Treatment of Diabetic Retinopathy by Light Coagulation

Abstract

THE idea for the treatment of advanced diabetic retinopathy by light-coagulation was first introduced by Meyer-Schwickerath (1954) of Essen, Germany. The instrument used was the light-coagulation apparatus developed by Dr. H. Littman and manufactured by the firm of Carl Zeiss. Some of the changes in diabetic retinopathy are similar to those found in the retina in certain other neovascular diseases which are benefited by lightcoagulation. These include Leber's aneurysms, Eales's disease, and angiomatosis. Since it has been established that light-coagulation can destroy certain vessels within the eye and that firm chorio-retinal adhesions can be formed, it was felt that this treatment might be of some value in reducing the incidence of recurrent intra-ocular haemorrhage and detachment of the retina associated with this disease. Material and Method This series consists of 28 patients (42 eyes) involving a total 117 treatments. There were seventeen women and eleven men, their ages ranging from 26 to 78 years. They all had advanced diabetic retinopathy as manifested by retinitis proliferans and a history of recurrent haemorrhage into the vitreous, and were referred by physicians, who continued their medical management while the lightcoagulation therapy was being evaluated. The eyes were observed for from 12 to 43 months after treatment. A pertinent medical history was taken, including the onset of diabetes, the onset of ocular symptoms, and the degree of control. Careful and complete physical examination of the eye was carried out to find the best correctable visual acuity and the visual fields when feasible, with slit-lamp examination, ophthalmoscopy, tonometry, and serial retinal photographs. The light-coagulation was performed under local anaesthesia using 2 per cent. retrobulbar Xylocaine, the pupil being maximally dilated before each treatment. The amount of light delivered to the involved area was varied in each case according to what was felt to be the minimal reaction necessary to produce a mild retinal burn. This was altered somewhat depending upon the degree of abnormality of the lesion being treated. The light was directed to the geographic site of the retina showing the maximum diabetic involvement. An attempt was made to delimit the retinitis proliferans and to obliterate the neovascular tissues. Care was taken to avoid the macular and paramacular regions. Proliferation on the nerve head was not treated directly. Aneurysms and vessels suspected of recent haemorrhage were coagulated. In general, the course of the large vascular trunks where the proliferation or neovascularization was most prominent was followed, treatment being