• diabetic retinopathy
• macular oedema
• vision loss
• vitrectomy

In patients with diabetic retinopathy, laser treatment is directed at the prevention of visual loss rather than at visual improvement. Treatment should therefore be applied before visual loss occurs, when the risk of visual loss justifies adverse effects of treatment. The risk of visual loss is linked to the likelihood of progression of retinopathy to sight threatening forms, which in turn depends on epidemiological factors such as sex, ethnicity, diabetes type, and duration; systemic factors such as hypertension, glycaemic control, and serum lipids; specific risk factors such as pregnancy, cataract surgery, and tightened glycaemic control; and, lastly, ophthalmoscopic signs (box 1).

This patient has type 2 diabetes, and data from the Wisconsin Epidemiological Study of Diabetic Retinopathy (WESDR)^1,2 (table 1) suggest that retinopathy is likely to progress slower than in type 1 disease, especially if insulin therapy is not required. Glycaemic control, on the other hand, is very poor and this is likely to accelerate retinopathy progression. In the UK Prospective Diabetes Study (UKPDS), patients with type 2 diabetes randomised to intensive glycaemic control had retinopathy progression rates 21% lower than the conventional treatment cohort.³ Mean glycosylated haemoglobin (HbA_1c) values were respectively 7.0% and 7.9%, much lower than in this case. UKPDS data indicate that the effect of poor glycaemic control is synergistic with that of poor hypertensive control, but fortunately in this patient hypertensive control is good, and there is no biochemical evidence of renal dysfunction, which might compromise hypertensive control in future. In the UKPDS, patients randomised to intensive control of blood pressure (⩽150/85) had a one third reduction in the rate of retinopathy progression compared to conventionally treated patients.⁴ This patient also has significantly elevated plasma cholesterol levels. Whereas there is no randomised controlled trial demonstrating a beneficial effect on retinopathy with reduction in plasma cholesterol, the ETDRS associated exudate deposition with higher plasma cholesterol values.⁵

In this patient, significant haemorrhage and venous beading are present in four quadrants, and intraretinal microvascular abnormalities (IRMA) in at least one. New vessels, fibrous proliferation, retrohyaloid, and intragel haemorrhage are not apparent. Based on the 4-2-1 rule⁶ (box 2), this would be classified as very severe non-proliferative diabetic retinopathy. In the Early Treatment Diabetic Retinopathy Study final retinopathy severity scale, eyes with this level of disease had a 17% probability of developing high risk proliferative retinopathy within a year (table 2).⁷ Exudate approximately one disc diameter temporal to the centre of the macula suggests the possibility of clinically significant macular oedema, albeit eccentric, with little immediate threat to vision.

This patient has fundus signs consistent with a 17% risk of developing high risk proliferative diabetic retinopathy in a year, possible macular oedema, poor glycaemic control, and elevated serum cholesterol. Improved glycaemic control may be beneficial, though close ophthalmological surveillance during the transition period is desirable. A reduction in serum cholesterol may reduce risks associated with macrovascular disease, even if there is no unequivocal benefit to retinopathy. Careful stereoscopic evaluation of the macula, coupled with fluorescein angiography if indicated, may reveal clinically significant macular oedema, which if present should be treated with macular laser therapy according to ETDRS guidelines. Panretinal laser therapy in the absence of other specific risk factors for retinopathy progression, and in the absence of high risk proliferative disease, confers little potential benefit to offset against side effects such as macular oedema. Provided the patient is a consistent attender, review within 3 months to examine for signs of proliferative disease is appropriate (table 2).