Postoperative corneal melts may be associated with infectious, inflammatory, or trophic causes. Dellen effects associated with structural or mechanical eyelid problems also may contribute to corneal melts. Nutritional causes are less common in developed countries. Proper management is directed at identifying and correcting associated conditions while supporting the corneal tissue at risk to minimize scarring and to prevent perforation.
The two most common causes of corneal melt are herpes simplex virus (HSV) keratitis and retained lenticular material. Although medroxyprogesterone may not influence the underlying incidence of melt-related complications, which are likely to be associated with other risk factors, especially HSV, it may have a protective effect with regard to melt onset and severity (Hicks, 2003; Eguchi, 2004). Although a history of HSV keratitis was a contraindication to AlphaCor in the past (Hicks, 2002), a history of HSV alone is no longer considered a contraindication. In cases of corneal melt, however, HSV should be ruled out. Progressive melts are treated with lamellar grafts or are “reversed” for repeated attempts at penetrating keratoplasty (PKP).
Corneal epithelial defects begin the melting process. Failure to reepithelialize leads either to infection or to a trophic process. Immune mediators and collagenase enzymes attack the exposed stroma, and inflammatory cells further compound progression of ulcerative melting. The corneal epithelium plays a very important role in maintaining the health of the corneal surface. This is because of its rapid self-growing capacity. Important progenitor cells are located at the limbus, which multiply and migrate to the area of disease. These cells are known as limbal stem cells, and their deficiency plays a very important role in postoperative corneal problems.
Among all corneal insults, chronic inflammation at the limbus appears to be a common denominator for postoperative corneal melting. The limbal stem cells serve as a proliferative barrier between corneal and conjunctival epithelia. Conditions that severely damage the limbal stem cells can result in an invasion of conjunctival epithelium onto the corneal surface. This process of conjunctivalization results in thickened, irregular, unstable epithelium often with secondary neovascularization and inflammatory cell infiltration. Epithelial defects are common in a conjunctivalized corneal surface and may lead to corneal ulceration, melting, and loss of vision.
A cornea denuded of epithelium resists collagenolysis poorly. Any delay in reepithelialization can favor corneal melting. For example, damage to the deep limbal crypts and their normal reserves of basal epithelial cells may destroy important sources for reepithelialization of the cornea. It also is possible that the chemically burned eye, metabolically deprived from changes in pH and glucose levels of the anterior chamber, may need the normally insignificant limbal vascular routes of nutrition to survive. If these routes are no longer functional because of massive thrombosis, then the integrity of the cornea is threatened, and sterile necrosis leading to melting syndrome may be inevitable.
Gottsch and Liu propose that a natural protein triggers an immune assault on the eye that can lead to corneal melt. They discovered that Mooren ulcer, the painful ulceration of the cornea, is an autoimmune disorder. The body launches an attack on CO-ag (cornea-associated antigen), located only in the cornea.
Postoperative corneal melts do not occur frequently. However, they tend to occur more in patients with the predisposing factors listed in Causes.
Depending on the severity and location of the melt, the vision may be minimally or severely affected.
Postoperative corneal melts are more common in less advanced counties, where nutritional deficiencies play a major part in the health of the cornea.
Because corneal melts are common in people with collagen disorders and in those with rheumatoid arthritis, they tend to occur more often in females than in males.
Postoperative corneal melts commonly occur in patients with compromised corneas who are in their fourth or fifth decades or even in those who are elderly.
Corneal melting (including post-operative corneal melting), a condition that may lead to corneal perforation (open injury), is often an indication of a systemic disease, such as rheumatoid arthritis or lupus, therefore requiring systemic treatment rather than just topical eye drop application.
It is extremely important that patients be treated by an expert physician who specializes and understands the process of eye melt, which can be a presenting sign of a serious systemic disorder that can benefit dramatically with systemic treatment. The team of physicians and ophthalmologists should be experts at providing ocular and systemic care to patients with such disorders. Drugs used in the treatment of these eye diseases can have significant adverse effects, including bone marrow suppression, and improper use or dosages can be devastating. However, the corneal melt itself can be equally devastating to one’s vision, potentially leading to perforation of the cornea and/or loss of vision. Therefore, the risks and benefits are heavily weighed, and an informed decision is made as to the best course of treatment.
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