Vitreopapillary traction in proliferative diabetic vitreoretinopathy

Aim—To present the clinical profile of a new entity in advanced proliferative diabetic vitreoretinopathy (PDVR). Mechanisms of vision loss due to vitreopapillary traction on the nasal optic disc are described, followed by an introduction of methods for prevention and treatment in such cases. Methods—17 patients with PDVR and traction on the nasal side of the optic disc, pallor of the optic nerve head, and reduced visual acuity were included in the study. Six patients were observed retrospectively and 11 patients prospectively before and after pars plana vitrectomy. Preand postoperative examinations included visual acuity, Goldmann’s visual field, fluorescein angiography, and measurements of visual evoked potentials (VEP). Results—During a postoperative follow up period of 3 to 24.5 months (mean 14.5 months) an improvement in optic disc appearance combined with an increased visual acuity (mean increase in VA = 0.171) was observed in 15/17 (88.3%) patients. In addition, 8/17 (47%) of these patients showed higher VEP amplitudes (mean 3.83 μV), and eight (6/8 of the same patients as VEP amplitudes) patients showed a reduction of latency (mean reduction 22.25 ms) during VEP assessment. Conclusion—These results suggest that vitreopapillary traction may damage the anterior optic nerve, via decreased axoplasmatic flow in the optic nerve fibres and/or mechanical reduction of perfusion in the posterior ciliary arteries. The eVects of each mechanism appear to be reversible, but in the long term might lead to irreversible optic nerve atrophy. Therefore, in patients with vitreopapillary traction, early vitrectomy should be considered as a method to prevent optic neuropathy. (Br J Ophthalmol 1999;83:261–264) Optic nerve atrophy may be due to intraorbital or CNS compression or ischaemia producing direct eVects on the optic nerve, or progressive damage to retinal ganglion cells caused by inflammation, degeneration, elevated intraocular pressure, or ischaemia. In patients with proliferative diabetic vitreoretinopathy (PDVR), another possible mechanism for nerve atrophy may be vitreopapillary traction of the optic disc, as described by De Bustros and co-workers in 1987. The concept of vitreopapillary traction and its relief during vitrectomy for PDVR has been debated over the past Table 1 Overview of patients investigated in this study. Preand postoperative visual acuity was measured in all patients. Available VEP results are shown. Evaluation mode, duration of symptoms, and determination of diabetic stage are displayed for every individual Patient No Visual acuity pre/post VEP latency (ms) pre/postop VEP amplitude (μV) pre/postop Duration of traction (years) Evaluation type Diabetes type 1 0.02/0.1 84/88 8.6/6.6 1 prospective II 2 0.3/0.5 168/130 3.7/3.9 1 prospective II 3 0.02/0.1 86/82 3.9/2.9 5 prospective II 4 0.02/0.05 85/78 2.8/14.8 1 prospective II 5 0.5/0.5 154/152 4.3/6.4 1 prospective I 6 0.05/0.1 118/230 2.3/12.1 1.5 prospective II 7 0.02/0.4 142/118 4.5/3.3 0.5 prospective II 8 0.02/0.2 NA/142 NA/3.9 2 prospective II 9 0.08/0.02 NA/138 NA/3.9 10 retrospective I 10 0.4/0.5 NA NA 1 retrospective II 11 0.2/0.3 NA NA 4 retrospective II 12 0.02/0.5 NA NA 2 retrospective I 13 0.3/0.4 NA NA 1.5 retrospective I 14 0.2/0.4 130/80 5.1/5.25 2 prospective II 15 0.1/0.3 124/124 4.7/6.0 3.5 prospective I 16 0.05/0.3 152/106 2.3/4.5 6 prospective I 17 0.02/0.4 142/135 3.9/5.8 2.5 prospective II NA = data not available. Br J Ophthalmol 1999;83:261–264 261 Department of Ophthalmology, Philipps-University Marburg, Marburg, Germany P Kroll W Wiegand J Schmidt Correspondence to: Professor Peter Kroll, Department of Ophthalmology, Philipps-University Marburg, Robert Koch Strasse 4, 35037 Marburg, Germany. Accepted for publication 30 July 1998 group.bmj.com on October 22, 2017 Published by http://bjo.bmj.com/ Downloaded from