Vein occlusions and their two types
The retina receives its blood supply from the central retinal artery that divides at the optic nerve into little arterioles. These arterioles then become the retinal capillaries and feed the retina, and return to the optic nerve as retinal venules. Then, they flow out of the eye as the central retinal vein.
The retinal vein can quickly become occluded either in its entirety as a central retinal vein occlusion or partly as a branch retinal vein occlusion. Patients who get a central retinal vein occlusion can get macular oedema, and their vision will be reduced. We investigate these patients with visual acuity testing, retinal imaging with OCT and SLO, and also cardiovascular tests. We can treat central retinal vein occlusion with either intravitreal steroids or intravitreal injection of Anti-VEGF agents such as Avastin, Lucentis or Eylea, to reduce macular oedema and help improve visual acuity.
Long-term effects of central retinal vein occlusion include distortion from macular oedema, even once macular oedema has settled. This effect can be a central distortion that affects reading and fine vision. Fortunately, although central retinal vein occlusion is a common cause of marked or total loss of vision in middle aged and elderly population, there are two types – one of which is less severe than the other.
What are the different types of vein occlusions?
There are the ischaemic type and the non-ischaemic type of vein occlusions. Ischaemia is a restriction in blood supply to tissues, causing a shortage of oxygen and glucose needed for cellular metabolism (to keep tissue alive). As you can imagine, the ischaemic type is likely to affect the vision much more profoundly, whereas the non-ischaemic central retinal vein occlusion (CRVO) is comparatively more benign. The latter results in a central scotoma from cystoid macular oedema, but does not develop the complications of ocular neovascularisation and secondary glaucoma.
In contrast, ischaemic central retinal vein occlusion can be a seriously blinding disease because of the following effects of anterior segment neovascularisation leading to neovascular glaucoma and blindness.
What is particularly fortunate is that over 75% of patients who get CRVO have the non-ischaemic type. So only about one-quarter to one fifth of patients suffer the kind of CRVO that can cause severe permanent visual loss.
It’s important that we differentiate between the two types and this involves the assistance of our medical colleagues working very closely with our medical retina colleagues such as Professor Michel Michaelides and Mr Jaheed Khan at Clinica London.