CLINICAL CHALLENGES
The Case of 6-Month Sadie
Problems can sneak up on diabetic patients, so it pays to see them regularly.

All eye doctors worth their salt talk to their patients about the need for regular, routine eye care. We harp on the importance of recall and pre-appointing to our staffs and reinforce the concept of annual exams to our patients. Some patients require more frequent monitoring, though.

Obviously diabetic patients need to be seen at least yearly, but as this case shows, it may be prudent to see even presumably stable diabetics every 6 months.

NVD of Sadie's optic nerve head.

Sadie's story

Sadie was one of my "regulars," whom I saw every 6 months. She was a 71-year-old type I diabetic who had been dependent on high doses of insulin to control her blood glucose for the past 11 years.

Sadie had originally been referred to me 5 years earlier by her internist to be monitored for ocular manifestations of her diabetes. The internist was having trouble controlling her blood glucose levels.

At the time I first examined Sadie, she was using 65 units of insulin in the morning and 50 units in the late afternoon. Despite this, her blood sugar level consistently stayed higher than 280 mg/dL, sometimes going as high as 350 mg/dL, and her internist was justifiably concerned about diabetic retinopathy (as well as other peripheral vascular disease).

Sadie didn't fit the description of a classic diabetic patient. She was slight of stature, certainly not overweight and maintained a relatively healthy diet. She did have a family history of diabetes, however. Her uncontrolled diabetes confounded her M.D. and frustrated her.

Initially Sadie's visual acuity (VA) was 20/30 OU. Over the years she developed cataracts, which were removed successfully and uneventfully. She maintained a VA of 20/25 OD, 20/30 OS after the cataract surgery. At every visit I examined Sadie's retinas and found no evidence of any diabetic retinopathy. I always talked with her about diabetes and the eye and scheduled her for 6-month follow-up appointments. I stressed that this was especially important because her disease was poorly controlled.

As time passed

In August of 2000, I once again saw Sadie for her 6-month checkup. Since her last visit, Sadie's insulin had been reduced to 30 units in the morning and 20 units in the afternoon, but her internist added nateglinide (Starlix) in hopes of controlling the highs and lows in her blood sugar level.

He also prescribed lisinopril (Prinivil) to improve Sadie's circulation. This new regimen had made her glucose control much more stable, averaging around 180 mg/dL.

As usual, Sadie had no complaints about her vision. She said that she wasn't experiencing any difficulty seeing and that her vision remained stable. I measured her VA to be 20/30 OD, 20/25 OS. Her pupils were 5 mm, round and briskly reactive. She had no extraocular muscle restrictions. Her anterior segments showed mild bulbar injection, but no corneal changes and no papillae. Posterior chamber implants were well positioned OU and I saw no posterior capsule opacities in either eye.

Uh oh

I dilated Sadie's eyes and once again embarked on a detailed examination of her retinas, half expecting to find nothing significant. As usual, the right eye revealed no diabetic changes. The cup-to-disk ratio was 0.4/0.4, with a slight ring of peripapillary atrophy. I saw some atrophy of the retinal pigment epithelium in the macular area, but no hemorrhages, exudates or neovascularization OD.

However, when I examined the OS I met with the unexpected. On the surface of the optic nerve head I saw a frond of neovascularization (see figure above). These fine vessels were delicate in appearance but occupied about half of the optic disk's surface. At first I thought they were collateral vessels, but after critically examining them in more detail with a 60D lens, I realized that these vessels were pathologic in nature. They extended anteriorly toward the posterior vitreous and formed loops back onto one another.

Sadie definitely had neovascularization of the disk (NVD). A few other dot hemorrhages were scattered throughout the posterior pole, but I found no areas of neovascularization elsewhere (NVE). No macular edema was present.

When it's NVD

Sadie had NVD, one of the lesions of proliferative diabetic retinopathy (PDR). Other clinical entities of PDR are NVE, preretinal hemorrhage and vitreous hemorrhage.

The lesions of PDR share certain characteristics. They're all located either in front of the retina or within the vitreous, and they're associated with greater incidence of vision loss. Clinically, NVD presents as a fine vascular network characterized by anterior growth. The new vessels also stand out because of their diameter. They're thinner than normal vessels on the disk.

NVD is defined as new vessels on the disk or within 1 disk diameter of the disk margin. They begin as fine loops on the surface and initially are devoid of any supporting connective tissue. As it proliferates, NVD incorporates itself into the vitreous. If left untreated, these vessels can con-tract and cause a vitreous hemorrhage or a traction retinal detachment.

PDR is defined clinically as:

• any new vessels (NVD or NVE)
• severe NVD (defined as NVD that occupies more than one-third of the disk area)
• a pre-retinal hemorrhage
• a vitreous hemorrhage.

The Diabetic Retinopathy Study (DRS) has shown that if a patient has three of these conditions she's considered to have high-risk PDR and would benefit from prompt therapy.

The chance of severe vision loss more than doubles when three of these risk factors are present. The Study also showed that PDR is more common in poorly controlled diabetics or in those who have had the disease for a period greater than 5 years.

The skinny on Sadie

Sadie met the first three criteria for high-risk PDR, indicating the need for pan-retinal photocoagulation (PRP). An intravenous fluorescein angiogram confirmed the disk vessels to be NVD; it also confirmed that there were no diabetic changes OD.

Sadie underwent PRP in the OS 4 days after I noticed the NVD. It took 6 months for these new vessels to completely regress, but they eventually did. Since undergoing the laser treatment, Sadie has worked diligent-ly to better control her blood sugar. Her VA has remained stable at 20/30 OU and she hasn't developed any further diabetic retinopathy. Of course she will continue to be "6-month Sadie," needing ongoing monitoring of her retinas.

Optometry trumpets itself as the primary eyecare profession, and this case is a good illustration of what that means. All of us need to expand our practices into managing cases like this. Not only will this approach be good for our profession and our practices, but most importantly, it will be a great benefit to our patients. OM

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