Blindness is one of the most feared complications of diabetes,
but also one of the most preventable. Diabetes is the
commonest cause of blindness in people aged 30 to 69 years.
Twenty years after the onset of diabetes almost all patients with
Type 1 diabetes and over 60% of patients with Type 2 diabetes
will have some degree of retinopathy, and even at the time of
diagnosis of Type 2 diabetes, approximately one-quarter of
patients already have established background retinopathy.
As treatment is now available to prevent blindness in the majority
of cases, it is essential to identify patients with retinopathy
before their vision is affected.
Classification of retinopathy
Diabetic retinopathy is due to microangiopathy affecting the
retinal precapillary arterioles, capillaries, and venules. Damage
is caused by both microvascular leakage due to break down of
the inner blood-retinal barrier and microvascular occlusion.
These two pathological mechanisms can be distinguished from
each other by fluorescein angiography, which is the “gold
standard” for assessing diabetic retinopathy.
Background retinopathy
Microaneurysms are small saccular pouches possibly caused by
local distension of capillary walls. They are often the first
clinically detectable sign of retinopathy, and appear as small
red dots commonly temporal to the macula.
Haemorrhages may occur within the compact middle layers of
the retina, and appear as “dot” or “blot” haemorrhages, or
rarely, in the superficial nerve fibre layer where they appear as
“flame shaped” haemorrhages (the latter better recognised as
related to severe hypertension).
Hard exudates are yellow lipid deposits with relatively
discrete margins. They commonly occur at the edges of
microvascular leakage, and may form a “circinate” pattern
around a leaking microaneurysm.
They may coalesce to form
extensive sheets of exudate. Vision is affected when hard
exudates encroach upon the macula.
Retinal oedema is due to microvascular leakage and indicates
breakdown of the inner blood-retinal barrier. It appears
clinically as greyish areas of retinal thickening, and may assume
a petal-shaped cystoid appearance at the macula, where it may
cause marked visual deterioration.
Clinically significant macular oedema (CSMO) requires
treatment. It is defined as any one of the following:
1• retinal oedema within 500 m (one-third of a disc diameter)
of the fovea
2• hard exudates within 500 m of the fovea, if associated with
adjacent retinal thickening
3• retinal oedema that is one disc diameter (1500 m) or larger,
any part of which is within one disc diameter of the fovea.
Twenty percent of eyes with untreated CSMO will suffer
significant visual loss in two years compared with 8% of
treated eyes.
Pre-proliferative retinopathy
Retinal ischaemia due to microvascular occlusion may lead to
neovascular proliferation. Signs of ischaemia include:
1• cotton wool spots, which appear as white patches with rather
feathery margins and represent nerve fibre layer
microinfarcts; they become highly significant when there are
more than five
2• large dark “blot” haemorrhages
3• venous beading and looping
4• intraretinal microvascular abnormalities (IRMA).
Proliferative retinopathy
New vessel formation may occur at the optic disc (NVD) or
elsewhere on the retina (NVE). Disc new vessels are particularly
threatening to vision and if allowed to progress commonly lead
to vitreous haemorrhage. If untreated, 26% of eyes with “highrisk”
and neovascular proliferation on the disc will progress to
severe visual loss within two years. With laser treatment this is
reduced to 11%.
Advanced eye disease
In advanced proliferative diabetic retinopathy, progressive
fibrovascular proliferation leads to blindness due to vitreous
haemorrhage and traction retinal detachment.
Rubeosis iridis and neovascular glaucoma occur when new vessels form on the
iris and in the anterior chamber drainage angle, leading to a
most painful blind eye which occasionally requires enucleation
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