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Postoperative Corneal Edema

  • Author: Michael Taravella, MD; Chief Editor: John D Sheppard, Jr, MD, MMSc  more...
Updated: Mar 03, 2016


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. See the image below.

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.

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.



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, 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]




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.

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, and 1.5% for iris fixated lenses.[3, 4, 5] 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).[6, 7] See the image below.

Pseudophakic bullous keratopathy. This patient has Pseudophakic bullous keratopathy. This patient has a closed-loop anterior chamber intraocular lens (Leiske model).

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.[8, 9] This overall drop in the incidence of PBK reflects the rapid development and improvement of both intraocular lens design and cataract surgical technique.


Trends similar to that in the United States have been noted in Canada, United Kingdom, Australia, and Scandinavia.[10, 11, 12, 13]


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).


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.


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

Contributor Information and Disclosures

Michael Taravella, MD Director of Cornea and Refractive Surgery, Rocky Mountain Lions Eye Institute; Professor, Department of Ophthalmology, University of Colorado School of Medicine

Michael Taravella, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, Eye Bank Association of America

Disclosure: Received none from AMO/VISX for consulting.


Mark Walker, MD Medical Director, Laser Eye Connection

Mark Walker, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Christopher J Rapuano, MD Professor, Department of Ophthalmology, Jefferson Medical College of Thomas Jefferson University; Director of the Cornea Service, Co-Director of Refractive Surgery Department, Wills Eye Hospital

Christopher J Rapuano, MD is a member of the following medical societies: American Academy of Ophthalmology, American Ophthalmological Society, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, International Society of Refractive Surgery, Cornea Society, Eye Bank Association of America

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cornea Society, Allergan, Bausch & Lomb, Bio-Tissue, Shire, TearScience, TearLab<br/>Serve(d) as a speaker or a member of a speakers bureau for: Allergan, Bausch & Lomb, Bio-Tissue, TearScience.

Chief Editor

John D Sheppard, Jr, MD, MMSc Professor of Ophthalmology, Microbiology and Molecular Biology, Clinical Director, Thomas R Lee Center for Ocular Pharmacology, Ophthalmology Residency Research Program Director, Eastern Virginia Medical School; President, Virginia Eye Consultants

John D Sheppard, Jr, MD, MMSc is a member of the following medical societies: American Academy of Ophthalmology, American Society for Microbiology, American Society of Cataract and Refractive Surgery, Association for Research in Vision and Ophthalmology, American Uveitis Society

Disclosure: Nothing to disclose.

Additional Contributors

Richard W Allinson, MD Associate Professor, Department of Ophthalmology, Texas A&M University Health Science Center; Senior Staff Ophthalmologist, Scott and White Clinic

Richard W Allinson, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, Texas Medical Association

Disclosure: Nothing to disclose.

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Pseudophakic bullous keratopathy. Large multiple bullae, such as depicted here, are associated with moderate to severe pain and discomfort.
Pseudophakic bullous keratopathy in a patient with a Binkhorst style iris-fixated lens.
Pseudophakic bullous keratopathy. This patient has a closed-loop anterior chamber intraocular lens (Leiske model).
Specular microscopy of a normal cornea. Note the compact, uniform hexagonal appearance of the endothelial cells.
Specular microscopy illustrating moderate polymegathism and polymorphism. This is thought to be evidence of endothelial physiologic stress.
Fuchs endothelial dystrophy. The apparently empty spaces are occupied by guttate.
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