2 The procedure
2.1.1 AMD is the most common cause of blindness in developed countries. A proportion of patients with AMD have wet AMD. Wet AMD is characterised by the abnormal growth of blood vessels in the choroid layer underneath the macular part of the retina. These vessels can threaten vision if they leak and cause scarring.
2.1.2 Current treatments for wet AMD include laser photocoagulation, photodynamic therapy and intravitreal injections of anti-VEGFs. Patients with advanced disease may benefit from optical aids such as magnifying glasses, eccentric viewing training and implantation of miniature lens systems.
2.2.1 Epiretinal brachytherapy for wet AMD aims to slow down the growth of blood vessels that cause wet AMD by administering beta radiation therapy targeted at the abnormal, leaking vessels.
2.2.2 The procedure is usually carried out with the patient under local anaesthesia, and is normally used in combination with an anti-VEGF agent. A vitrectomy is performed, and an intraocular epiretinal probe is placed in the vitreous cavity, over the fovea. Beta radiation is delivered by the probe. The radiation dose received by the patient is less than the dose received during a typical chest X-ray. The sclera is closed with an absorbable suture and the eye is patched. Prophylactic antibiotics and steroids are usually administered.
2.2.3 A number of different devices are available for this procedure.
Sections 2.3 and 2.4 describe efficacy and safety outcomes from the published literature that the Committee considered as part of the evidence about this procedure. For more detailed information on the evidence, see the overview
2.3.1 A case series of 34 patients treated by epiretinal brachytherapy (concomitant treatment not described) reported that 63% and 50% of patients receiving 24 Gy and 15 Gy of radiation respectively gained 1 or more letters of visual acuity at 12-month follow-up (absolute figures not given). In the same study, visual acuity improved by more than 15 letters in 21% and 0% of patients respectively (absolute figures not given).
2.3.2 A different case series of 34 patients treated by epiretinal brachytherapy plus anti-VEGF injections reported a gain of 8.9 letters in best-corrected visual acuity after the procedure; 38% (13/34) of patients demonstrated a clinically significant improvement of 3 lines or more at a median follow-up of 12 months. At 36-month follow-up, the mean change in visual acuity was a gain of 3.9 letters (n = 19); 21% (4/19) of patients had gained 15 letters or more.
2.3.3 The Specialist Advisers listed key efficacy outcomes as retention of visual acuity, number of anti-VEGF injections required, and time to recurrence of AMD.
2.4.1 The case series of 34 patients treated by epiretinal brachytherapy plus anti-VEGF injections reported that 25% (6/24), 50% (12/24) and 54% (7/13) of phakic eye patients developed cataracts at follow-up periods of 12, 24 and 36 months.
2.4.2 The case series of 34 patients treated by epiretinal brachytherapy alone reported that there were no radiation-induced toxicity adverse events at 12-month follow-up. The other case series of 34 patients, treated by epiretinal brachytherapy plus intravitreal VEGF therapy, reported non-proliferative radiation retinopathy in 1 patient at 36-month follow-up. These changes were not considered to have an adverse effect on visual acuity.
2.4.3 Retinal tear was reported in 6% (2/34) and 3% (1/34) of patients in the 2 case series.
2.4.4 The case series of 34 patients treated by epiretinal brachytherapy plus anti-VEGF injections reported raised intraocular pressure in 6% (2/34) of patients (follow-up not stated).
2.4.5 The Specialist Advisers listed anecdotal or reported adverse events as cataract formation, retinal haemorrhage, retinal detachment, infective endopthalmitis, and radiation retinopathy. They considered theoretical adverse events to include radiation optic neuropathy and radiation-induced malignancy.