Postoperative Corneal Edema 

  • Author: Michael Taravella, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: May 11, 2009
 

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 bPseudophakic 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.

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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 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]

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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.

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]

Pseudophakic bullous keratopathy. This patient hasPseudophakic 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] 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.[9, 10, 11, 12]

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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Contributor Information and Disclosures
Author

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, and Eye Bank Association of America

Disclosure: Nothing to disclose.

Coauthor(s)

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, and Contact Lens Association of Ophthalmologists

Disclosure: Nothing to disclose.

Specialty Editor Board

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, and Texas Medical Association

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD  Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

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 Institute

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

Disclosure: Allergan Honoraria Speaking and teaching; Allergan Consulting fee Consulting; Alcon Honoraria Speaking and teaching; RPS Ownership interest Other; EyeGate Pharma Consulting fee Consulting; Bausch & Lomb Honoraria Speaking and teaching; Bausch & Lomb Consulting; Merck Honoraria Speaking and teaching

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD  Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

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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