Excerpt from Corneal Edema, Postoperative

Synonyms, Key Words, and Related Terms: postoperative corneal edema, pseudophakic bullous keratopathy, PBK, aphakic bullous keratopathy, ABK, pseudophakic corneal edema, aphakic corneal edema, cataract surgery

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Background: Pseudophakic bullous keratopathy (PBK) and aphakic bullous keratopathy (ABK) refer to the development of irreversible corneal edema as a complication of cataract surgery. As corneal edema progresses and worsens, first stromal and then intercellular epithelial edema develops. Epithelial edema is associated with the development of bullae; hence, the name bullous keratopathy. The history of PBK parallels the history of the development of the intraocular lens. As surgical techniques and lens design have improved, the incidence of this complication has decreased dramatically. However, it still represents an important cause of visual disability following routine and complicated cataract surgery.

Pathophysiology: Corneal transparency is, in a large part, dependent on the ability of the cornea to remain in a dehydrated state. It is affected by several interdependent factors. The epithelium and the endothelium are both semipermeable membranes that create a barrier to the flow of water and other electrolytes into the cornea. Evaporation from the corneal tear film results in slightly hypertonic tears that tend to draw fluid out of the cornea. Intraocular pressure tends to drive fluid into the cornea. Osmotic forces and the electrolyte balance within the corneal stroma also tend to draw water into the cornea. However, the most important influence on corneal deturgescence is the presence of an active metabolic pump in the endothelium.

The endothelium is a single layer of cells present on the back of the cornea. The site of the metabolic pump is within the lateral cell membrane; it is temperature dependent, associated with the enzyme Na⁺/K⁺ ATPase, and it is inhibited by ouabain. Endothelial cells produce a basement membrane (Descemet membrane), and they are of neuroectodermal origin. Cell density at birth can be as high as 7500 cells/mm², decreasing to an average of about 2500-2700 cells/mm² in older adults.

Endothelial cells are not capable of significant mitotic activity. The normal rate of endothelial loss after age 20 is approximately 0.5% per year. Surgical trauma, inflammation, and corneal dystrophies can accelerate this normal aging loss. The final common pathway in the development of bullous keratopathy is damage to the corneal endothelium; when the cell density reaches a critically low level of about 300-500 cells/mm², corneal edema develops.

Frequency:

In the US: Exact incidence of PBK is unknown; however, it currently is estimated that 0.1% of patients undergoing cataract surgery will develop this problem. Food and Drug Administration premarket approval studies for intraocular lenses performed from 1978-1982 found an incidence of postoperative corneal edema of 0.06% for posterior chamber lenses, 1.2% for anterior chamber lenses, and 1.5% for iris fixated lenses. Certain styles of intraocular lenses introduced in the mid 1980s were reported to have an incidence as high as 5% (Leiske and Hessburg closed loop anterior chamber intraocular lenses, ORC Stableflex, and Azar model 91Z).
From 1984-1989, ABK and PBK accounted for the majority of corneal transplants performed in the US (about 33%). Since then, the number of cases has decreased, despite an increase in the number of overall cataract surgeries performed. Keratoconus surpassed PBK in 1990 as the leading indication for corneal transplantation in some studies in the US. This overall drop in the incidence of PBK reflects the rapid development and improvement of both intraocular lens design and cataract surgical technique.

Internationally: Trends similar to the US have been noted in Canada, United Kingdom, Australia, and Scandinavia.

Race: No known association of PBK with se .....