CLINICAL CHALLENGES
The Artist's Rendition
A patient's artwork leads this doctor on the road to diagnosing her condition.
By Eric Schmidt, O.D.

For many of us who see a considerable number of patients each day, it can become easy to trivialize some of our patients' complaints. We may say things such as, "It's just dry eye," or, "You're just experiencing glare," without realizing how these occurrences are really affecting each patient.

The following case brought this point home in a dramatic fashion. You'll see what I mean, but first, meet the patient.

A visually disturbed artist

Anne is a fascinating woman and, as our conversation would uncover, obviously talented as well. She told me that when she was 20 she left North Carolina to enroll in the Berklee College of Music in Boston. She eventually gravitated to visual arts rather than music and over the past 35 years had worked as a designer, a studio artist and an artist in residence. She also illustrated children's books before moving back to North Carolina, where she's now a graphic design artist. But Anne was obviously in my office for reasons other than just lively conversation! She was having a persistent visual disturbance that concerned her.

Seeing the artist's rendition

Anne said that one morning three months earlier she awakened to see a large black spot in the temporal portion of her vision OS. She said that the spot was absolutely black and about the size of a silver dollar. She also said that her vision to the right of the black spot was blurred moving into the central and nasal field of vision OS only.

For some inexplicable reason, Anne didn't seek any care right away and said that in about five days her vision began to improve and the spot in the temporal field became smaller. Now, three months later, that image still persists and the nasal field is still mildly blurred but she describes her central vision as much better.

To make matters more interesting, Anne brought in an illustration that she generated on her computer to show me more or less what she experienced originally and what the image looks like now (Figs. 1a & 1b). Her graphic illustrates that originally the majority of her vision was involved but that now a much smaller negative scotoma persisted in her temporal field OS.

I asked Anne if, at the time of the initial onset, she had any other associated symptoms such as headache, paresthesia, nausea or disequilibrium. She denied all of this but said that she occasionally does get "terrific" headaches that concentrate around her temples. Anne also denied seeing any flashes of light over the past three months.

I asked her if this spot moved at all and she informed me that it had always stayed stationary in the same general location and hadn't changed in size or appearance for the past two-and-a-half months. She was concerned about it still being present and finally came to have it checked out.

Sorting through the findings

Anne was healthy and took only conjugated estrogens/med-roxyprogesterone acetate tablets (Prempro). Her visual acuity (VA) through her bifocal glasses was 20/20 -2 OD and 20/20 OS. A refraction of +0.75 -125 x 90 OD and +0.25 sph OS gave Anne a crisp 20/20 in each eye. Her pupils were 6-mm round and equally reactive. I noted no afferent pupil defect. Extraocular muscles were full without restriction or pain and her confrontation visual fields were full OU. Amsler grid testing was normal OD but revealed a semi-circular blurred -- but not black -- area superior-temporal to fixation. Color testing revealed no dyschromatopsia.

Anne's slit lamp exam was absolutely normal. Her cornea was clear with no infiltrates or guttata. The anterior chamber was a deep, well-formed Grade 4 chamber with no cell or flare and no tobacco dust present. No posterior synechiae had formed. There was no iris atrophy or transillumination. Goldmann tonometry measured 19 mm Hg OD, 18 mm Hg OS.

As I dilated her eyes, I mentally sorted out the possibilities of what this image could represent. I had effectively ruled out angle-closure glaucoma and an iritis or any other anterior segment problem. The persistent scotoma and her description pointed to a retinal pathology, but the optic nerve could be involved as well.

My differential diagnosis at this point included optic nerve diseases such as ischemic optic neuropathy and optic neuritis, and maculopathies such as central serous choroidopathy, subretinal neovascular membrane from macular degeneration, epiretinal membrane, macular edema or inflammatory entities such as toxoplasmosis or ocular histoplasmosis.

I also was concerned about a retinal tear or focal retinal detachment. It was also possible that the underlying etiology was a carotid artery insufficiency. A migraine syndrome was also possible, but the visual phenomena associated with that usually doesn't persist. A thorough dilated fundus examination should allow me to uncover the cause of Anne's visual obscuration.

Diagnosing a PVD

My examination of Anne's right retina was normal. Her optic disk wasn't elevated or edematous, there were no retinal or disk hemorrhages or edema, her arteries and veins were of normal caliber and there was no retinal detachment, tears or holes. No retinal plaques or sign of infarction were present either.

However, when I examined Anne's OS with a 78-D lens, a huge vitreous opacity jumped out at me! A detailed look confirmed this opacity as a large posterior vitreous detachment (PVD). It was rather ill-defined, but I estimated it as > 3 disk diameters (DD) in size vertically and about 1DD horizontally.

This PVD was free-floating just nasal to the disk and had no attachment to the retina or optic nerve head. Using a 20-D lens and a binocular indirect ophthalmoscope, I examined the retina peripherally to the ora serratta to make sure that there was no vitreoretinal traction and to rule out any retinal holes, tears or detachment. The PVD was complete, it wasn't exerting any traction on the retina and there weren't any retinal breaks present.

Understanding PVD's pathogenesis

The vitreous is a transparent, gel-like structure that takes up about two thirds of the volume of the globe. Though it appears optically empty, it's actually a meshwork of collagen arranged in a regular pattern. The vitreous contacts the retina, optic disk, ciliary body and lens, but has its firmest attachment at the vitreous base at the anterior peripheral retina.

A PVD most likely occurs at its attachment to the optic nerve head. Liquefaction and degeneration of the vitreous causes it to shrink and pull anteriorly away from the optic nerve head. As this process occurs, traction can be exerted on the retina and tears can occur, especially in areas of the retina that are inherently weaker. Retinal degenerations such as lattice degeneration or cystic retinal tufts as well as meridional folds are more likely to develop tears secondary to a PVD.

The vitreous base will rarely develop a tear but it's the traction on this area that produces the classic flashes that patients experience with PVD. Anterior/ posterior motion of the vitreous body produces an arc of vitreous traction. This arc-shaped traction on the retina causes the characteristic arc flashes usually seen temporally with PVD.

Just a PVD

After the examination, I described in detail what Anne's condition was and that I would follow her closely for the next few months but that there was no treatment indicated at this time. I also took care not to minimize her PVD. Because of the sheer size of the PVD, the vitreoretinal traction created had to be greater than normal, thus, I surmised, the visual phenomena created by this was also more dramatic than typically seen with a PVD.

The blurry vision centrally at the onset was most likely caused by heavy traction at the papillomacular bundle area. The traction may have been so great as to induce milc macular edema transiently. The scotoma that remains is the actual PVD that Anne is seeing. Because of its large size, she may see this for quite a long time. I told her not to worry though because it's "just a PVD!"

Contributing Editor Eric Schmidt, O.D., is director of the Bladen Eye Center in Elizabethtown, N.C. E-mail him at KENZIEKATE@aol.com.