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      Drugs & Diseases > Ophthalmology

      Postoperative Corneal Edema

      Updated: Jan 18, 2023
      • Author: Michael Taravella, MD; Chief Editor: John D Sheppard, Jr, MD, MMSc  more...
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      Overview

      Background

      Pseudophakic bullous keratopathy (PBK) and aphakic bullous keratopathy (ABK) refer to the development of irreversible corneal edema as a complication of cataract surgery. [1] 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. 

      Pseudophakic bullous keratopathy. Large multiple b Pseudophakic bullous keratopathy. Large multiple bullae, such as depicted here, are associated with moderate to severe pain and discomfort.
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      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.

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      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 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, it is associated with the enzyme Na+/K+ ATPase, and it is inhibited by ouabain. Endothelial cells produce a basement membrane (the 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 years 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. [2]

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      Epidemiology

      Frequency

      United States

      The exact incidence of PBK is unknown; however, it is estimated that 0.1% of patients undergoing cataract surgery will develop this problem. It is higher is patients with Fuchs dystrophy with a rate of PBK requiring endothelial keratoplasty of 3.3% at 1 year after cataract surgery. [3]

      The US Food and Drug Administration (FDA) 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, 1.5% for iris fixated lenses, and up to 4% for scleral fixated lenses. [4, 5, 6]   [7] Certain styles of intraocular lenses introduced in the mid 1980s were reported to have an incidence as high as 5% (eg, Leiske and Hessburg closed loop anterior chamber intraocular lenses, ORC Stableflex, Azar model 91Z). [8, 9]  

      Pseudophakic bullous keratopathy. This patient has Pseudophakic bullous keratopathy. This patient has a closed-loop anterior chamber intraocular lens (Leiske model).
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      From 1984-1989, ABK and PBK accounted for most corneal transplants (about 33%) performed in the United States. 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 United States. [10, 11] This overall drop in the incidence of PBK reflects the rapid development and improvement of both intraocular lens design and cataract surgical technique.

      International

      Trends similar to that in the United States have been noted in Canada, United Kingdom, Australia, and Scandinavia. [12, 13, 14, 15]

      Race

      No known association of PBK with race exists.

      Patients of Northern European descent do have an increased incidence of Fuchs corneal dystrophy. This dystrophy does predispose to the development of corneal edema (see Pathophysiology, Causes, Histologic Findings).

      Sex

      No known association of PBK with sex exists.

      Fuchs corneal dystrophy, a known predisposing factor in the development of postoperative corneal edema, occurs approximately 3 times more frequently in women than in men.

      Age

      Older patients who have less endothelial reserve are more prone to develop this problem.

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      Prognosis

      Prognosis is good following surgical intervention for PBK. Corneal transplant is a definitive treatment. It can be done in the form of penetrating keratoplasty (PK), Descemet membrane endothelial keratoplasty (DMEK), or Descemet stripping automated endothelial keratoplasty (DSAEK). A patient who undergoes EK can expect mean corrected distance visual acuity (CDVA) 20/25 to 20/30 at 1 year after DSAEK, and 89% of DMEK patients can expect CDVA ≥20/25 also at 1 year. [16, 17]

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