A new technique for the vital staining of the corneal endothelium

tion and irrigation of the anterior chamber, and although lens design with surface protuberances may be of some importance, it is clear that a biophysical interaction between methacrylate and the corneal endothelial surface produces extensive cell damage. It appears that the methacrylate adheres instantaneously to the endothelial surface, and with separation of the two surfaces the anterior membranes of the endothelial cells are torn off. The membranes are seen, by SEM, to remain adherent to the methacrylate surface. Other substances such as glass and stainless steel are capable of producing similar endothelial damage. In contrast, the natural lens appears to cause no damage when it is touched to the endothelium. We feel, therefore, that this is a surface problem of these materials and is not due to the chemical makeup of the materials per se. When a portion of the glass sphere is covered with a soft lens, corneal endothelial damage occurs only in areas of direct contact between the endothelium and the glass. If, in fact, the intraocular lens could be kept away from the endothelium and the chamber never lost, during lens implantation, the type of damage described in this investigation would not occur. It has been our experience, however, that placement of the intraocular lens into the eye with removal of the lens holder and suturing of the wound, is not always possible without brief touch between the endothelium and the lens. The risk of such touch is greatly increased when the vitreous face bulges forward. Because of the conclusive evidence that contact (no matter how brief) between lens and corneal endothelium can produce significant endothelial damage, we undertook a second investigation to see if we could modify the surface of the lens. We found that a variety of substances could prevent endothelial damage when the lens was dipped into the substance prior to being touched to the endothelium. Two patients have undergone uneventful lens implantation after the lens was dipped into protective solutions and cell loss was 11 per cent with a methylcellulose solution and 9 per cent with a polyvinyl pyrrolidone solution. The importance of endothelial damage at the time of surgery is not absolutely certain, but it is clear that if damage is extensive enough, corneal edema supervenes. Since the human corneal endothelium seems not to regenerate, it may be that if enough endothelial cells are lost at the time of surgery, even if the cornea clears, the death of additional endothelial cells with aging may result in an area of endothelial surface that can no longer be covered by the spreading cells. It seems likely, therefore, that late corneal edema may result in at least some of the patients. If endothelial contact with the methacrylate surface is a major cause of endothelial damage, and if such damage can be easily eliminated, it may not be necessary to withhold intraocular lens insertion from patients with mild endothelial changes. Also, the age criterion for lens insertion may become more flexible if further studies confirm our findings that intraocular lenses do not cause progressive damage to the endothelium and that the major cause of endothelial cell death at the time of surgery can be eliminated.