Ophthalmology Dx: The Hole Truth

Slideshow

  • Figure 1.

    At a dilated fundus exam, the patient’s right eye had a retinal hole/tear in the periphery at approximately 11:00.

  • Figure 2.

    This retinal drawing from the ophthalmologist’s notes shows a shallow retinal detachment approaching the superotemporal arcades. Credit: Edward Ryan, MD

  • Figure 3.

    This fundus photo shows the same eye 3 months postoperatively. Can you identify the underlying ocular condition that instigated these findings? Credit: Edward Ryan, MD

A 22-year-old male patient presented to the clinic for a first visit for a routine exam and a contact lens update. He had his last eye exam 1 year ago in his home country, Norway. His best-corrected visual acuities were 20/20 OD, and 20/25 OS. Pupillary, slit lamp, and fundus exams were all normal. His confrontation fields also appeared normal. His uncorrected refractions were -5.50 OD, and  -7.00 OS. He declined dilation, and was asked to return for a dilated exam, intraocular pressures, and with his current contact lens prescription. At the follow-up visit, 17 days later, his pressures were 12 mm Hg OD, and 13 mm Hg OS. Upon dilation, he was found to have a retinal hole in the right eye (Figure 1), and a shallow retinal detachment, that was approaching the superotemporal arcades (Figure 2). The dilated exam of the left eye was normal. He was immediately referred to a retinal surgeon. The first surgical procedure was uncomplicated and the retina was reattached. At the 1 week follow up, however, the superior retina was detached again, and in the inferior temporal area, a new detachment had developed. Additional surgeries were unable to repair the detachments.

Proliferative vitreoretinopathy (PVR) is caused by the growth and contraction of the cellular membrane within the vitreous cavity and on both sides of the retinal surface as well as intraretinal fibrosis.1 Many risk factors have been associated with the development...

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Proliferative vitreoretinopathy (PVR) is caused by the growth and contraction of the cellular membrane within the vitreous cavity and on both sides of the retinal surface as well as intraretinal fibrosis.1 Many risk factors have been associated with the development of PVR. Almost all risk factors are associated with dispersion of retinal pigment epithelial (RPE) cells, formation of membranes, breakdown of the blood-ocular barrier, many surgical interventions, or chronic untreated retinal detachments.1

Researchers estimate the incidence of PVR are 5% to 10% of all retinal detachment cases.1,2 This figure has largely remained unchanged in prospective studies for 25 years, despite the evolution of new vitreoretinal management techniques.1 Approximately 77% of postoperative forms of PVR appear within 1 month after retinal detachment surgery and 95% appear within 45 days.3,4  

PVR is graded on a 3-point scale:

• Grade A: Limited to the vitreous cells and/or haze.

• Grade B: The edges of the tear are either rolled or irregular or the inner retinal surface is irregular.

• Grade C: Most challenging repair, includes preretinal or subretinal membranes.

Although consensus exists on a pharmacologic agent for the treatment or prevention of PVR, some medical interventions that target inflammation, cell proliferation, and fibrosi may hold promise.1 These include taxol and colchicine, which could reduce migration and proliferation of cells and kinase inhibitors, which have shown positive results in preclinical PVR studies.1,5 

Primarily, PVR is treated surgically, with a goal of reattaching the retina. However, for patients with Grade 3 PVR, the preretinal and subretinal membranes and intraretinal fibrosis may require additional maneuvers to relieve traction to reattach the retina and prevent recurrence.1 Scleral buckling is one such option, but research shows its success rate is approximately 34% to 47%. One study shows a combined approach (scleral buckling and vitrectomy) may have a higher success rate for patients at high-risk for postoperative PVR than vitrectomy alone. No agreement yet exists on the timing of surgery for these patients.1

This patient underwent 3 additional surgeries, but they were not successful in repairing the detachments (Figure 3). Visual acuities after all surgical attempts were, at best, hand motion.

References

1. Idrees S, Sridhar J, Kuriyan A. Proliferative retinopathy, a review. Int Ophthalmol Clin. 2019;59(1):221-240. doi:10.1097/IIO.0000000000000258

2. Lean JS, Stern WH, et al. Classification of proliferative vitreoretinopathy used in the silicone study. Ophthalmol. 1989;96:765-771. doi:10.1016/s0161-6420(89)32821-1

3. Pastor JC. Proliferative vitreoretinopathy: an overview. Surv Ophthalmol. 1998;43:3-18. doi:10.1016/s0039-6257(98)00023-x

4. Pastor JC, de la Rua ER, Martin F. Proliferative vitreoretinopathy: risk factors and pathobiology. Prog Retin Eye Res. 2002;21:127-144. doi:10.1016/s1350-9462(01)00023-4

5. Imai K, Loewenstein A, Koroma B, et al. Herbimycin A in the treatment of experimental proliferative vitreoretinopathy: toxicity and efficacy study. Graefes Arch Clin Exp Ophthalmol. 2000;238:440-447. doi:10.1007/s004170050376

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