Abstract
Purpose: :
To investigate the hypothesis that panretinal photocoagulation (PRP) stops progression of proliferative diabetic retinopathy (PDR) by increasing intraretinal PO2 over the lesion and the surrounding region.
Methods: :
O2 diffusion in the retina was simulated using a two–dimensional mathematical model in cylindrical coordinates. A central cylinder of lesioned retina was surrounded by an annular cylinder of undamaged retina. In the lesioned area, the outer retina (OR) was either absent, or replaced by scar tissue that did not consume oxygen. In the undamaged tissue, the OR was represented by the three–layer O2 diffusion model developed previously. The inner retina (IR) of both regions was assumed to have a uniform oxygen consumption that followed Michelis–Menten kinetics. The IR had no retinal circulation, representing severe capillary dropout in DR. Parameters used in the study came from intraretinal measurements in the photocoagulated retina of healthy cats and from previously determined values from normal retina. Finite element modeling (Femlab v. 3.1) was used to solve the model. Parameters, such as choroidal PO2, lesion size, IR O2 consumption, and the presence or absence of scar tissue, were varied to understand their effects on retinal PO2.
Results: :
PO2 in IR was higher both in the lesion and in the region immediately adjacent to the lesion than in an unphotocoagulated (control) region far from the lesion. In all cases, the effect of the lesion was most pronounced on inner retinal PO2 within the lesioned area. For most cases simulated, a 10% increase in IR PO2 adjacent to the lesion compared to control extended only about 50–100 µm from the edge of the lesion. Placing the IR right next to the choroid (i.e. eliminating scar tissue) and reducing IR metabolism had the largest positive effect on PO2. Smaller (200 µm vs. 500 µm in diameter) lesions were more effective at increasing the fraction of retina in which PO2 was increased.
Conclusions: :
The results supported the hypothesis that PRP stops progression of PDR by increasing PO2 in photocoagulated retina, and to a smaller extent in non–photocoagulated regions of the retina.
Keywords: diabetic retinopathy • retina • metabolism