PMCCPMCCPMCC

Search tips
Search criteria 

Advanced

 
Logo of omanjophthalHomeCurrent issueInstructionsSubmit article
 
Oman J Ophthalmol. 2017 Jan-Apr; 10(1): 38–39.
PMCID: PMC5338052

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

Abstract

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.

Keywords: Epiretinal membrane, pars plana vitrectomy, visual fields, vitreomacular traction, vitreopapillary traction

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 ...

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.

References

1. Rumelt S, Karatas M, Pikkel J, Majlin M, Ophir A. Optic disc traction syndrome associated with central retinal vein occlusion. Arch Ophthalmol. 2003;121:1093–7. [PubMed]
2. Karatas M, Ramirez JA, Ophir A. Diabetic vitreopapillary traction and macular oedema. Eye (Lond) 2005;19:676–82. [PubMed]
3. Lam HD, Blumenkranz MS. Treatment of central retinal vein occlusion by vitrectomy with lysis of vitreopapillary and epipapillary adhesions, subretinal peripapillary tissue plasminogen activator injection, and photocoagulation. Am J Ophthalmol. 2002;134:609–11. [PubMed]
4. Wang MY, Nguyen D, Hindoyan N, Sadun AA, Sebag J. Vitreo-papillary adhesion in macular hole and macular pucker. Retina. 2009;29:644–50. [PubMed]
5. Modarres M, Sanjari MS, Falavarjani KG. Vitrectomy and release of presumed epipapillary vitreous traction for treatment of nonarteritic anterior ischemic optic neuropathy associated with partial posterior vitreous detachment. Ophthalmology. 2007;114:340–4. [PubMed]
6. Kim YW, Jeoung JW, Yu HG. Vitreopapillary traction in eyes with idiopathic epiretinal membrane: A spectral-domain optical coherence tomography study. Ophthalmology. 2014;121:1976–82. [PubMed]
7. Katz B, Hoyt WF. Gaze-evoked amaurosis from vitreopapillary traction. Am J Ophthalmol. 2005;139:631–7. [PubMed]
8. Kroll P, Wiegand W, Schmidt J. Vitreopapillary traction in proliferative diabetic vitreoretinopathy [ssee comments] Br J Ophthalmol. 1999;83:261–4. [PMC free article] [PubMed]
9. Katz B, Hoyt WF. Intrapapillary and peripapillary hemorrhage in young patients with incomplete posterior vitreous detachment. Signs of vitreopapillary traction. Ophthalmology. 1995;102:349–54. [PubMed]
10. Meyer CH, Schmidt JC, Mennel S, Kroll P. Functional and anatomical results of vitreopapillary traction after vitrectomy. Acta Ophthalmol Scand. 2007;85:221–2. [PubMed]

Articles from Oman Journal of Ophthalmology are provided here courtesy of Wolters Kluwer -- Medknow Publications