GLAUCOMA GRAND ROUNDS

Diabetes and MS Influence Case

J. James Thimons, O.D.

A 42-year-old white female diabetic patient presented after a recent drop in visual acuity in her left eye. The episode was sudden but painless. Her prior visual history included diabetic changes in her retina approximately a year earlier. (She had not followed through with a vitreoretinal specialist.)

Additionally, the patient had a 4-year history of multiple sclerosis, as well as severe hypertension for 7 years. Her medical therapy included both Inderal (propranalol HCl), an oral beta-blocker, and Norvasc (amlodipine besylate), an ACE inhibitor, for her blood pressure. The patient was also on Glucophage (metformin hydrochloride) for diabetes and Neurontin (gabapentin) for MS.

Physical Examination
Visual acuity with her existing correction was 20/25-1 O.D. and 20/40-2 O.S. Pinhole testing showed improvement to 20/20 O.D. and 20/25-1 O.S. Extraocular muscle testing demonstrated full excursions of the globe but saccades were not fluid. Pupil examination showed 4/4, 2+, and a minimally positive Marcus Gunn in the left eye. Slit lamp examination demonstrated normal corneal architecture, and the anterior chamber was deep and quiet. The iris showed no neovascularization. Both lenses had a slight evidence of nuclear sclerosis and some early cortical changes that did not approach the visual axis.

Applanation tensions were 23mm Hg O.D., 26mm Hg O.S. at 4 p.m. Gonioscopy demonstrated ciliary body 360° O.U. Dilated fundus examination revealed bilateral background and pre-proliferative retinopathy changes with the left eye showing an infarcted arterial exiting the disc just inferior to the macula. Both eyes demonstrated microaneurysms, and dot and blot hemorrhages, with exudation in the left eye more dramatic than that of the right. Angiography showed retinal ischemia, with a significantly more involved left eye. Cup-to-disc ratio was 0.25 O.D., and 0.40-0.45 O.S. with a vertical elongation of the optic cup. While there was no evidence of nerve fiber layer loss, the general nerve fiber pattern was significantly dulled in both eyes, most likely secondary to the diffuse diabetic changes.

Visual field testing showed non-specific changes in the right eye not typical of glaucoma, and the left eye showed a relatively deep depression immediately superior to fixation.

Physically, the patient demonstrated mild weakness of the right arm, apparently related to an MS episode a year earlier. She also showed unstable gait. Her blood pressure had been rising steadily during her treatment, but she had difficulty adjusting to several of the medications. The goal of her management now is to further reduce systemic hypertension.

Management
The challenge in assessing this complex patient's clinical picture is to account for the systemic disease elements with possible glaucoma. First, I contacted the patient's general practitioner to discuss current systemic therapy. He said her glucose as well as blood pressure varied considerably even with good compliance. Additionally, her MS had progressed over the last five years with the weakness on her right side.

The next step in our management was to assess the ocular status, as well as manage the ocular manifestations of the systemic elements. The patient returned for repeat IOP checks at a morning visit with no significant changes, and repeated the visual fields with minimal variability. We also referred the patient back to the managing physician for a vascular assessment to determine the etiology of the infarctive event in the left retina.

How do we start to treat a patient like this? First, we must address the etiology of the visual field loss. In this patient there are these three possibilities:

Glaucoma. Going against this diagnosis are the relatively normal cup-to-disc ratio in the left eye, the intensity of the field loss and the proximity to fixation. While the latter two are certainly possible in advanced disease, this type of change in early glaucomatous loss is atypical.

Retinal abnormality. The retinal findings, both on angiography and clinical observation, reflect the patient's visual field loss, given the frank ischemia of the macular bundle inferior to fixation in the left eye.

MS. Because there is no history of significant visual abnormality, MS probably isn't the culprit.

Our next step was to consider therapeutic intervention, which we had to weigh in light of her current systemic conditions. In a case such as this, continue the dialogue with the managing clinician, and the neurologist and internist if you can. In this case, they were comfortable with beta-blockers and alpha-agonists, but were unfamiliar with using prostaglandins to treat glaucoma in patients with MS.

Now do we initiate anti-hypertensive therapy, or simply monitor this patient for long-term changes? While the pressure control from the oral beta-blocker is less predictable than that from topical application, the patient's IOP is certainly likely to be decreased by the oral drug. This indicates that the pressure in both eyes is probably ordinarily higher. Taking into account the additional systemic risk of the marginally controlled diabetes, the better choice seemed to be therapeutic intervention to lower pressure and to prevent optic nerve damage.

With a goal pressure of 18mm Hg in each eye, I initiated a monocular trial of Alphagan (brimonidine) 1 drop bid in the left eye. In three weeks, IOPs were 24mm Hg O.D. and 18mm Hg O.S., so I added therapy in the fellow eye. At follow-up 10 weeks later, IOPs were 16mm Hg O.D., 18mm Hg O.S. at 10 a.m., and visual fields were unchanged. Meanwhile, the patient continued to see the vitreoretinal specialist, and underwent selective focal laser therapy with some success.

We monitored this patient carefully every month over the first 3 months for both progression of field change in the left eye as well as for retinal manifestations of diabetes. Because both were stable over that time, we now follow up every 3 months for both her glaucoma and diabetic retinopathy.

While this patient has multiple systemic issues that bear on glaucoma management, our management of the glaucoma itself was not out of the ordinary. Still, we must direct our clinical pathways toward the patient's systemic issues in light of the ophthalmic findings. Additionally, communication between the managing practitioners is invaluable so we can assure that changes in systemic therapy do not impact ophthalmic treatment and vice versa.

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