An 86-year-old woman was referred by her optometrist after several months of worsening vision. Ocular history was significant for cataract surgery two years prior and a 25-year history of open-angle glaucoma with a seven-year history of treatment using brimonidine tartrate 0.1% BID OU and artificial tears (ATs). She had no history of contact lens use or eyelid disorders (i.e., styes, blepharitis, and meibomian gland disease) and no history of corneal disorders including recurrent corneal erosion, meibomian gland disease, rosacea blepharitis, blepharokeratoconjunctivitis, or ulcers. The patient reported worsening of her vision since her cataract surgery, most noticeably in the three months prior to her referral, requiring her to use a magnifying glass to read. The referring eyecare provider reported no identifiable corneal lesions prior to 2016, with slow development and progression of bilateral peripheral corneal opacities since that time. The patient also noted photosensitivity in both eyes. She had no pertinent medical history, including hyperlipidemia.
On examination, best-corrected distance visual acuity (BCDVA) was 20/60 OD and 20/70 OS. Manifest refraction was +0.75-1.00 x 160 OD and +0.50-1.25 x 165 OS, and IOP was within normal limits in both eyes. Slit lamp examination was remarkable for bilateral dermatochalasis, superficial punctate keratitis (SPK), and peripheral corneal scarring from 4 o'clock to 5 o'clock position and 7 o'clock to 8 o'clock position with superior corneal neovascularization consistent with sectoral interstitial keratitis and lipid keratopathy OU. There was no guttata or corneal lattice, but crocodile shagreen was noted in both eyes. Dilated fundus examination revealed blunted macular reflex OU and C/D ratio of 0.65 OD and 0.75 OS. Findings were consistent with bilateral lipid keratopathy secondary to interstitial keratitis. Infectious and autoimmune workup was ordered in coordination with the patient's primary care physician (PCP), including complete blood count with differential, erythrocyte sedimentation rate, C-reactive protein, auto-antibody titers (ANA, C-ANCA, and P-ANCA), rheumatoid factor, anti-SSA/Ro and anti-SSB/La, purified protein derivative (PPD) skin test and interferon-gamma release assay (IGRA) for tuberculosis, chest X-ray, ACE and lysozyme levels for sarcoidosis, throat and nasal swabs for methicillin-resistant Staphylococcus aureus, stool for ova and cysts, dental and tonsillar exam, Lyme disease titers, and syphilis testing. All tests resulted as negative or within normal limits. The patient's PCP reported no findings in the review of systems or on physical exam consistent with rheumatoid arthritis, systemic lupus erythematosus, Sjogren syndrome, or other similar systemic diseases.
The patient was continued on BT and artificial tears (ATs) and then started on difluprednate drops TID OU. Slit lamp photographs taken three weeks later (shown in Figure 1) demonstrated no tangible change in the areas of lipid keratopathy. After excluding all other possibilities, we have concluded that the BT is the most likely cause of this patient's lipid keratopathy. As such, we are planning to discontinue BT in this patient; however, an appropriate alternative glaucoma treatment must be found, and we are in discussion with our glaucoma specialist to determine this.