ROCK Inhibitor (Ripasudil) as Coadjuvant After Descemetorhexis Without an Endothelial Graft
We read with interest the article by Moloney et al on descemetorhexis without grafting for Fuchs endothelial dystrophy using an Rho-associated kinase (ROCK) inhibitor (ripasudil, previously known as K-115) as a coadjuvant in 2 eyes that failed to clear by month 2 and in a third case with a small area of persistent focal edema.1 Our first concern is that the age of the patients was not indicated. How many of the eyes were phakic and how many were pseudophakic? Were any of the descemetorhexis procedures performed along with phacoemulsification?
In a case that we reported on, a patient who underwent descemetorhexis without grafting along with phacoemulsification and intraocular lens implantation, we noted a persistent area of paracentral edema, which eventually generated a fibrotic leukoma (Fig. 1).2 Moloney et al mentioned that in case 9 of their series, a patch of microcystic edema persisted outside the visual axis, within the stripped area at month 5. The patient received ripasudil 6 times a day during 2 weeks, and edema disappeared. According to their results, we believe that if we had used such an approach in our patient, the visual results would have been even better.
Retrospectively reviewing the case we reported, we found that the shape of the descemetorhexis was rather irregular, and the size was approximately 5.5 to 5.8 mm high and 3.5 to 3.8 mm wide, including the peripheral superior cornea. Although the patient reached a distance-corrected visual acuity of 20/30-2, 16 months after surgery, 5 months later in her last visit, it decreased to 20/70. Now, we believe that the rhexis size and the involvement of the superior peripheral endothelium could have been related to the persistence of the patch of paracentral edema that eventually led to the presence of a paracentral leukoma (Fig. 1). As mentioned by Moloney et al, sizes of the descemetorhexis larger than 4 mm in diameter have been linked to persistent edema.1–5 In addition, after a failed descemetorhexis without an endothelial graft, the case might become challenging for Descemet membrane endothelial keratoplasty (DMEK) because of the presence of fibrosis in stroma or prevention of attachment of the DMEK graft on areas with endothelial cells.2,5 However, recently, Rao et al6 (from the group of Colby) reported good outcomes of DMEK in 3 patients with Fuchs endothelial dystrophy after failed Descemet stripping without an endothelial graft. They did not attempt to scrape the posterior stroma in any case and achieved complete corneal clearance without the need for rebubbling.
We consider that the results shown by Moloney et al using short-term supplementation with a topical ROCK inhibitor (ripasudil) are very encouraging and might open a way to apply this approach more frequently. However, a big concern is the low final values of the endothelial cell count at the last follow-up visit (12 ± 8.2 months on average, with a range between 4 and 30 months). The mean was only 765.6 ± 226 cells/mm2. Four eyes (33.3% of the group) had less than 600 cells/mm2, with one of those with 494 cells/mm2 (which is below the traditionally accepted limit for corneal edema). Furthermore, almost all eyes (11 of 12, ie, 91.7%) showed a cell density below 1000 cells/mm2.1
Lee and Munir recently reported a case of eventual corneal endothelial cell failure after initial spontaneous resolution of corneal edema following failed DMEK, in a patient with Fuchs dystrophy (a 9.00-mm diameter descemetorhexis had been performed).7 The cornea gained transparency, and an endothelial cell count of 1139 cells/mm2 was found 8 months after surgery.