Let’s face it, time is passing. Day by day and year by year, we are all aging—admit it or not. Our patients’ eyes and those eyes with corneal grafts are also aging.

Consider also that the graft material—the corneal button—had an earlier life as well. A graft button has been through the works, so to speak. It lived, some longer than others, before passing through death only to be brought back to life to enable another to see. Graft buttons suffered severe anoxia; the trauma of being wrenched from their original cornea-eye; and re-invigoration, stitches, antibiotics, and steroidal and perhaps other anti-inflammatory agents for months on end. The greater chance is that at least once in their second lives, the grafts experience a rejection episode that require more medications. And—perhaps the greatest insult to corneal buttons—contact lens wear to compensate for the astigmatism induced into the graft or for the anisometropia resulting from the surgery.

Considering everything that corneal buttons go through, you may wonder how long full-thickness penetrating keratoplasty (PK) grafts last. A paper published in 2009 concluded that only 27% of grafts would be viable at 20 years (Borderie et al, 2009). I have been in contact lens practice in a hospital setting for more than 30 years. Gradually, some old grafts have been coming my way.

A Common Finding

Over the past five years or so, patients who underwent PK procedures during the 1990s and whose grafts were considered successful have begun to return. One of the most vivid developments common to all of these grafts has been an increase in topographically measurable corneal astigmatism. This cylinder is startling because of its quantity. It frequently measures more than 20.00D.

Figures 1 through 3 show one such patient who, now in his 70s, underwent PK in 1993. His refraction to excellent acuity in 2000 required only 1.00D of cylinder. In 2008, his refraction required 10.00D of cylinder. We terminated the refraction in 2013 with more than 12.00D when his cornea boasted 22.00D of cylinder; and before scleral lens fitting in 2014, it had nearly 26.00D of corneal cylinder.

Figure 1. Corneal topography of Patient #1 in January 2008. The sim k curvatures translate to 48.25D and 38.50D or 9.75D of anterior corneal astigmatism. This is nearly identical to his refractive cylinder of 10.00D.

Figure 2. In July 2013, the topography of Patient #1’s graft showed a jump to nearly 22.00D of cylinder.

Figure 3. Patient #1’s graft just over a year after the Figure 2 image now shows nearly 26.00D of graft astigmatism on anterior surface topography.

When I first encountered this augmented astigmatism, I began to consider its potential source. My first idea was that throughout the years since the PK, the host cornea continued to develop its keratoconus. But, in every case, the current presentation was of recently reduced habitual visual acuity. We needed to understand the cause for the sudden enormous increase in corneal cylinder. Beginning with a gradually increasing pull by the host cornea as its keratoconus continued to develop, the only available other plausible factor is the deterioration of the grafted tissue itself. It was no longer able to take the pull.

Fitting Challenges

Another patient, then in her mid-30s, with whom we have worked since she was first diagnosed with keratoconus more than 20 years ago, had undergone PK in each eye and subsequent near total retinal detachment with surgical re-attachment in her right eye. She had been doing well physically and visually with her corneal lens in that eye. During a periodic follow-up visit, I noticed that the lens was eroding her graft at the margin between 10 o’clock to 12 o’clock. She was treated for a mild rejection episode and sent back to me for a refitting.

I soon learned that corneal lenses—small, large, intralimbal, steep, or flat—were all out of the question. They would either fall off or ride up and abrade. I also tried silicone hydrogel mini-scleral lenses, but the haptic could not be steep enough to prevent fluting.

So began the epic saga of fitting this eye (Figures 4 and 5) with scleral lenses, which have also been problematic for this grafted cornea. I first tried lenses with a very high vault so as to not irritate her graft, but their curvatures were so steep with the high minus required that the lenses bulged in a cosmetically unacceptable manner.

Figure 4. Anterior corneal topography of Patient #2 10 years after her transplant showing 3.7D of graft cylinder.

Figure 5. The same eye as in Figure 4. The cylinder now has reached 9.36D. Perhaps more important is the overall shape of the graft. Much more pronounced ectasia is discernible in the areas in which both corneal and scleral lenses abrade.

In consultation with colleagues here and abroad, I attempted many other designs. Each, in its own way, brushed and caused erosion staining on the peripheral graft surface. Thus, over the past six months or so, I have observed larger and larger areas of peripheral graft show more and more staining. I have concluded that what I saw three or more years ago was only an early indication of the worse that was yet to come.

As of our last examination, the graft-host interface had risen a full 360° (Figure 6). Currently, and after many fitting iterations, my patient seems to be doing well with a custom prosthesis generated via a 3-D scan of a surface impression of her eye. The future of fitting seems to have arrived.

Figure 6. The elevation maps showed that the peripheral bulge continued to rise over the past two years more than 20 microns in some areas and that the annular curvature continues to grow around the much flatter central surface of the graft. One further note is that the curvature in the historically highest part of the cornea between 10 o'clock to 12 o'clock continues to steepen here from 63D to nearly 66D.

A More Forgiving Approach in the Future

Many eyes that require corneal transplantation secondary to keratoconus are those of young people or of others who have never worn contact lenses but spontaneously develop scarring or other causes of vision deterioration. However, many other keratoconus patients develop scarring secondary to the use of contact lenses. I believe that corneal lenses fit with any degree of bearing over years of wear are likely to cause superficial and deep scarring in the cornea.

It is quite likely that, in general, our contact lens fitting paradigm for keratoconus needs rethinking—and most possibly a radical overhaul. By fitting lenses in a more forgiving manner, even minor insults to the health of corneal structures can be avoided; and perhaps, in the long run, fewer corneal transplants will be required.

In any event, better lens designs and fitting will result in delayed transplant surgery, which will permit a transplanted cornea to live comfortably while gradually aging together with its new host or until synthetic transplant material becomes available. CLS

Acknowledgement: As always, my respect and thanks must be expressed to my patients for choosing me to help them confront their visual adversities invoked by their corneal ectasias.