Screening--see "Management of Type 2 Diabetes"
I. Epidemiology & natural history
- Earlier onset in type II than in type I
- Clearly related to degree and duration of hyperglycemia, as well as HTN
- Risk of blindness greater for African-Americans than for whites with NIDDM
- Progression can be accelerated by pregnancy, puberty, and cataract surgery
- Vision loss can result from macular edema or capillary nonperfusion (central vision loss), distortion and detachment of retina by new blood vessels and contraction of accompanying fibrous tissue, or hemorrhage in preretinal or vitreous spaces.
II. Nonproliferative form (earlier stage)
- Present in 20% at time of dx
- Few scattered microaneurysms with or without occas. blot hemorrhagesIn "preproliferative" stage get exudates (yellow), cotton-wool spots (infarcted nerve fiber layer), and other vascular changes, e.g. vessel "sausaging"
- Usually not associated with vision impairment
- Macular edema can occur and lead to vision loss
III. Proliferative form (later stage)
- New vessel formation (neovascularization) of disk or posterior pole; eventually vitreous hemorrhage, secondary retinal detachment, and blindness
- Photocoagulation (by argon laser or xenon arc light) prevents further visual loss and may improve vision for some
- Vitrectomy is helpful if have vitreous hemorrhage, scarring, or retinal detachment
IV. Prevention
- Good glycemic control
- ACEI's may be protective! (see notes on Ann. Int. med. 128:982, 1998 in Nephropathy section)
V. Treatment
- Lased photocoagulation reduces risk of vision loss; may be ass'd with risk of modest loss of visual acuity and contraction of visual field; usually recc'd only for pts with proliferative DM retinopathy or severe non-proliferative DM retinopathy