An Elderly Patient's Blurry Right Eye Raises Questions

Karima S. Khimani; Rod Foroozan, MD


July 24, 2017


VPT can occur as part of the normal aging process, whereby the vitreous gradually detaches from the retina while the hyaloid membrane is persistently attached to the optic nerve head.[1] The shear forces of the separation of the vitreous from the retina cause elevation of the optic disc, which has been described by Schepens[2] as pseudopapilledema.[3] Traction from the vitreous can also traumatize the vessels, leading to optic disc hemorrhages and disc leakage, which can be best visualized on fluorescein angiography.[1]

Isolated optic disc elevation secondary to VPT can be misdiagnosed as other causes of optic disc edema and can mimic the clinical presentation of other ocular and systemic diseases, such as papilledema, central retinal vein occlusion, and non-arteritic anterior ischemic optic neuropathy.[1] Patients with VPT may also report transient photopsias.[4]

OCT can clearly illustrate the vitreopapillary interface and is a noninvasive and valuable tool for distinguishing VPT from true optic disc edema.[1,3] One series[3] noted the use of OCT to evaluate patients with isolated optic nerve head elevations, thereby eliminating the need for more extensive procedures. Another group[1] highlighted the use of spectral domain OCT 5 line raster (5LR), which was used to confirm the diagnosis of VPT in two patients who presented with optic disc hemorrhages. The 5LR allowed for high-resolution imaging of multiple cross-sections of the tissue being scanned, which helped identify VPT, monitor its progression, and distinguish it from etiologies that would pose a risk for progressive optic nerve damage.[1]

The best treatment of VPT is still being debated. Surgical release by vitrectomy has been reported by some groups[4,5] to improve visual impairment. Longstanding traction forces of the vitreous cause bending of the retinal nerve fibers, as well as stretching and thinning of the ganglion cell axons, which decreases axonal transport and causes sensory blockade of neuronal signals.[5] Surgical release of VPT has been hypothesized to improve the anatomy and functionality of retinal ganglion cells.[4,5] However, the roles of duration and degree of traction from VPT in determining treatment remain undefined. Furthermore, pars plana vitrectomy carries a risk of causing iatrogenic complications such as excision of nerve fibers and retinal breaks during aspiration of the vitreous.[4] Thus, milder degrees of VPT, with stability in visual function, may be monitored for progression.


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