Neovascular glaucoma

Abstract

Neovascular glaucoma (NVG) is a severely blinding, intractable disease. The objective of this review is to provide detailed information on its basic and clinical aspects, to enable us to manage it logically. Therefore, its causes, pathogenesis and pathology, methods of early diagnosis and management are discussed. To prevent or reduce the extent of visual loss caused by NVG, the first essential is to have a high index of suspicion of its development. The most common diseases responsible for development of NVG are ischemic central retinal vein occlusion (CRVO), diabetic retinopathy and ocular ischemic syndrome. In the management strategy, the first priority should be to try to prevent its development by appropriate management of the causative diseases. If NVG develops, early diagnosis is crucial to reduce the extent of visual loss. Management of NVG primarily consists of controlling the high IOP by medical and/or surgical means to minimize the visual loss. Currently, we still do not have a satisfactory means of treating NVG and preventing visual loss in the majority, in spite of multiple modes of medical and surgical options advocated over the years and claims made. This review discusses the pros and cons for the various advocated treatments.

Fig. 1

A graphic representation of cumulative chances (in %) of developing various types of ocular NV in ischemic CRVO in relation to time from onset of the disease (in days). (Reproduced from Hayreh et al. 1983)

Fig. 2

Diagrammatic representation of sequence of events in eyes with ocular ischemia.

Fig. 3

Visual fields of 2 eyes with ischemic CRVO before and after PRP (Reproduced from Hayreh et al 1990b). (A). Visual fields of left eye of a 63-year-old man - top pre-PRP and bottom 6 months after PRP. The eye had 1754 argon laser burns, starting 81 days after onset of ischemic CRVO. Pre-PRP peripheral fields were normal with I4e and V4e but post-PRP fields showed marked deterioration and constriction. This eye developed iris NV 2 months after PRP and it lasted for almost 4½ years. (B). Visual fields of left eye of a 57-year-old man - top pre-PRP and bottom 2 years after PRP. The eye had 2250 argon laser burns, starting 112 days after onset of ischemic CRVO. Pre-PRP peripheral fields were normal with I4e and V4e but post-PRP fields showed marked constriction and deterioration. This eye developed retinal NV 5 months after the PRP, produced vitreous hemorrhage, and the NV persisted till the patient died 4 years after PRP.