Excerpt from Corneal Melt, Postoperative

Synonyms, Key Words, and Related Terms: postoperative corneal melt, corneal melting, corneal perforation, corneal scarring, corneal epithelial defect, corneal tissue, corneal ulcer, corneal ulceration, cornea, vision loss

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Background: 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.

Pathophysiology: 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.

Frequency:

In the US: Postoperative corneal melts do not occur frequently. However, they tend to occur more in patients with the predisposing factors listed in Causes.

Mortality/Morbidity: Depending on the severity and location of the melt, the vision may be minimally or severely affected.

Race: Postoperative corneal melts are more common in less advanced counties, where nutritional deficiencies play a major part in the health of the cornea.

Sex: 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.

Age: 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.