Abstract
Purpose
To report a case in which netarsudil ophthalmic solution 0.02% improved refractory corneal edema after laser peripheral iridotomy (LPI) and Descemet’s membrane endothelial keratoplasty (DMEK).
Observations
A 63-year-old female presented with decreased vision due to corneal edema secondary to iatrogenic endothelial cell loss from previous YAG and argon laser peripheral iridotomy. Initial treatment with topical sodium chloride 5% solution was unsuccessful in resolving the edema. As a result, topical netarsudil was initiated off-label. Improvement in corneal thickness and visual acuity was noted, but after a few months, the left eye decompensated with worsening edema. Cataract surgery with DMEK was performed. Surgery was prolonged and intraoperative floppy iris was encountered. Post-operatively, the patient’s best-corrected visual acuity (VA) fluctuated between 20/30 to 20/70 with persistent corneal edema. The central corneal thickness (CCT) ranged from 758 to 779 three months after surgery. Topical netarsudil was started again off-label for cornea edema once nightly. Over the next two months, visual acuity and CCT improved to 20/25 and 650, respectively. Stabilization of visual acuity and cornea edema has been maintained for eight months after initiation of topical netarsudil.
Conclusions
Netarsudil, a commercially available rho-kinase inhibitor, may be an effective, non-invasive adjunctive therapy for refractory corneal edema. Our case demonstrates improvement in BCVA and CCT using topical netarsudil, which has been maintained without any vision threatening side effects.
1
Introduction
Netarsudil ophthalmic solution 0.02%, was approved by the U.S. Food and Drug Administration for the treatment of elevated intraocular pressure in patients with primary open-angle glaucoma. Rho-associated protein kinase (ROCK) inhibitor, such as netarsudil, act by disrupting actin fibers and decreasing smooth muscle contraction and stiffness in the trabecular meshwork, thereby increasing the flow of aqueous humor.
Interest has also arisen regarding ROCK inhibitors and endothelial function. Rho-Kinase inhibitors have been shown to improve corneal endothelial cell function by decreasing apoptosis and increasing cell proliferation in animal models. , ROCK inhibitor Y-27632 has been studied in Fuch’s endothelial dystrophy and shown to preserve corneal clarity and visual acuity. Ripasudil (K-115) has also been shown to improve corneal edema in patients after failed central descemetorhexis. To date, there is limited data on netarsudil (AR-13503), which we hypothesized would have a similar effect on endothelial cell function.
2
Case report
A 63-year-old female patient presented for decreased vision in her left eye. Her past ocular history was significant for narrow anatomical angles, status post argon LPI in both eyes at age 54, and subsequent touch up YAG LPI in the left eye at age 58. Initial BCVA was 20/20 OD and 20/60 OS. On exam, there was edema of the superior cornea extending to the visual axis in both eyes (OU) with left eye (OS) ( Fig. 1 A) greater than the right (OD). There were no signs of Fuchs endothelial dystrophy. The anterior chamber was narrow and stable compared to previous exams, with no signs of inflammation. The iris was convex and the angle was open to trabecular meshwork (TM) in all quadrants on gonioscopy. The intraocular pressure (IOP) was 18. On optical biometry, anterior chamber depth was 2.55 mm OU, and central corneal thickness (CCT) was 607 OD, 747 OS. Specular microscopy showed regular endothelial cells OD with a count of 2151. No cells could be visualized OS due to the corneal edema [ Fig. 2 ].
