|Year : 1983 | Volume
| Issue : 5 | Page : 667-668
Management of corneal thinning and perforation
Deptt. Of Ophthal., West Virginia University, School of Medicine, Morgantown, WV 26506, USA
V K Raju
Deptt. Of Ophthal., West Virginia University, School of Medicine, Morgantown, WV 26506
|How to cite this article:|
Raju V K. Management of corneal thinning and perforation. Indian J Ophthalmol 1983;31:667-8
The problems of corneal thinning and perforation are not uncommon and require prompt and proper treatment. This paper essentially deals with some principles for better understanding of these problems and guidelines to follow in their prevention and management.
Etiology and Pathogenesis:
The conditions in which corneal thinning and perforation occur involve disease processes such as infection, inflammation, trauma, and degeneration. Herpes Simplex, rheumatoid arthritis, and alkali burns account for the majority patients seen. The single most important event leading to corneal thinning and perforation is persistent epithelial defect. The importance of corneal epithelium in maintaining the corneal integrity has been extensively reviewed by Dohlman.  Regardless of the cause of the epithelial defect, if re-epithelialization does not occur, the potential for corneal thinning and perforation exists. Alterations in the basement membrane of the epithelial cells may be the cause of persistent epithelial defects in most of the cases.
Although the epithelium is an effective barrier to infection, some organisms can penetrate the intact corneal epithelium (eg: gonococccus, Koch-Weeks bacillus, and C. Diphtheriae).
Stromal melting by proteolytic enzymes elaborated by altered epithelial cells and polymorphonuclear leucocytes has been demonstrated in experimental animals and in vitro in human corneas. , Topical steroids potentiate this melting process. In conditions like rheumatoid arthritis and chemical burns there may be altered stromal collagen that contributes to further corneal melting. Stromal wound repair seems to be defective in these conditions leading to perforation. Bowman's membrane and corneal stroma are not effective barriers to microorganisms, but the elastic Descemet's membrane is an effective barrier which prevents perforation of the cornea for a number of days. When most of the stroma melts away, the Descemet's membrane bulges forward, forming a descemetocele.
Corneal thinning: The general principles for treatment of corneal thinning are the same regardless of cause. Treatment is directed toward healing of the epithelial defect, inhibiting stromal melting, and stimulating stromal fibroplasia and vascularization. A simple and effective measure to promote re-epithelization of the cornea is a pressure bandage. Soft contact lenses used as a bandage are a significant advance in the treatment of corneal thinning. These lenses may be used in conjunction with all forms of eye drops. Ointments should not be used with soft contact lenses since the ointment base can accumulate on the lens.
The value of collagenase inhibitors in the treatment of corneal thinning is still debated. There may be many proteolytic enzymes just as important as collagenase. There is no general agreement about which inhibitor to use. The commonly recommended inhibitors are cysteine, acetyl cysteine, and ethylene diaminetetracetic acid (EDTA). Of these, acetyl crysteine is the only readily available drug. It should be used at least one drop every two hours around the clock and continued until complete re-epithelialization occurs. A thin total conjunctival flap as described by Gunderson  is a very effective method for management of corneal thinning. This method is especially useful when other methods have failed. If needed, penetrating corneal transplantation can be performed through the conjunctival flap at a later date. It is best to avoid penetrating keratoplasty during active inflammatory process. Lamellar keratoplasty may be useful in certain patients with corneal thinning.
Regardless of the etiology, when the corneal perforation occurs the general methods of treatment are the same (i.e. pressure bandage, soft lens, conjunctival flap, etc.). The use of a pressure bandage can often aid in healing a non-infected perforation. Prophylactic antibiotics such as Gentamycin drops should be used. Tissue adhesives (eg. cyanoacrylate glue) may be used to seal small corneal perforations.
Perforations larger than 1 mm. are usually not successfully sealed with this adhesive. For larger perforations or if tissue adhesive is not available, a blowout patch of preserved cornea may be used or lamellar keratoplasty may be performed. A bandage soft contact lens can be used postoperatively to facilitate re-epithelialization.
If perforations are due to infectious ulcers, specific treatment of the offending organism must be instituted. Herpes Simplex keratitis presents unusual problems in the management, and injudicious use of cortico-steroids in this disease should be avoided. If steroids are given, the smallest possible dose in conjunction with an antiviral agent should be used. It is important to remember that overuse of antiviral agents or antibiotics will inhibit reepithealization.
| Summary|| |
The single most important even in the etiology of corneal thinning and perforation is persistent epithelial defect. The treatment modalities should be aimed at correcting the condition creating the defect as well as facilitating re-epithelialization.
| References|| |
|1.||Dohlman, C.H., Invest. Ophthalmol., 10, 376, 1971. |
|2.||Brown, S.I., & Hook, C.W., Am. J. Ophthalmo1, 72, 1138, 1971. |
|3.||Slansky, H.H., et al. Arch. Ophthalmol., 82,108, 1969. |
|4.||Gunderson, T., Arch. of Ophthalmol, 60, 880, 1958. |