10.5.3  Metabolic Alteration in Diabetes Mellitus

branch occlusion. Thus, early detection of such changes should be possible by fluorescence lifetime measurements. It is conceivable to be able to detect such unsupplied fields. In individually adapted therapy, these fields might be coagulated first.

To find such alterations, time-resolved fluorescence measurements were performed on a 77-year-old male diabetic type II patient. There were few signs of early non-exudative diabetic retinopathy in the eye with crystalline lens. Fluorescence lifetime measurements were considered for

comparison of an 82-year-old healthy subject. As in arterial branch occlusion, a definite difference was detectable in lifetime t2 in the short-wavelength channel. Figure 10.11 shows the histograms of t2 in K1 of both subjects.

The distribution of the lifetime t2 in K1 of the older healthy subject exhibits a single maximum at 497 ps. In diabetic patients, the maximum of t2 in K1 is shifted to 662 ps and an additional shoulder appears around 1,200 ps. This lifetime range around 1,200 ps was expected as a sign of reduced oxidative metabolism. It corresponds to the lifetime t2 in K1, which was detected in the non-supplied area in the arterial branch occlusion. This prolonged lifetime t2 is the result of an increasing contribution of protein-bound NADH, produced as an augmented effect of glycolysis.

The fields of reduced metabolic activity can be selected at the fundus. Figure 10.12 shows an image of lifetime t2 in K1. In this image, regions with lifetimes shorter than

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Lifetime T2 in ps

1,000 ps are red and fields of reduced metabolism with lifetimes longer than 1,000 ps are marked in green. For better orientation, the images of fluorescence intensity are also given. The contrast is weak in the image of fluorescence intensity in K1 (490–560 nm) because of the fluorescence of the lens. The contrast is much better in the long-wavelength channel, where no fluorescence of the crystalline lens is detectable. The coagulations of the fields of reduced metabolism might be a subject of further research into individually adapted therapy.

The histograms of lifetime t2 in K2 are identical to maxima at 467 ps. Further typical changes in lifetime in diabetic and healthy subjects were detected for t1 also. In channel 1 (490–560 nm), the frequency of t1 was maximal at 92 ps in the healthy subjects. For the diabetic subjects, this histogram was double humped at 97 and 132 ps. In K2 (560– 700 nm), the most frequent lifetime t1 = 92 ps in diabetics was shorter than t1 = 102 ps in the healthy subject.

Large differences between the diabetic and healthy subjects were detectable for lifetime t3 in K1. The most frequent lifetime t3 = 5,530 ps in diabetic subjects was

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considerably longer than t3 = 4,000 ps in the healthy subjects. In K2 (560–700 nm), the difference was much smaller in the diabetic subjects (t3 = 2,980 ps) than in healthy subject (t3 = 2,590 ps). As the lifetime t3 in eyes with crystalline lens is predominantly determined by the fluorescence lifetime of the lens, the prolonged lifetime in diabetic subjects is caused by metabolic changes in the lens. The main reason is the forming of glycolysed proteins (AGE), exhibiting long lifetime. An early sign of diabetic metabolic alteration is observable in the lens. Owing to excitation by blue light at 448 nm, diabetic lenses emit a strong green fluorescence.

10.5.3.2  Lifetime Images in Diabetes After Laser

Coagulation

Laser coagulation is the most frequent therapy in severe diabetic retinopathy. Changes in time-resolved autofluorescence after laser coagulation have been demonstrated in a 77-year-old diabetic patient in Fig. 10.13. An intra-

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