CLINICAL CHALLENGES
The Nervous Crossing Guard
Use good listening skills and good doctoring to uncover dysthyroid ophthalmopathy.
By Eric Schmidt, O.D.

If you've ever doubted the importance of a comprehensive history, this case should put those doubts to rest. The patient's history was instrumental in following the proper diagnostic path.

Nervous, with bulging eyes

J.M. is a 41-year-old white female whose major ocular complaint was excessive tearing, especially when she got tired. She said the tearing, present for 4 months, seemed worse in her left eye and had gotten worse and become more bothersome as time progressed.

I noticed that her eyes were bulging and the lids seemed swollen. J.M. was fidgeting, almost nervous. I asked her for more details about her eyes. She said that when they teared no pus or mucus appeared. Her eyes didn't hurt, but she was having more trouble reading, and attributed the tearing to this.

I asked her about pain, redness or double vision. She denied pain, stated that her eyes got a "little red" at times, and admitted that she did sometimes see double. She only noticed the diplopia when lying in bed or in a recliner watching TV -- not when sitting up or standing.

I asked whether the diplopia went away when she closed one eye, but said she didn't know because she'd never tried that. I also asked whether the double vision was horizontal or vertical. She replied that she saw two TVs, one atop the other. Again, this only occurred when she was reclining and had existed for about the last month.

Finally, I asked if she felt nervous or hyperactive. She said that she felt "unsure of herself" and that she was short with the children she worked with as a school crossing guard. J.M. took no medications.

Following the path

J.M.'s unaided visual acuity (VA) was 20/20 OD, 20/25 OS. She struggled to read 20/30 at near but didn't see double. Her pupils were 5 mm, round and reactive OU, with no afferent defect. Cover testing showed orthophoria with no tropia and Hirschberg's test showed orthophoria equally in each eye.

When I performed the physiological H test with a transilluminator, I discovered why she was seeing double. Her left eye wouldn't completely invert when she looked down and to the right. When she looked down and to her left, the lack of inversion and restriction of gaze was even more apparent. Subjectively, J.M. said she saw two lights, one atop the other, in those positions of gaze.

As I watched her eyes during these tests, I saw more sclera superiorly and inferiorly OS than OD. Her palpebral apertures measured 11.5 mm OD, 13 mm OS. I also palpated the eyelids, finding soft edema of the upper and lower lids OU, but no palpable nodules or tenderness.

I tried to move her eyeball downward using a cotton swab but couldn't. This forced duction test was also positive when I unsuccessfully attempted to rotate the eyeball downward using a jeweler's forceps. Using my thumbs, I was easily able to retropulse both eyes, which indicated that there was no mass retro-orbitally. I measured no exophthalmos OU.

Still on the road

Next, I examined J.M.'s eyes with the slit lamp, which revealed a normal lacrimal lake OD, but a mildly thickened lake OS. I saw no lagophthalmos, but the lower punctum OS wasn't appositional to the globe because of the lid edema. I saw no bulbar injection or sodium fluorescein staining.

I conducted a Zone Quik test to further assess the epiphora, getting measurements of 15 mm OD, 22 mm OS. The rest of the exam was normal. Intraocular pressure (IOP) was 16 mm Hg OU and didn't change when measured in upgaze. Retinal grounds were normal and the optic disks were flat with a cup-to-disk ratio of .3/.3 OU. J.M.'s blood pressure measured 140/80 mm Hg. Lenses of +100D more than her refraction of +0.25 OD and +0.25 -0.50 x 180 yielded crisp 20/20 vision at near.

Destination: thyroid

Though J.M.'s chief complaint was tearing, my greater concern was the diplopia. Based on my exam, J.M.'s left inferior rectus muscle wasn't moving her left eye down completely. The positive forced duction test indicated that the diplopia was restrictive rather than a result of a paretic muscle. Some mass or material was probably impinging on the superior rectus muscle OS. This fact, along with the discovery of lid retraction and jitteriness, led me to suspect a hyperthyroid condition.

I ordered a thyroid panel [T3, T4 and thyroid stimulating hormone (TSH) tests], plus a complete blood count (CBC) and a blood glucose level. I told J.M. that I suspected an overactive thyroid.

I received her lab results a few days later. The CBC was normal and the fasting glucose was 100 mg/dL, but the thyroid panel was grossly abnormal. The T3 and T4 levels were elevated, indicating a high level of thyroid proteins in the bloodstream.

The TSH barely registered. The pituitary gland was trying to shut off the thyroid by not releasing TSH. These tests are conclusive for hyperthyroid-ism. I referred J.M. to her internist, who immediately placed her on methimazole (Tapazole) to regulate her thyroid gland.

Getting better

At the 3-month follow-up visit, J.M. said the diplopia was gone and the tearing was greatly improved. She felt "normal."

I examined her and found a normal pair of eyes (though she still needed reading glasses). Her eyes weren't restricted in any portion of gaze and the lid edema was resolved. The palpebral apertures were equal at 10.5 mm OU. Her medical doctor assured me that she was now euthyroid.

I advised J.M. to use artificial tears as needed for grittiness and explained the need for annual eye exams. I told her to return to my office if any of the symptoms returned.

A masquerader

You'll need all of your skills to uncover thyroid eye disease, or disthyroid ophthalmopathy.

An overactive thyroid causes an autoimmune-type reaction and releases "extracellular material" with an affinity for the extraocular muscles (EOMs) and eyelids. This results in classic lid retraction, edema, diplopia and proptosis. Further accumulation leads to infiltration, inflammation and congested ocular tissues and orbit.

The most common symptoms are tearing caused by exposure, bulging eyes, photophobia, diplopia and a foreign body sensation. Graves' disease, as hyperthyroidism not restricted to the eye is called, affects individuals differently.

Usually the eye signs resolve when the systemic condition is properly treated. The patient may need simple supportive therapy such as lubricants during the day and ointment at night for proptosis.

The condition rarely threatens sight unless the enlarged EOMs compress the optic nerve. Compressive optic neuropathy is caused by accumulation of the extracellular material into EOMs, which enlarge and disrupt axoplasmic flow to the optic nerve head by compressing it. VA rapidly decreases. It's diagnosed by strong clinical suspicion and magnetic resonance imaging of the orbit.

Early on, decreased color vision and contrast sensitivity herald optic neuropathy. Prompt neurosurgical intervention is usually necessary.

Know about Grave's disease

Diplopia is a big problem for Graves' disease patients. Short term, I recommend patching, if needed. I don't prescribe prism; the diplopia usually disappears once you can control the system-ic disease.

Graves' disease patients need annual optometric exams. They may experience exacerbations of the eye signs even if the thyroid is normalized. Be aware of the many faces of this disease, be ready to treat the eyes and be prepared to counsel patients.

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