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Handbook of Diabetes, 4th Ed., Excerpt #14: Diabetic Eye Disease

New vessel growth or neovascularisation is the hallmark of proliferative retinopathy and results from the local release of growth factors (such as vascular endothelium-derived growth factor; VEGF) in response to ischemia (Figures 15.9, 15.10). These vessels are fragile, fine outgrowths from retinal veins and grow forward into the vitreous. Because of this, they are prone to shear stress and rupture, resulting in preretinal or vitreous hemorrhage and sudden visual loss (Figure 15.11).

LANDMARK CLINICAL TRIAL

Kroc Collaborative Study Group. Blood glucose control and the evolution of diabetic retinopathy and albuminuria. A preliminary multi-centre trial. N Engl J Med 1984; 311: 365-372.

This was an international, multicenter trial of improved versus conventional glycemic control on microvascular complications in the eye and kidney. Seventy patients were randomized to either CSII or conventional insulin (CIT) for 8 months. All had non-proliferative retinopathy at baseline. Twenty-four hour average blood glucose from a seven-point profile collected at home using plastic fluoridated tubes was 11 mmol/L (198 mg/dL) and 10.4 mmol/L (187 mg/dL) at baseline in the CSII and CIT groups respectively. Baseline total HbA 1c (normal range 6.5 – 7.8%) was 10.3% and 10.1% respectively. During the 8-month trial glycemia did not change in those on CIT but mean 24-hour glucose was 6.4 mmol/L (115 mg/dL) and HbA1c 8.1% in those on CSII. Retinopathy worsened with the appearance of IRMAs and cotton wool spots suggestive of ischemia. Albuminuria, however, was significantly reduced in the 10 patients with baseline values > 12 ì g/min on CSII with no change in the 10 on CIT. The authors concluded that medium-term maintenance of glycemic separation was possible (previously this had been extremely difficult to achieve) but that the worsening of retinopathy was a concern. They concluded: ‘These preliminary observations indicate the need for longer trials (particularly of primary prevention)’.
This study set the stage for the much bigger DCCT – it could almost be considered as the pilot. The finding of acute worsening of retinopathy was confirmed by the Stockholm and Oslo studies and was seen in the secondary prevention arm of the DCCT. Later analysis of the Kroc patients showed that in the long term, eye complications were less severe in the CSII group, thus providing reassurance for the DCCT.
The study also showed that CSII was an effective, safe and practicable research tool.
The study name derived from the Kroc Family Foundation which funded the trial. Dr Robert Kroc was one of the founders of the McDonalds hamburger chain.

 

New vessels are associated with fibrous bands that can cause traction retinal detachment or tearing of vessels, leading to further hemorrhage (Figure 15.12). Sometimes the hemorrhage remains encapsulated between these fibrous bands, the retina and the vitreous, leading to a fluid level and a flat-topped (boat-shaped) appearance.

Tractional detachment results in ‘tenting’ or folding of the retina with grey-white bands and occasional tears (Figure 15.13). Ophthalmic ultrasound is often helpful at detecting detachment, particularly if the retina is obscured by hemorrhage (Figure 15.14).

The most common cause of visual loss, however, is maculopathy, which results from ischemia and subsequent edema of the central retina. Focal maculopathy is usually associated with areas of circinate or star-shaped exudate within one optic disc diameter of the macula (Figure 15.15). Diffuse macular edema results from ischemia and causes thickening of the retina. It is harder to detect clinically and needs either stereo ophthalmoscopy or optical coherence tomography (OCT), which can generate clear images of the retina and accurate estimates of thickness (Figure 15.16).