The superficial fibroplastic nodule (SFN) and I go back some 25 years, only then I found it called a proud nebula. In those days, most keratoconic corneae were fit with relatively small, relatively flat, GP lenses. The constant rubbing…abrasion…erosion at the apex of the cones on some of these corneae eventually gave way to the buildup of heaped scar tissue, which would subsequently re-abrade and grow higher. These eyes would be painful, and if the heaped up scar was large enough and centrally located, vision would suffer. The selection of lens designs in those days was not very forgiving to the SFN.
The first patient for whom I fought this battle—in retrospect, probably not very successfully—caused me to visit the library. There, I found an article by Moodaley et al (1994) calling this phenomenon a “proud nebula.” I also found a design article in Contact Lens Spectrum describing what the authors called a “duozone lens,” (Mandell et al, 1995). This lens featured a very steeply curved and tiny (1mm to 2mm) central zone surrounded by a fitting zone meant to match the flatter (generally superior) corneal curve of the midperipheral cornea. The fitting curve represented the vision-providing area of the lens.
Working with our local lab (which reportedly broke many diamonds lathing these lenses for us), we generated many duozone lenses. Several are in our library, and some might even still be walking around, although the lab no longer exists.
We used corneal topography to guesstimate the curves we wanted, and we were to some extent successful. Mostly, these lenses were not verifiable; what we got was what we got, and we had to trust that we received what we had asked for.
Managing SFNs Today
SFNs still happen because patients do not come in for follow-up visits as often as I would wish; they try to overextend the life of their contact lenses, and basically they deny that the ocular aggravation from which they are suffering might be caused by a poor fitting relationship between their sore cornea and their vision-restoring contact lens.
This week, a veteran patient dropped by for a check-up. I have noted in her file over the years the fluorescein image of the open scar of an abraded SFN. I even endeavored to fit her three or four years ago with a scleral lens to stop the recurrent abrasion, but she had declined.
She asked a typical question during the exam: “Isn’t there a corneal surgery that can cure me of this problem?” The answer from our department over the years has been “No.” I suppose that this is the conservative approach, implying that as long as vision can be acceptable with contact lenses, we continue with contact lenses. Only thereafter would we need to consider penetrating keratoplasty or perhaps the more subtle anterior lamellar keratoplasty. You might wonder whether this scar can be removed either with a physical or an optical knife (laser).
I was more successful in stating my case for her cornea this time. She was amazed at the improvement in comfort with the first trial lens. The OCT image in Figure 1 shows, from top to bottom: the scleral lens, the saline-filled fluid reservoir, and the cornea with an obvious sub-epithelial SFN to the right of center.
Is Prevention Possible?
The question begging an answer is: Can SFNs be prevented? Given the peculiarities of the keratoconic cornea and how it does not heal as well from even minor insults compared to a normal cornea, anything that can prevent apical rubbing and subsequent abrasion should help to protect the cornea and prevent SFN development. Because vision remediation in keratoconus in most cases requires the use of GP lenses, first and foremost the lenses must be fit with at least minimum clearance over the cone; minimal touch, feather touch, and other fitting approaches that closely approximate the corneal surface are likely to result in unwanted corneal irritation, though achieving good visual acuity. I don’t like the tradeoff; the health and integrity of the corneal anterior anatomy is paramount.
We don’t know who will develop an SFN, we only know what is likely to contribute to its formation. So, careful corneal lens fitting as well as careful control and evaluation at periodic follow-up visits—with lens replacement when the ectasia begins to progress—are vital.
I have reported one case of “cyclic keratoconus” (Schendowich, 2008) (and I have seen several others). In a patient who had very mild keratoconus (not yet wearing contact lenses), I plotted his corneal ectasia progression and regression over a year, documenting six cycles. Combined with an earlier observation that many of our patients experience “good eye days and bad eye days” (Schendowich, 2000), I concluded that a flattish-fitting corneal lens on a keratoconic cornea was likely causing an apical abrasion during those “bad eye days” when their ectasia would be cyclically progressing.
For patients who are not yet wearing contact lenses but who show progression/regression cycles, I wonder whether corneal cross-linking (CXL) might not effectively prevent SFN formation. Once the cornea has been “frozen” by the procedure, it should not need to be refit as frequently as a cornea that has not undergone CXL.
For advanced corneae for which CXL is not an option, or for any ectasia showing a very high flat-steep curvature difference, I recommend a scleral rather than a corneal lens. The scleral lens with its saline-filled pre-corneal cell will prevent scenarios leading to SFN formation. CLS
Acknowledgement:
As always, I express my respect and thanks to my patients for choosing me to help them confront their visual adversities invoked by their corneal ectasias.
For references, please visit www.clspectrum.com/references and click on document #258.