A 77-year-old woman came to my office in mid-July 2025 seeing only counting fingers with her right eye, with a decompensated cornea and an endothelial cell count between 800 and 1000 cells per square millimeter. Five months later, in January 2026, that same eye saw 20/40 with correction, with a transparent, functional cornea. There was no transplant. The rescue was achieved with topical medical management alone: a Rho-kinase inhibitor, Ripasudil, combined with hypertonic saline.

Transparent cornea rehabilitated after endothelial decompensation.
Transparent cornea rehabilitated after endothelial decompensation.

That fact is what makes this case worth writing about. A cornea with that level of endothelial damage, in an eye with the history this one had, was until recently almost exclusively transplant territory. That it recovered useful visual function without going into the operating room marks one of the most interesting frontiers we have today in corneal rehabilitation.

I want to be clear from the outset about something important. I did not manage the initial cataract surgery or the endophthalmitis that complicated it. The patient was referred to my office afterward, with the corneal problem already established, for management of the decompensation. My role began in July 2025, when the corneal picture was the active front.

The starting point: an eye with a difficult history

The patient had undergone bilateral cataract surgery in May 2025. One week after the right-eye surgery she developed postoperative endophthalmitis, which is a severe intraocular infection. Managing that complication required intraocular injections of antimicrobials and, because of an insufficient response, a pars plana vitrectomy with placement of silicone oil inside the eye. The oil was removed in early July 2025.

That entire sequence, necessary to save the eye from the infection, took a toll on the cornea. After the vitreoretinal surgery, corneal decompensation appeared with a very low endothelial cell count in the right eye. At that point the patient was referred to my office for corneal management.

When I first evaluated her, the visual acuity of the right eye was counting fingers. To put that in perspective: counting fingers means the person can only tell how many fingers are being held up at close range. That is not functional vision. The cornea was decompensated and the endothelium, the layer responsible for keeping it transparent, was critically compromised.

What the corneal endothelium is and why it does not regenerate

To understand this case, you have to understand the endothelium. The cornea is the transparent lens at the front of the eye, and its transparency is not passive: it depends on active work. The innermost layer of the cornea, the endothelium, is made of a single sheet of cells that function as a pump. These cells constantly remove excess fluid from the corneal tissue. As long as the pump works, the cornea stays dry and transparent. When the pump fails, water accumulates, the cornea swells, and it becomes cloudy. That, in essence, is corneal decompensation.

The problem is that the human corneal endothelium has a very limited proliferative regenerative capacity. Unlike the surface epithelium, which renews itself constantly, endothelial cells essentially do not reproduce in the living eye. We are born with a certain number, and with age, surgeries, trauma, and inflammation, that population only declines. A healthy young adult has on the order of 2500 to 3000 cells per square millimeter, a figure that decreases progressively with age, and below roughly 500 cells the cornea tends to decompensate.

This patient was between 800 and 1000 cells per square millimeter in the right eye. A low count, in an eye that had already been through endophthalmitis, vitrectomy, and silicone oil. In my experience, that is exactly the profile of eye where one begins to talk with the patient about endothelial keratoplasty.

Why a transplant was not the first step

Corneal transplantation, and in particular selective endothelial keratoplasty, solves the problem by replacing healthy cells from a donor. It is a surgery we perform with good results, but it requires a donor, an operating room, and a recovery with its own risk of rejection and of graft failure over time. In an eye with the history of this one, adding another intraocular surgery was not a minor decision.

For that reason, before proposing a transplant, the reasonable protocol was to try to rehabilitate the endothelial function that remained. And that is where Rho-kinase inhibitors come in.

How a Rho-kinase inhibitor works in the cornea

Ripasudil belongs to a family of drugs called Rho-kinase inhibitors, or ROCK inhibitors. This medication was originally approved in Japan for another indication, glaucoma, where it helps lower the pressure in the eye. But its effect on endothelial cells opened a different line of research in the cornea.

The concept is the following. Rho-kinase is an enzyme that regulates the behavior of endothelial cells: their shape, their adhesion, and their ability to move. By inhibiting that enzyme, Ripasudil appears to favor the remaining cells migrating to cover the damaged areas and, to some degree, proliferating, something they normally do very little. If those cells manage to repopulate and reorganize, the endothelial pump regains capacity and the cornea clears again.

That is why this approach is called endothelial rehabilitation. No new tissue is transplanted: the patient's own tissue is stimulated to reorganize and work better. It is a shift in philosophy, from replacement to rehabilitation. These drugs have been studied in other scenarios of endothelial damage, such as Fuchs endothelial dystrophy and various forms of corneal decompensation. The evidence continues to build, and that is why it should be presented honestly: it is a promising, cutting-edge tool, not a universal substitute for transplantation.

The treatment and the patient's response

The regimen we started in July 2025 combined two fronts. On one side, topical Ripasudil, to stimulate endothelial rehabilitation. On the other, topical hypertonic saline, which helps draw water out of the cornea through a physical concentration mechanism, reducing the edema while the endothelium recovers function. The two work in complementary directions: one repairs the pump, the other relieves the fluid load in the meantime.

The progress was gradual, which is how this type of response usually behaves. It is not a switch that turns on. The cornea cleared progressively and vision climbed over the months.

These were the milestones for the right eye:

At the May 2026 evaluation, the refraction of the right eye allowed a corrected vision of 20/40, with the cornea showing only minimal inferior thickening and no overt corneal edema. The intraocular pressure was normal and the posterior segment, after the vitrectomy, remained healthy. The recent endothelial cell count was still in the range of 800 to 1000 cells per square millimeter, which is consistent with the idea that the benefit came more from better organization and function of the cells present than from a dramatic increase in their number.

Going from counting fingers to 20/40 in an eye with that history, without going into the operating room, is a result that in my experience fully justifies having tried the medical route first.

What this case does mean, and what it does not

It is worth putting this result in proper perspective. This case shows that, in selected patients, medical management with Rho-kinase inhibitors can rehabilitate a decompensated cornea and avoid, or at least postpone, a transplant. That is clinically relevant because it broadens the options before reaching the operating room.

What this case does not mean is that every decompensated cornea will be resolved with drops. It is not a universal solution. It is one more option, available for cases in which there is still endothelium capable of responding and the cause of the damage has been controlled. There are decompensations where the endothelium is so depleted, or the cornea so scarred, that a transplant remains the best and sometimes the only way out. This depends on the case, and that individual evaluation is precisely the work of the cornea specialist.

For anyone who wants to understand the other end of the spectrum, where the rescue does require surgery and donor tissue, I wrote about a tectonic corneal patch to save a Boston keratoprosthesis. That case and this one are two sides of the same principle: using the right tool for the degree of damage in front of you.

The role of the cornea specialist

Deciding when to try the medical route and when to go straight to a transplant is not trivial. It requires reading the endothelium well, the state of the surface, the cause of the damage, and the patient's reality. A low endothelial cell count does not automatically condemn an eye to a transplant, just as an acceptable count does not guarantee that the cornea will behave well. The decision is built from the complete picture.

As Medical Director of the Eye Bank of the Dominican Republic, I work daily at that intersection between the medical and surgical management of the cornea. Having direct access to donor tissue gives me the peace of mind to try the conservative route first when it makes sense, knowing that, if the cornea does not respond, the transplant option is available without delay. That safety net is what allows one to be patient with a medical treatment without putting the eye at risk. If you are interested in the full spectrum of options for the cornea and the ocular surface, you can review our cornea services.

Frequently asked questions

Does every damaged cornea need a transplant?

No. Many corneal disorders are managed with medical treatment, and some endothelial decompensations, in selected cases, can be rehabilitated without surgery. A transplant is reserved for when the damage exceeds the tissue's own capacity to recover. The decision depends on the case and is made by a cornea specialist after evaluating the endothelium and the cause of the damage.

Does the corneal endothelium regenerate?

Very little. The human corneal endothelium has a very limited proliferative capacity in the living eye, so the cells that are lost are not easily replaced. What some treatments aim for is not to create large numbers of new cells, but to stimulate the existing ones to migrate, reorganize, and work better to restore pump function.

What is Ripasudil?

It is a Rho-kinase inhibitor, a type of drug applied as eye drops. In the cornea it has been studied for its ability to promote the migration and function of endothelial cells, which can help clear a decompensated cornea in selected cases. It was originally approved for another ophthalmic indication, and its endothelial use is a cutting-edge line of work.

When is a corneal transplant actually needed?

When the endothelium is so depleted that it does not respond to medical management, when there is scarring or structural opacity that drops cannot reverse, or when the cornea cannot stay transparent despite treatment. In those scenarios a transplant, particularly selective endothelial keratoplasty, remains the best option to restore vision.

Can any patient with a decompensated cornea be treated with Ripasudil?

Not necessarily. It is an option for cases in which there is still endothelium capable of responding and the cause of the damage is under control. The indication, the dose, and the follow-up must be defined by an ophthalmologist who specializes in the cornea, who assesses whether the eye is a candidate before starting.

What this case makes clear

Corneal rehabilitation is changing. For years, a decompensated cornea with a low endothelial cell count pointed almost inevitably to a transplant. Today, Rho-kinase inhibitors give us a tool to first try to get the patient's own tissue to recover, and in selected cases that attempt works, as it worked in this patient who went from counting fingers to 20/40 without going into the operating room.

It does not replace transplantation in every case. It is one more option in the arsenal, valuable precisely because it broadens what we can offer before surgery. If you or a family member is facing corneal decompensation and a transplant has been proposed, a second evaluation with a cornea specialist who knows these alternatives in depth is worth it. The right decision always depends on the particular case.

Disclaimer

This content is for educational and informational purposes. It does not replace professional ophthalmic consultation, diagnosis, or treatment. The use of Ripasudil and other Rho-kinase inhibitors in the cornea must be indicated and supervised by an ophthalmologist. The results described correspond to a specific patient and may vary according to the clinical conditions of each person. Corneal decompensation requires specialized evaluation to determine whether an eye is a candidate for medical management or for a transplant.

References

  1. Garnock-Jones KP. Ripasudil: First Global Approval. Drugs. 2014;74(18):2211-2215. PMID 25414122.
  2. Okumura N, Koizumi N, Ueno M, et al. Enhancement of corneal endothelium wound healing by Rho-associated kinase (ROCK) inhibitor eye drops. Am J Pathol. 2012. PMID 22704232.
  3. Deng Y, et al. Rho-associated kinase (ROCK) inhibitors in corneal endothelial therapy: a systematic review. 2025. PMC12292609.
  4. Okumura N, et al. Topical Rho-associated kinase inhibitor ripasudil for corneal endothelial dysfunction in Fuchs endothelial corneal dystrophy. Am J Ophthalmol. 2021.
  5. Erdinest N, et al. Clinical outcomes of topical ripasudil in corneal endothelial dysfunction: a retrospective cohort. J Clin Med. 2025. PMID 40807192. PMC12347265.
  6. Review of evidence for in vivo corneal endothelial regeneration. Exp Eye Res. 2017.

Last updated: June 23, 2026