European Journal of Molecular & Clinical Medicine

Abstract

24-year-old apparently healthy male presented with sudden diminution of vision with confirmed clinical findings of Eales disease in both eyes.
Eales disease is an idiopathic obliterative vasculopathy. It was discovered in 1880, by Sir Henry Eales, who first described the Eales disease in a cluster of young males.^[1]. All patients were young and presented with complaints of vomiting, headache, constipation, epistaxis. Eales believed it to be a vasomotor neurosis, lead to rupture of retinal and nasal vessels with consequent haemorrhage.^[2] Eale’s disease affects healthy young adults. Male predominance (97.6%) has been reported in majority of cases. The predominant age of onset is between 20 and 40 years. One in 200-250 ophthalmological patients were detected to have Eale’s disease. Retinal changes include perivascular phlebitis, peripheral nonperfusion, and neovascularization. Visual loss is characteristically caused by bilateral recurrent vitreous haemorrhage and its sequelae.^[2] It is believed hypersensitivity to tuberculoproteins play an important role in etiology of Eales disease. Corticosteroids remain mainstay of therapy in active perivasculitis stage of Eales disease. Photocoagulation is the mainstay of treatment in proliferative stage of Eales disease. Pars plana vitrectomy has shown improvement in visual acuity in cases of recurrent vitreous haemorrhage. Application of endolaser is mandatory at the end of vitreous surgery. Additional procedures such as lensectomy and buckling may be done as and when required. ^[3]