Vitrectomy for vitreopapillary traction in a nondiabetic 16-year-old girl.

Vitreopapillary traction (VPT) is an unusual clinical entity and its management and prognosis have been sparsely studied. It has been described in adults with various vitreomacular pathologies and the possible effects on visual functions. However, the role of surgical intervention in altering the course of the disease is not well understood. Hereby, we describe a case of idiopathic VPT in a 16-year-old girl who presented with decreased vision and visual field changes corresponding to the area of retinal traction. This case was managed with pars plana vitrectomy and epiretinal membrane removal that resulted in improved visual field sensitivity; thus, emphasizing the role of surgical intervention in such eyes.

Introduction

Vitreopapillary traction (VPT) is a recently recognized condition characterized by vitreous traction over the optic disc caused by fibrocellular proliferative membrane or incomplete posterior vitreous detachment.[1] In adults, VPT is associated with diabetic retinopathy,[2] central retinal vein occlusion (CRVO),[3] macular hole,[4] nonarteritic anterior ischemic optic neuropathy (NAAION),[5] and epiretinal membrane (ERM).[6] However, little is known about VPT in children or adolescents. Hereby, we describe a case of VPT in a 16-year-old girl successfully managed with vitrectomy.

Case Report

A 16-year-old girl presented with gradually progressive vision loss in the right eye of 6 years duration. There was no history of trauma, pain, or redness. Her medical history was noncontributory. Best-corrected visual acuity (VA) was 10/300 in the right and 20/20 in the left eyes. The left eye was essentially normal. Fundus examination of the right eye revealed mild disc pallor, obscured disc margins from overlying vitreous condensation, and retinal traction caused by peripapillary membrane [Figure 1 – upper left]. Clinical findings were confirmed on optical coherence tomography (OCT) [Figure 1 – middle left]. Humphrey visual field (30-2) analysis showed paranasal and superotemporal defects [Figure 1 – lower left]. Investigations done to rule out tuberculosis (Quantiferon-TB gold test and Mantoux test), and sarcoidosis (high-resolution computed tomography of the chest and serum angiotensin-converting enzyme) were negative.

Figure 1

At baseline, the right eye reveals peripapillary membrane (upper left). Six weeks after vitrectomy, there is resolution of disc elevation (upper right). At baseline, optical coherence tomography image (middle left) shows obliteration of optic cup and traction over peripapillary retina. Optical coherence tomography image 6 weeks later reveals traction relief (middle right). At baseline, pattern deviation plot of Humphrey's visual field (24-2) shows central defect (lower left) corresponding to vitreopapillary traction. Six weeks after vitrectomy, pattern deviation plot reveals improvement of visual field defect (lower right)

The patient underwent 25G pars plana vitrectomy with complete removal of posterior hyaloid, epiretinal, and peripapillary membranes and internal limiting membrane peeling with complete relief of traction. Postoperative recovery was uneventful. Six weeks later, fundus examination revealed relief of traction [Figure 1 – upper right] with settling retinal folds. OCT showed resolution of traction over the optic disc [Figure 1 – middle right]. Repeat visual fields revealed the improvement in field defects [Figure 1 – lower right]. VA was maintained at 10/300; improvement was impaired due to amblyopia. Six months later, examination revealed further reduction in retinal schitic changes with decrease in overall central macular thickness (384 µm) and VA being stable stable at 10/300.

Discussion

Anatomical evaluation of vitreopapillary interface is facilitated by spectral domain OCT and functional evaluation by visual field analysis. Traction exerted by the posterior hyaloid over retina has been implicated in vitreomacular and VPT. VPT has been proposed as possible cause of temporary or chronic functional impairment.[7] In a multivariate analysis by Kim et al., significant field defects in patients with ERM associated with VPT were noted as compared to ERM group alone.[6] Significant changes in central 30-2 visual fields, foveal visual evoked potentials, and decreased VA have been observed in various studies due to sole traction over optic nerve head.[8]

Furthermore, long-standing optic nerve traction might result in optic atrophy either by impeding the axoplasmic flow or by changing laminar flow through the peripapillary blood vessels.[8] The latter may decrease the blood flow, create turbulence, and increase the formation of thrombi leading to permanent functional damage. Katz and Hoyt followed up eight patients presenting with intra- and peripapillary hemorrhage due to VPT over 6 months. In no patient did the vitreous detach completely and no patient had any sequela or impairment of visual function. Authors were of the opinion that the benign nature of this condition did not necessitate surgery to relieve vitreous traction.[9]

On the other hand, surgical release may seem logical to reestablish normal anatomical and functional potentials. Supporting this, anecdotal evidence has shown that release of traction resulted in improved surgical outcomes in cases of VPT associated with NAAION,[5] CRVO,[3] and diabetic retinopathy.[8] Meyer et al. reported a case of VPT managed with vitrectomy showing improvement in vision and unaltered foveal thickness. However, visual field changes were not studied in that case.[10] In our case, we analyzed visual field changes before and after vitrectomy and changes in peripapillary and foveal thickness with respect to visual function.

Conclusion

Our case adds to evidence of traction relief and functional improvement following surgical release of VPT. However, the role of duration and intensity of VPT in pathogenesis of optic nerve damage needs further study.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.