|LETTER TO EDITOR
|Year : 2000 | Volume
| Issue : 1 | Page : 71-2
Is there a minimum endothelial cell count for a clear cornea after penetrating keratoplasty?
SK Rao, AT Leung, AL Young, DS Fan, DS Lam
S K Rao
Source of Support: None, Conflict of Interest: None
Keywords: Adult, Cell Count, Contrast Media, administration & dosage, Corneal Dystrophies, Hereditary, surgery, Endothelium, Corneal, cytology, Female, Fluorescein, administrat
|How to cite this article:|
Rao S K, Leung A T, Young A L, Fan D S, Lam D S. Is there a minimum endothelial cell count for a clear cornea after penetrating keratoplasty?. Indian J Ophthalmol 2000;48:71
In January 1997, we performed a 7.5 x 7.0 mm corneal graft in the left eye of a 33-year-old woman with granular corneal dystrophy. Surgery and early postoperative period were uneventful. She developed allograft rejection in March 1997 and received treatment with intravenous methyl prednisolone (500 mg), cyclosporine A (50 mg b.i.d.), and oral and topical steroids. Although the rejection was reversed, she developed steroid-induced glaucoma and this was controlled with topical anti-glaucoma medications. In May 1999, slitlamp biomicroscopy of the left eye revealed a clear graft. Specular microscopy (Konan noncon Robo ca sp 8000, Konan Inc., Hyogo, Japan), revealed an endothelial cell count of 445 cells/mm2 (Figure); and central graft pachymetry (Corneo-GageTM plus, Sonogage Inc., Cleveland, Ohio) was 451 μm. Comparative values in the right eye were 2906 cells /mm2 and 536 μm respectively. Allograft rejection resulted in endothelial damage and low cell count in our patient 28 months after penetrating keratoplasty. The borderline intraocular pressure could also have contributed to the severe graft thinning. The apparent paradox of a low endothelial cell count and thin corneal graft has been reported earlier,[1-3] although the mechanism for the same is not clear.
Bourne reported significantly decreased endothelial cell density, deswelling rate, and endothelial permeability to fluorescein in 12 eyes with corneal grafts, compared to normal control subjects. He related this to the decreased cross-sectional area of the intercellular space facing the anterior chamber, due to the decreased number of cells in the endothelial monolayer. The leakage of fluid into the corneal stroma and the endothelial pump, which are hypothesized to occur mainly through this paracellular pathway between cells, is thus reduced. In contrast, endothelial permeability is increased in eyes with an inherently unhealthy endothelium, as in Fuch?s endothelial dystrophy, resulting in stromal edema and increased corneal thickness. Corneal guttae were seen in only 2 of the 20 eyes described by Kus et al although 8 of the eyes in their study had an endothelial count < 700 cells/mm2. This is considered by some specialists to be the critical limit for corneal decompensation. The absence of guttae in graft endothelium could indicate that the endothelial cells in corneal grafts, though reduced in number, are essentially healthy. It is therefore interesting to speculate that with such reduced endothelial permeability, the normal endothelial cells in a corneal graft are able to maintain corneal clarity in the thin graft.
If the above hypothesis were accepted, we would expect grafts with a long follow-up and normal or decreased thickness to have a bimodal distribution of endothelial cell counts. Those with adequate cell counts and a physiological endothelial cell count-corneal thickness relationship would form one peak. Eyes with low endothelial counts, but still well compensated due to the reduced pump-leak hypothesis described above, would form the other. However, further loss of endothelial cells in the latter group of eyes would result in graft oedema and increased thickness. The data from our patient and that reported recently by Kus et al support this hypothesis. In their series, in 9 grafts with central thickness < 600 μm, the endothelial cell counts showed 2 peaks: 6 eyes with counts <700 cells/mm2 and the other 3 eyes with counts > 900 cells/mm2.
Abbott et al in their study reported 4 eyes with a central endothelial cell count less than that in our patient. The endothelial cell count was 320, 336, 416, and 432 cells/mm2 respectively. The graft thickness in these eyes was 0.54, 0.46, 0.45 and 0.43 mm respectively. The two grafts with cell counts < 400 cells/mm2 had a corneal graft thickness greater than the two other grafts with higher cell counts. It is therefore interesting to speculate that in the post-graft endothelium, 400 cells/mm2 may be the critical limit at which graft failure occurs. However, in individual eyes, other factors such as age of the recipient, host corneal pathology, uveitis and glaucoma may also influence the critical endothelial cell count necessary to maintain corneal deturgescence.
In conclusion, we feel that the functional status of the endothelium after corneal grafting is best assessed by serial monitoring of both endothelial cell counts and corneal pachymetry.
| References|| |
Lin JG Jr, Stuart JC, Warnicki JW, Sinclair RA, Marsh GM. Endothelial morphology in long-term keratoconus transplants. Ophthalmology
Abbott RL, Fine M, Guillet E. Long-term changes in corneal endothelium following penetrating keratoplasty. A specular microscopic study. Ophthalmology
Kus KM, Seitz B, Langenbucher A, Naumann GOH. Endothelium and pachymetry of clear corneal grafts 15 to 33 years after penetrating keratoplasty. Am J Ophthalmol
Bourne WM. Functional measurements on the enlarged endothelial cells of corneal transplants. Trans Am Ophthalmol Soc
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