Retinal Pathology after Central Retinal Vein Occlusion.

OCCLUSION of the central retinal vein causes incomplete haemorrhagic infarction of the inner layers of the retina. Haemorrhagic infarction describes a situation in which the venous backflow of an area of tissue is interrupted. As a result the flow of blood has to stop; ischaemia and resulting increase of vascular permeability lead to retinal oedema and extensive haemorrhages. The central retinal artery remains open and goes on pushing more blood into the retina. In the inner retina the ischaemia soon results in degeneration of the neurons of the inner retinal layers. The glia and the mesodermal retinal structures, however, survive and form a scar. This incompleteness of the haemorrhagic infarction of the inner retina in central vein occlusion has its explanation in the double blood supply of the retina. The inner retinal layers are normally supplied by the retinal blood system, while the chorio-capillaris supplies the outer retinal layers. After central vein occlusion the supply from the chorio-capillaris is obviously sufficient for a survival of the glia and the mesodermal structures of the inner retina until the retinal circulation is re-established by venous collaterals and recanalization of the thrombus. The high metabolic needs of the neurons of the inner retina, however, cannot be supplied from the chorio-capillaris and these cells suffer irreversible damage which causes blindness. Secondary (haemorrhagic) glaucoma is a very common complication of central vein occlusion, and occurs about 2 to 5 months after the occlusion. The above description of the retinal changes which follow venous occlusion may be sufficient to explain this pathological process to a student. The ophthalmologist, however, should add all the available details which can be gained by every possible approach of research. It is the purpose of this study to demonstrate the early and late pathology of the second neuron of the visual pathway which is the direct cause of the blindness which finally results from central vein occlusion. Along with the pathology of the retinal part of the second neuron-the ganglion cells and the nerve fibres-the neuroglia and the retinal blood vessels will be considered. Two typical cases of occlusion of the central retinal vein-one early and one late-are used as examples for this demonstration. Halfof each involved