temperature increase of 10ºC to 20ºC is sufficient to produce the desired chemical changes. Photocoagulation is used in the management of retinal diseases such as diabetic retinopathy, diabetic maculopathy, subretinal neovascularization, retinal vascular abnormalities, and retinal breaks or tears of various types.3 Panretinal argon photocoagulation (PRP) is commonly performed for the treatment of proliferative diabetic retinopathy, ischemic central retinal vein occlusion, and other causes of retinal ischemia.4 Complications of PRP include thermal injury to the cornea, iris and lens, visual field loss, haemorrhage, macular edema, and elevated intraocular pressure with or without angle closure.4–6 Many transient changes after PRP occur only when a large area of the retina is treated in one session or in closely spaced sessions.5 In the study, we investigated the effects of PRP on anterior chamber depth changes and early and late period intraocular pressure. We studied 170 eyes with diabetic retinopathy (Type 2 diabetes). All patients had proliferative or high-risk preproliferative retinopathy. PRP was applied to all eyes under topical anesthesia. Patients with closed angle, rubeosis iridis, open angle or neovascular glaucoma, and other intraocular disorders were excluded. Examination before and after PRP comprised the fundus, chambers angle, visual acuity, slit-lamp examination, fundus Fluorescein angiography and IOP. IOP was measured with a Goldman applanation tonometer. Eyes with IOP over 30 mm Hg were treated with timolol maleate 0.05%. Anterior chamber depth was evaluated by the same person using A-scan ultrasonography. IOP measurements and anterior chamber depth were measured after cycloplegia. Cycloplegia was applied using cyclopentolate hydrochloride 1%. The intraocular pressure of each eye was measured during the first examination before PRP and at the first hour, first day, and the first, third and sixth months after PRP. Anterior chamber depth was also measured before PRP, and after the first hour and first day after PRP. Patients with an IOP >30 mm Hg were treated by antiglaucomatous agents. The initial treatment protocol of PRP was 850 to 1200 burns, the intensity varied from 0.2 to 1.0 W, the duration of exposure varied from 0.1 to 0.2 second, and the spot size 200 to 500 μ. Additional photocoagulation was performed if deemed necessary by the treating ophthalmologist. The paired t-test was used in the statistical analysis. The study included 85 patients with Type 2 diabetes mellitus, aged 38 to 77 years (mean, 62.0 years). In the first examination, we found high-risk nonproliferative diabetic retinopathy in 68 eyes and proliferative diabetic retinopathy in 102 eyes. While IOP was significantly elevated in the first hour after PRP, it was not significantly different in the following measurements (Table 1). IOP over 30 mm Hg was seen in four eyes in the first hour after PRP, and these eyes were treated with timolol maleate 0.05%. IOP decreased to normal levels on the first day after PRP in all these eyes. While anterior chamber depth was significantly shallow in the first hour after PRP, it was not statistically different from the first day after PRP (Table 2). None of the eyes developed neovascular glaucoma or rubeosis iridis during the observation period.