When an eye problem isn't just an eye problem.
Systemic diseases often manifest in the eye. Diagnosing the eye condition can be easy, but the underlying etiology challenges our clinical investigative skills. Remember this in your practice.
THE CASE: Rosetta was frustrated. She said that for the past 1 1/2 years she'd been treated "by the same doctor for the same infection," but her eye problem had never totally resolved. Not only was her left eye sore and red now, but her vision in that eye was decreased as well.
Rosetta described the eye pain as intermittent but throbbing, "like a toothache," around the eye and toward her right temple. Both eyes were extremely photophobic. She said that since 1995 she'd been treated off and on for iritis. She showed me the drops that her past eye doctor had prescribed. One was atropine sulfate 1% 1 drop b.i.d. OU. The second was prednisolone acetate 1% (Pred Forte) 1 drop b.i.d. OS. Rosetta said that she'd been using the prednisolone off and on for 1 1/2 years but that the atropine was a recent addition.
Rosetta's medical history wasn't completely normal. This 51-year-old woman was taking a medication, whose name she didn't know, for hypertension and had arthritis for which she was using 4 to 8 ibuprofen tablets (Advil) per day. She described the arthritis as affecting all her fingers and both wrists.
Examination revealed some unexpected findings. Her uncorrected visual acuity (VA) was 20/40 OD and 20/80 OS. The right eye improved to 20/20 with pinhole occlusion; the left eye improved to 20/50. Both of her pupils were 8 mm and fixed, the result of the atropine. Extraocular muscle (EOM) evaluation showed no restrictions or pain on movement.
A refraction of +1.00 -0.50 x 90 OD and -0.75 -1.00 x 90 OS yielded VAs of 20/20 and 20/502 OD and OS, respectively.
When I examined her right eye with a slit lamp, I found a healthy, quiet anterior segment. I saw no anterior chamber cell or flare, the cornea and conjunctivae were clear and no cataract was evident.
Problems with her left eye
More was going on with Rosetta's left eye. The left eye showed 1+ bulbar injection with prominent ciliary flush (below). The cornea was free of infiltrates or edema.
The anterior chamber showed 3+ cell and 3+ flare (see page 84). No posterior synechiae had formed, but a 3+ posterior subcapsular cataract had. Her intraocular pressure (IOP) was 14 mm Hg OD, 16 mm Hg OS.
Dilated fundus examination OD showed a normal retina and healthy optic nerve with a cup-to-disk ratio of .2/.2. The overlying vitreous was clear.
The left eye revealed a clear vitreous that was free of cells and an intact retina with no hemorrhages, edema or detachment. I estimated the cup-to-disk ratio to be .35/.35, but my view was blurred to a 20/50 level.
With a gonioscope, I could see Grade 3 anterior chamber angles OU. There was no debris or precipitate in the angle. However, mild peripheral anterior synechiae were developing throughout the angle of Rosetta's left eye.
Rosetta did have an iritis. Because it was persistent, I treated it as something other than ordinary acute iritis.
My first challenge was to make her comfortable by decreasing the inflammation. I asked her to increase the prednisolone to q2h OS and to discontinue the atropine. I felt that she'd already used it long enough to prevent a ciliary body spasm and subsequent worsening of inflammation. I told her to wear sunglasses outdoors and see me again in 5 days. I also requested her old records.
At her return visit, I saw a marked improvement. Her eye felt much better, looked less red and was no longer sensitive to light. VA was still 20/20 OD but was now 20/300 OS, which improved to 20/60 with a pinhole. Her pupils were round and sluggishly reactive and her anterior chamber reaction had decreased to 1+ cell with no flare.
The posterior subcapsular cataract was still present and IOP was 14 mm Hg OD, 20 mm Hg OS. I decreased the prednisolone to q4h and ordered the following blood tests to uncover any systemic causes:
complete blood count (CBC)
antinuclear antibody (ANA)
angiotensin converting enzyme (ACE)
rheumatoid factor (RF)
rapid plasma reagent (RPR)
erythrocyte sedimentation rate (ESR)
I saw Rosetta again in 1 week. Her symptoms had completely abated except for the blurred vision OS, which still improved to only 20/50 with the pinhole.
My examination revealed that the anterior chamber reaction had completely resolved. Her IOP was 20 mm Hg OD, 24 mm Hg OS. Gonioscopy was unchanged. I decided to very slowly taper the prednisolone in hopes of preventing a recurrence.
Rosetta's blood work showed an elevated cholesterol level of 235 mg/dl, a positive rheumatoid factor and a mildly elevated erythrocyte sedimentation rate (37 mm/hr). Her old records revealed a VA of 20/20 OS 1 1/2 years earlier. There wasn't mention of a posterior subcapsular cataract.
I decided that the cataract was steroid-induced and that, based on the results of the blood work, Rosetta probably had an arthritic disease that was causing the iritis. I referred her to a rheumatologist and scheduled follow-up for 2 weeks.
Over the next year, I saw Rosetta often. She had bouts of iritis OS whenever I discontinued the prednisolone. Once, her right eye developed a mild iritis. She underwent cataract extraction OS last year and did remarkably well. Her corrected vision is now 20/20 OD and OS.
I've twice tried to put Rosetta on maintenance doses of less potent steroids, but both times her iritis recurred. She's been taking prednisolone OS every morning for the past 3 months and has had no recurrences. She'll probably remain on this maintenance dosage for many years.
The rheumatologist is also treating Rosetta for sero-negative arthritis. He concurs that the iritis was a manifestation of this problem. I'll continue to monitor her every 3 months for the next year. After that, I hope to schedule her appointments less often. She knows to return promptly if the eye should flare up.
Contributing Editor Eric Schmidt, O.D., is director of the Bladen Eye Center in Elizabethtown, N.C.
Copyright Boucher Communications, Inc. Jun 1999
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