Diabetic retinopathy and cataract surgery.

Two papers in the current issue, one from Pollack, Dotan, and Oliver of Israel and the other from Cunliffe and colleagues of Cambridge, deal with the effects of cataract surgery on diabetic retinopathy and its complications. All ophthalmologists are aware that there are possible extra hazards when cataract extraction has to be done in the presence of diabetic retinopathy, but in view of the fact that about 10% ofcataract patients have diabetes, and that most of those whose diabetes is of fairly long duration are also likely to have retinopathy, it is surprising that in the ordinary course of events serious postoperative complications of the sort one might fear seem to happen so seldom. Galloping rubeosis and/or accelerated retinopathy ought to be almost everyday occurrences in busy cataract programmes, yet they do not appear to be. There is no doubt that the postoperative visual prognosis of diabetics with retinopathy is worse than of those without, but that is only what one would expect. Perhaps a more important consideration is whether the retinopathy 'is itself exacerbated by the patient being rendered aphakic. If microvascular ischaemia is the primary event in diabetic retinopathy, with neovascularisation of retina and eventually iris to follow, what would be the most likely effect ofaphakia? One would have thought that the freer movement of fluids between anterior and posterior segments, with a general tendency towards the anterior part ofthe eye, would shift the neovascularising stimulus (whatever it is) forwards. Rubeosis ought to be more likely and retinal neovascularisation less likely. There is indeed some evidence that the risk ofrubeosis is increased by extraction,' but the evidence for a relative improvement in retinal neovascularisation does not seem to be forthcoming, and indeed one of the papers in the present issue indicates the exact opposite. It is even suggested that the increase of neovascularisation which is said to occur might be directly due to the absence of the lens, which is thought normally to contribute a component to the anti side of the pro-anti neovascularisation balance thought to exist in the normal eye. That there is evidence for an antineovas-cularising factor in the lens is not disputed (the matter is referenced in the paper by Pollack et al), but it is only one component in what is probably a complex interplay of factors and seems unlikely to play a major role in view of the large numbers of diabetic …