Ophthalmic Surgery, Lasers and Imaging Retina

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Imaging 

Progression of Diabetic Tractional Retinoschisis by Optical Coherence Tomography

Ella Leung, MD; Robert A. Sisk, MD; Harry W. Flynn Jr, MD

Abstract

A 63-year-old woman presented with proliferative diabetic retinopathy with extensive posterior neovascularization in both eyes. Visual acuities were 20/40 in the right eye and 20/400 in the left eye with eccentric fixation. Tractional retinoschisis in the left eye that initially spared the fovea progressed over 3 years to involve the entire macula. Findings were documented by optical coherence tomography. No surgical intervention was offered. Tractional retinoschisis in proliferative diabetic retinopathy may become progressive due to cicatricial contraction of the posterior hyaloid face.

Abstract

A 63-year-old woman presented with proliferative diabetic retinopathy with extensive posterior neovascularization in both eyes. Visual acuities were 20/40 in the right eye and 20/400 in the left eye with eccentric fixation. Tractional retinoschisis in the left eye that initially spared the fovea progressed over 3 years to involve the entire macula. Findings were documented by optical coherence tomography. No surgical intervention was offered. Tractional retinoschisis in proliferative diabetic retinopathy may become progressive due to cicatricial contraction of the posterior hyaloid face.

Progression of Diabetic Tractional Retinoschisis by Optical Coherence Tomography

From Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, Florida.

The authors have no financial or proprietary interest in the materials presented herein.

Address correspondence to Robert A. Sisk, MD, Cincinnati Eye Institute, 1945 CEI Drive, Cincinnati, OH 45242. E-mail: rsisk@CincinnatiEye.com

Received: February 22, 2009
Accepted: February 22, 2010
Posted Online: October 28, 2010

Introduction

Retinoschisis, or separation of the layers of the neurosensory retina, has been reported as a complication of severe proliferative diabetic retinopathy (PDR).1 Pathological studies have demonstrated this results from contraction of the vitreous body, which creates traction on a thick posterior hyaloid face and areas of preretinal fibrovascular proliferation.2,3 In contrast to senile retinoschisis, which typically follows a nonprogressive course, retinoschisis in PDR may be progressive as traction increases. Although patients with retinal detachment from degenerative retinoschisis may benefit from prophylactic barrier laser photocoagulation, extension into the macula may limit its utility in PDR.

Retinoschisis can be difficult to differentiate clinically from retinal detachment. Visual field testing demonstrates an absolute scotoma corresponding to retinoschisis and a relative scotoma corresponding to retinal detachment. Lincoff et al. suggested the application of a test spot of laser retinopexy, which produced retinal whitening when outer retinal layers were present in retinoschisis.1 Retinal whitening did not occur in the presence of subretinal fluid. Using this method, they found that 43% (85 of 200) eyes with PDR and tractional elevations had retinoschisis and the remainder had retinal detachment. A more recent study using optical coherence tomography (OCT) found that 29% of eyes with PDR and tractional elevations had both retinoschisis and retinal detachment,4 suggesting that these conditions are comorbid rather than mutually exclusive.

Case Report

A 63-year-old woman with type 2 insulin-dependent diabetes mellitus presented with gradual onset of decreased vision in her left eye. Visual acuities were 20/40 in the right eye and 20/400 in the left eye with eccentric fixation. Both eyes had high-risk PDR with extensive neovascularization and preretinal fibrosis along the temporal arcades and evidence of prior panretinal photocoagulation. The left eye had a translucent preretinal membrane with striae toward fibrovascular fronds at each temporal arcade (Fig. 1). OCT demonstrated tractional retinoschisis in the left eye that involved the superior and temporal macula (Fig. 2). Additional panretinal photocoagulation was applied to both eyes. Over the next 3 years, visual acuity remained stable but the extent of the retinoschisis cavity increased to involve the entire macula (Fig. 3).

Montage Fundus Photograph of the Left Eye with Advanced Proliferative Diabetic Retinopathy with White Translucent Preretinal Membrane Tethered to Regressed Fibrovascular Membranes Most Prominent Temporally. Retinal Vessels Were Attenuated and Whitened, Indicating Severe Ischemia. Although Retinoschisis Progressed Through the Fovea, This Was Clinically Difficult to Appreciate Without Stereoscopic Examination.

Figure 1. Montage Fundus Photograph of the Left Eye with Advanced Proliferative Diabetic Retinopathy with White Translucent Preretinal Membrane Tethered to Regressed Fibrovascular Membranes Most Prominent Temporally. Retinal Vessels Were Attenuated and Whitened, Indicating Severe Ischemia. Although Retinoschisis Progressed Through the Fovea, This Was Clinically Difficult to Appreciate Without Stereoscopic Examination.

Stratus OCT 3 (Carl Zeiss Meditec, Inc., Dublin, CA) Horizontal and Vertical Scans Obtained Using the Radial Lines Protocol. (A) Tractional Retinoschisis Involved the Superior and Temporal Macula with Partial Splitting at the Foveal Center on Initial Presentation. Note Increased Transmission to the Choroid in Areas of Retinoschisis, Loss of Retinal Lamination, and Müller Cell Bridges. (B) One Year Later, There Was Increased Splitting of the Fovea. (C) Three Years After Initial Presentation, a Large Schisis Cavity with Inner Layer Holes Involved the Remainder of the Macula. (D) Cirrus HD-OCT (Carl Zeiss Meditec, Inc.) Horizontal and Vertical Scans from 512 × 128 Cube Scans Taken 3 Years After Initial Presentation Were Affected by Media Opacity and Inversion Artifact by the Extent of the Posterior Hyaloid Separation in the Z-Plane.

Figure 2. Stratus OCT 3 (Carl Zeiss Meditec, Inc., Dublin, CA) Horizontal and Vertical Scans Obtained Using the Radial Lines Protocol. (A) Tractional Retinoschisis Involved the Superior and Temporal Macula with Partial Splitting at the Foveal Center on Initial Presentation. Note Increased Transmission to the Choroid in Areas of Retinoschisis, Loss of Retinal Lamination, and Müller Cell Bridges. (B) One Year Later, There Was Increased Splitting of the Fovea. (C) Three Years After Initial Presentation, a Large Schisis Cavity with Inner Layer Holes Involved the Remainder of the Macula. (D) Cirrus HD-OCT (Carl Zeiss Meditec, Inc.) Horizontal and Vertical Scans from 512 × 128 Cube Scans Taken 3 Years After Initial Presentation Were Affected by Media Opacity and Inversion Artifact by the Extent of the Posterior Hyaloid Separation in the Z-Plane.

Stratus OCT 3 (Carl Zeiss Meditec, Inc., Dublin, CA) Fast Macular Thickness Maps Created Using the Proprietary Software. Mild Hourglass Artifact Was Seen on Both Scans. (A) On Initial Presentation, There Was Increased Distance Between the Internal Limiting Membrane and Retinal Pigment Epithelium–Choriocapillaris Complex in the Superior and Temporal Macula. Central Macular Thickness of the 1-mm Subfield Was 225 Microns. (B) Three Years Later, Extension of the Retinoschisis Cavity to the Remaining Macula Is Evident with Increased Central Macular Thickness of 954 Microns.

Figure 3. Stratus OCT 3 (Carl Zeiss Meditec, Inc., Dublin, CA) Fast Macular Thickness Maps Created Using the Proprietary Software. Mild Hourglass Artifact Was Seen on Both Scans. (A) On Initial Presentation, There Was Increased Distance Between the Internal Limiting Membrane and Retinal Pigment Epithelium–Choriocapillaris Complex in the Superior and Temporal Macula. Central Macular Thickness of the 1-mm Subfield Was 225 Microns. (B) Three Years Later, Extension of the Retinoschisis Cavity to the Remaining Macula Is Evident with Increased Central Macular Thickness of 954 Microns.

Discussion

The posterior hyaloid membrane–internal limiting membrane complex is thickened and tightly adherent in PDR.3 Complete vitreous separation is unusual in patients with previous advanced proliferative disease. Preretinal neovascular membranes arborize on the scaffold of the posterior hyaloid face during the angiogenesis phase. Both treated and untreated eyes subsequently progress to a cicatricial phase with tractional retinal detachment, retinoschisis, or a combination of both.

Ischemia has long been postulated to be a predisposing factor to retinoschisis. Degenerative retinoschisis is thought to preferentially occur in the temporal peripheral retina because this region, which is farthest from the optic nerve, is the last to vascularize developmentally. Vitreoretinal tractional forces alone typically cause retinal tears or detachment rather than retinoschisis, as illustrated by rhegmatogenous retinal detachments, macular holes, and proliferative vitreoretinopathy. This suggests that the adhesive forces of Müller cells in a nonischemic eye are greater than the mechanical adhesion of the retina to the retinal pigment epithelium or the retinal pigment epithelium fluid pump.

In the setting of severe PDR, damage to retinal capillary endothelial cells leads to inner retinal ischemia and death of Müller cells. However, the outer retina remains perfused by the choriocapillaris, permitting the retinal pigment epithelium fluid pump to function, promoting retinal attachment. This may allow anterior and tangential tractional forces from the contracting posterior hyaloid face to overcome the integrity of the Müller cell processes and permit retinoschisis at the intraretinal watershed zone. Our patient’s poor visual acuity on presentation with a partially intact fovea on OCT is consistent with severe macular ischemia.

OCT is a useful tool in differentiating retinoschisis from retinal detachment, providing two-dimensional information about the location and severity of tractional forces, identification of surgical planes, and integrity of retinal lamination. In our patient, OCT demonstrated retinal thinning and disorganization with loss of lamination, confirming a degenerative process in addition to tractional forces. Spectral domain OCT technology offers the advantages of faster acquisition time, enhanced transverse resolution, better visualization of the vitreoretinal interface, and three-dimensional reconstruction from parallel horizontal scans. However, it is more susceptible to reduced contrast from media opacity and has tighter limitations in the z-plane, which can create inversion artifacts.

To the best of our knowledge, this is the first report demonstrating progression by OCT of tractional retinoschisis in PDR. We suspect this is not an uncommon finding, but both ischemic and mechanical factors must be present to create posterior tractional retinoschisis. Differentiation of retinoschisis from retinal detachment has surgical implications. Visual acuity recovers poorly following repair of tractional retinoschisis in PDR compared to repair of tractional retinal detachment.1 We believe tractional retinoschisis from PDR involving the foveal center is a relative contraindication to surgery.

References

  1. Lincoff H, Serag Y, Chang S, Silverman R, Bondok B, el-Aswad M. Tractional elevations of the retina in patients with diabetes. Am J Ophthalmol. 1992;113:235–242.
  2. Faulborn J, Ardjomand N. Tractional retinoschisis in proliferative diabetic retinopathy: a histopathologic study. Graefes Arch Clin Exp Ophthalmol. 2000;238:40–44. doi:10.1007/s004170050007 [CrossRef]
  3. Davis MD. Vitreous contraction in proliferative diabetic retinopathy. Arch Ophthalmol. 1965;74:741–751.
  4. Imai M, Iijima H, Hanada N. Optical coherence tomography of tractional macular elevations in eyes with proliferative diabetic retinopathy. Am J Ophthalmol. 2001;132:458–461. doi:10.1016/S0002-9394(01)01176-X [CrossRef]
Authors

From Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, Florida.

The authors have no financial or proprietary interest in the materials presented herein.

Address correspondence to Robert A. Sisk, MD, Cincinnati Eye Institute, 1945 CEI Drive, Cincinnati, OH 45242. E-mail: rsisk@CincinnatiEye.com

10.3928/15428877-20101025-07

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