A 60-year-old woman was referred to the dry eye clinic at JEC Eye Hospital Kedoya for chronic recurrent redness of her left eye (LE) in the past 6 months prior to her visit. Her past medical history was negative for autoimmune disease and thyroid dysfunction. She had been using spectacles since her early adulthood period and was also diagnosed with anisometropia of the LE. She did not have any history of ocular surgery in either of her eyes. At the time of the referral, she had been using cyclosporine 0.1% eye drop once per day and fluorometholone eye drop four times per day for 1 month and tear substitute every three hours. However, she did not feel any improvement under these medications. The history of her right eye (RE) was unremarkable.
On examinations, the best corrected visual acuity (BCVA) was 20/20 in the RE with S3.25 correction and 20/40 in the LE with S-18.00 correction. Intraocular pressure (IOP) of both eyes was within normal limits. At slit lamp examination, the LE showed significant conjunctival hyperemia and redundancy in the superior bulbar area (Figure 1). Positive fluorescein staining was observed on the superior bulbar conjunctiva and superior limbus. The lens of LE showed grade 2 nuclear sclerosis. There was plugging of meibomian gland orifices consistent with MGD in both eyes. The tear break-up time (TBUT) was shortened to 4 seconds in RE and 2 seconds in LE. Schirmer's test without anesthesia was 5 mm on the RE and 2 mm on the LE at 5 minutes. Meibography (Oculus Keratograph 5M, Oculus, Wetzlar, Germany) was performed to evaluate the degree and severity of MGD in both eyes (Figure 2) which revealed grade 1 meibomian gland loss.
Her final diagnosis at initial presentation was SLK, mixed type of dry eye disease related to aqueous deficiency and MGD, and senile cataract of the LE. Several treatment alternatives were discussed, including the option to continue cyclosporine 0.1% eye drop which she refused due to intolerable stinging sensations. She was also not keen on punctal occlusion. Accordingly, she opted for treatment combination of auto-SED 50% concentration and silicone hydrogel contact lens (Air Optix Aqua, Alcon, 33% water content) which acted as therapeutic BCL and myopia correction, together with non-preserved lubricants every 1 to 2 hours. She agreed to wear the contact lens during her working hours (6 to 8 hours per day) and administer auto-SED at home (at least 6 times per day), since it was bothersome for her to use the auto-SED at work. In terms of MGD, we decided to perform intense pulsed light (IPL) therapy using the E-Eye  device (E-Swin, Houdan, France), which was done in 3 sessions with 4-weeks interval. We also discussed the possibility of cataract surgery for her LE once the ocular surface condition has improved, to prevent worsening of symptoms after the surgery.
On review 3 months after her initial visit, the patient had symptomatic relief in her LE. Slit lamp examination revealed significant reduction of inflammation on the superior bulbar conjunctiva of the LE (Figure 3A), and no fluorescein staining was visible. Treatment regimens with auto-SED, contact lens wear, and non-preserved lubricants were continued.
Two years following her presentation, the patient remained asymptomatic. Mild superior conjunctival hyperemia without fluorescein staining was found on examination of the LE (Figure 3B). TBUT of both eyes were more than 5 seconds. Schirmer test was done, and the results were 6 and 5 mm of RE and LE, respectively. Meibography was suggested in order to evaluate the extent of meibomian gland loss after treatment. Unfortunately, she refused to do the examination. As for the treatment, she did not mind continuing to wear contact lens and administer auto-SED, especially now that she only needed to use the auto-SED 3 to 4 times per day.