Diabetes can affect the eyes in a number of ways. The most common and characteristic form of involvement is diabetic retinopathy. About one in three young patients is likely to develop visual problems, and in the UK 5% have in the past become blind after 30 years of diabetes; diabetes is the commonest cause of blindness in the population as a whole up to the age of 60 years. Other forms of eye disease may also occur: THE LENS may be affected by reversible osmotic changes in patients with acute hyperglycaemia-causing blurred vision-or by cataracts.
NEW VESSEL FORMATION IN THE IRIS (rubeosis iridis) may develop as a late complication of diabetic retinopathy and can cause glaucoma.
EXTERNAL OCULAR PALSIES, especially of the sixth nerve, can occur (a mononeuritis). The natural history of retinopathy.
Diabetes causes increased thickness of the basement membrane and increased permeability of the retinal capillaries. Aneurysmal dilatation may occur in some vessels while others become occluded. These changes are first detectable by fluorescein angiography: a fluorescent dye is injected into an arm vein and photographed in transit through the retinal vessels. This technique is not necessary to screen effectively for retinal disease. After 20 years of IDDM, almost all patients have some retinopathy- 60% progress to proliferative retinopathy. After 20 years of NIDDM >80% have some retinopathy, 20% have proliferative changes.
BACKGROUND RETINOPATHY. The first abnormality visible through the ophthalmoscope is the appearance of dot ‘haemorrhages’, which are actually due to capillary microaneurysms. Leakage of blood into the deeper layers of the retina produces the characteristic ‘blot’ haemorrhage, while exudates of fluid rich in lipids and protein give rise to hard exudates. These have a bright yellowwhite colour and are often irregular in outline with a sharply defined margin. These changes rarely develop in young patients with a duration of diabetes under 10 years, but by 20 years virtually all eyes will at least manifest the occasional dot haemorrhage on careful ophthalmoscopy. In contrast, retinopathy may be present at diagnosis or shortly thereafter in older patients.
Background retinopathy does not in itself constitute a threat to vision but may progress to two other distinct forms of retinopathy: maculopathy or proliferative retinopathy. Both are the consequence of damage to retinal blood vessels and resultant retinal ischaemia.
DIABETIC MACULOPATHY. This may lead to blindness in the absence of proliferation and particularly affects the older patient with IDDM. Macular oedema is the first feature of maculopathy and may in itself result in permanent macular damage if not treated early. The first, and only, sign of this is deteriorating visual acuity and the condition cannot be diagnosed with standard ophthalmoscopy.
This is why it is essential to screen patients with diabetes regularly for changes in visual acuity. In most cases, however, maculopathy does not generate sufficient oedema to cause early loss of acuity. The process may then be detected in its later stages as encroachment of hard exudates and haemorrhages on the macular area. These changes are easily visible on ophthalmoscopy, but only through fully dilated pupils.
PREPROLIFERA TIVE RETINOPATHY. Progressive retinal ischaemia leads to further changes which herald proliferative, sight-threatening retinopathy. The earliest sign is the appearance of ‘cotton-wool spots’, representing oedema resulting from retinal infarcts. Unlike hard exudates they may also occur in severe hypertensive retinopathy. The term ‘soft exudate’ is often used synonymously but is best avoided. Cotton-wool spots are greyish-white, have indistinct margins and a dull matt surface, unlike the glossy appearance of hard exudates. Venous beading and/or venous loops are other recognized preproliferative changes.
PROLIFERATIVE RETINOPATHY. Hypoxia is thought to be the signal for formation of new vessels. These lie superficially or grow forward into the vitreous, resembling fronds of seaweed. They branch repeatedly, are fragile, bleed easily (because they lack the normal supportive tissue) and may give rise to a fibrous-tissue reaction. With advanced retinopathy, haemorrhages can be preretinal or into the vitreous. A vitreous haemorrhage presents as a loss of vision in one eye, sometimes noticed on waking, or as a floating shadow affecting the field of vision. Ophthalmoscopy gives the appearance of a featureless, grey haze. Partial recovery of vision is the rule, as the blood is reabsorbed, but repeated bleeds may occur. Loss of vision may also result from fibrous proliferation associated with new vessel formation. This may give rise to traction bands that contract with the course of time, producing retinal detachment.
Senile cataracts develop some 10-15 years earlier in diabetic patients than in the remainder of the population. Juvenile or ‘snowflake’ cataracts are much less common. These are diffuse, rapidly progressive cataracts associated with very poorly controlled diabetes. They should be distinguished from temporary lens changes that occasionally appear during hyperosmolar coma and resolve when the coma is brought under control.
Examination of the eye
Careful systematic examination of the eye is essential. Visual acuity and eye movements are tested, and the pupils are dilated with a quick-acting mydriatic such as tropicamide 0.5%. Dilating drugs should not be used in patients with a history of glaucoma, except with the advice of an ophthalmologist.
The examination begins at arm’s length. At this distance, cataracts are silhouetted against the red reflex of the retina. The ophthalmoscope is advanced until the retina is in focus. The examination begins at the optic disc, moves through each quadrant in turn, and ends with the macula (since this is least comfortable for the patient). The ophthalmoscope is then adjusted to the +10 dioptre lens for examination of the cornea, anterior chamber and lens. The location of abnormalities should always be sketched in the notes for future reference. Management of diabetic eye disease.
There is no specific medical treatment for background retinopathy, but patients are advised not to smoke and hypertension should be treated. Rapid progression may occur in pregnant patients and in those with nephropathy, and these groups need frequent monitoring. All patients with retinopathy should be examined regularly by a diabetologist or ophthalmologist. Early referral to an ophthalmologist is essential in the following circumstances:
• Deteriorating visual acuity
• Hard exudates encroaching on the macula
• Preproliferative changes (cotton-wool spots or venous beading)
• New vessel formation
The ophthalmologist may perform fluorescein angiography to define the extent of the problem. Maculopathy and proliferative retinopathy are treatable by retinal laser photocoagulation; in the latter condition early effective therapy reduces the risk of visual loss by about 50%. The value of photocoagulation is particularly marked in those with disc (as against peripheral) new vessels. In one trial only 15% of treated, as against 50% of untreated, eyes with disc new vessels progressed to legal blindness. Treatment in this case is by panretinal photocoagulation with 2000–5000 laser burns to each eye.