The Challenge of Maintaining Visual and Anatomic Stability for a Lifetime

Case #2: Persistent and unstable bilateral diabetic macular edema complicated by poor attendance at clinic appointments.

By Seenu M. Hariprasad, MD

The patient with diabetic macular edema (DME) who responds suboptimally to anti-VEGF therapy poses a distinct clinical challenge, prompting us to change course and tailor our treatment to the individual. As this case illustrates, our increasing understanding of the pathogenesis of DME along with our expanding array of therapeutic options helps guide our treatment approach for patients.

Case Report

A 55-year-old man with type 2 diabetes, hypertension, and hyperlipidemia has been managed at our service for several years. He is phakic and does not have glaucoma. This patient has a complex ocular history, which includes panretinal photocoagulation, pars plana vitrectomy, membrane peeling, endolaser photocoagulation, and intravitreal triamcinolone acetonide (Kenalog, Bristol-Myers Squibb) in both eyes. He has also received bevacizumab (Avastin, Genentech), ranibizumab (Lucentis, Genentech), and focal laser treatment for bilateral DME, which stabilized his vision but produced minimal improvement.

The patient has a history of missing appointments at our service because of his work schedule and the number of appointments he has with other medical specialists at our hospital. Given our long history in treating this patient, I present here a slice of his management by our service.

At a visit in March 2014 (Figure 1), the patient’s visual acuities were 20/70 OD and 20/100 OS. Significant edema was present in each eye. I administered Lucentis 0.3 mg OU, as this was the only FDA approved pharmacotherapy at the time.

Figure 1. Both eyes were treated with Lucentis 0.3 mg at this visit.

At the patient’s follow-up visit (Figure 2), his visual acuities had improved to 20/50 OD and 20/80 OS. Given persistent edema, I administered Lucentis 0.3 mg in each eye.

Figure 2. Given the persistent edema, both eyes were treated with Lucentis 0.3 mg during a follow-up visit.

The next time this patient presented (Figure 3), his visual acuities were 20/60 OD and 20/80 OS. The macular edema was a little less in the right eye but about the same in the left eye. As most of my colleagues would have done, I administered Lucentis for a third time in each eye.

Figure 3. Given his visual acuities and persistent edema, the patient received a third Lucentis injection.

On follow-up, I determined that the patient’s visual acuity did not improve in either eye and the macular edema was slightly worse in the right eye and about the same in the left eye (Figure 4). I adjusted my treatment paradigm and proceeded with an injection of Ozurdex 0.7 mg in each eye.

Figure 4. With little change in vision or anatomy, I switched from anti-VEGF therapy to Ozurdex.

The patient and I were happy with the dramatic improvement in anatomic response as shown on OCT and visual acuity in both eyes (20/40 OD, 20/70 OS) after switching our course of action (Figure 5). Given that the central macula was dry in both eyes almost 2 months after administering Ozurdex, we decided to withhold treatment at this visit.

Figure 5. Visual acuity and central foveal thickness were maintained for 2 months after the switch to Ozurdex.

Summary

This case is just one example of the multifactorial nature of DME. In a patient who is not responding to monotherapy, it is critical to consider adding a treatment with a different mechanism of action. ■

Seenu M. Hariprasad, MD, is the Shui-Chin Lee Professor of Ophthalmology and Visual Science at the University of Chicago. Dr. Hariprasad serves on the speakers bureaus for or is a consultant to Alcon, Alimera Sciences, Allergan, Bayer, Clearside Biomedical, Genentech, Janssen, Ocular Therapeutix, OD-OS, Optos, Regeneron, Spark, and Takeda. Dr. Hariprasad can be reached at retina@uchicago.edu.